meta/bib.txt

@ARTICLE{Ji2020-dp,
  title     = "Multimodal analysis of composition and spatial architecture in
               human squamous cell carcinoma",
  author    = "Ji, Andrew L and Rubin, Adam J and Thrane, Kim and Jiang, Sizun
               and Reynolds, David L and Meyers, Robin M and Guo, Margaret G
               and George, Benson M and Mollbrink, Annelie and
               Bergenstr{\aa}hle, Joseph and Larsson, Ludvig and Bai, Yunhao
               and Zhu, Bokai and Bhaduri, Aparna and Meyers, Jordan M and
               Rovira-Clav{\'e}, Xavier and Hollmig, S Tyler and Aasi, Sumaira
               Z and Nolan, Garry P and Lundeberg, Joakim and Khavari, Paul A",
  abstract  = "To define the cellular composition and architecture of cutaneous
               squamous cell carcinoma (cSCC), we combined single-cell RNA
               sequencing with spatial transcriptomics and multiplexed ion beam
               imaging from a series of human cSCCs and matched normal skin.
               cSCC exhibited four tumor subpopulations, three recapitulating
               normal epidermal states, and a tumor-specific keratinocyte (TSK)
               population unique to cancer, which localized to a fibrovascular
               niche. Integration of single-cell and spatial data mapped
               ligand-receptor networks to specific cell types, revealing TSK
               cells as a hub for intercellular communication. Multiple
               features of potential immunosuppression were observed, including
               T regulatory cell (Treg) co-localization with CD8 T cells in
               compartmentalized tumor stroma. Finally, single-cell
               characterization of human tumor xenografts and in vivo CRISPR
               screens identified essential roles for specific tumor
               subpopulation-enriched gene networks in tumorigenesis. These
               data define cSCC tumor and stromal cell subpopulations, the
               spatial niches where they interact, and the communicating gene
               networks that they engage in cancer.",
  journal   = "Cell",
  publisher = "Elsevier BV",
  volume    =  182,
  number    =  2,
  pages     = "497--514.e22",
  month     =  jul,
  year      =  2020,
  keywords  = "CRISPR screen; MIBI; intra-tumoral heterogeneity; multi-omics;
               scRNA-seq; skin cancer; spatial transcriptomics; squamous cell
               carcinoma; tumor immunology; tumor microenvironment",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Chen2023-zm,
  title    = "{STmut}: a framework for visualizing somatic alterations in
              spatial transcriptomics data of cancer",
  author   = "Chen, Limin and Chang, Darwin and Tandukar, Bishal and
              Deivendran, Delahny and Pozniak, Joanna and Cruz-Pacheco, Noel
              and Cho, Raymond J and Cheng, Jeffrey and Yeh, Iwei and Marine,
              Chris and Bastian, Boris C and Ji, Andrew L and Shain, A Hunter",
  abstract = "Spatial transcriptomic technologies, such as the Visium platform,
              measure gene expression in different regions of tissues. Here, we
              describe new software, STmut, to visualize somatic point
              mutations, allelic imbalance, and copy number alterations in
              Visium data. STmut is tested on fresh-frozen Visium data,
              formalin-fixed paraffin-embedded (FFPE) Visium data, and tumors
              with and without matching DNA sequencing data. Copy number is
              inferred on all conditions, but the chemistry of the FFPE
              platform does not permit analyses of single nucleotide variants.
              Taken together, we propose solutions to add the genetic dimension
              to spatial transcriptomic data and describe the limitations of
              different datatypes.",
  journal  = "Genome Biol.",
  volume   =  24,
  number   =  1,
  pages    = "273",
  month    =  nov,
  year     =  2023,
  language = "en"
}

@ARTICLE{Andersson2021-nr,
  title     = "Spatial deconvolution of {HER2-positive} breast cancer
               delineates tumor-associated cell type interactions",
  author    = "Andersson, Alma and Larsson, Ludvig and Stenbeck, Linnea and
               Salm{\'e}n, Fredrik and Ehinger, Anna and Wu, Sunny Z and
               Al-Eryani, Ghamdan and Roden, Daniel and Swarbrick, Alex and
               Borg, {\AA}ke and Fris{\'e}n, Jonas and Engblom, Camilla and
               Lundeberg, Joakim",
  abstract  = "In the past decades, transcriptomic studies have revolutionized
               cancer treatment and diagnosis. However, tumor sequencing
               strategies typically result in loss of spatial information,
               critical to understand cell interactions and their functional
               relevance. To address this, we investigate spatial gene
               expression in HER2-positive breast tumors using Spatial
               Transcriptomics technology. We show that expression-based
               clustering enables data-driven tumor annotation and assessment
               of intra- and interpatient heterogeneity; from which we discover
               shared gene signatures for immune and tumor processes. By
               integration with single cell data, we spatially map
               tumor-associated cell types to find tertiary lymphoid-like
               structures, and a type I interferon response overlapping with
               regions of T-cell and macrophage subset colocalization. We
               construct a predictive model to infer presence of tertiary
               lymphoid-like structures, applicable across tissue types and
               technical platforms. Taken together, we combine different data
               modalities to define a high resolution map of cellular
               interactions in tumors and provide tools generalizing across
               tissues and diseases.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  12,
  number    =  1,
  pages     = "6012",
  month     =  oct,
  year      =  2021,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

% The entry below contains non-ASCII chars that could not be converted
% to a LaTeX equivalent.
@ARTICLE{He2020-de,
  title     = "Integrating spatial gene expression and breast tumour morphology
               via deep learning",
  author    = "He, Bryan and Bergenstr{\aa}hle, Ludvig and Stenbeck, Linnea and
               Abid, Abubakar and Andersson, Alma and Borg, {\AA}ke and
               Maaskola, Jonas and Lundeberg, Joakim and Zou, James",
  abstract  = "Spatial transcriptomics allows for the measurement of RNA
               abundance at a high spatial resolution, making it possible to
               systematically link the morphology of cellular neighbourhoods
               and spatially localized gene expression. Here, we report the
               development of a deep learning algorithm for the prediction of
               local gene expression from haematoxylin-and-eosin-stained
               histopathology images using a new dataset of 30,612 spatially
               resolved gene expression data matched to histopathology images
               from 23 patients with breast cancer. We identified over 100
               genes, including known breast cancer biomarkers of intratumoral
               heterogeneity and the co-localization of tumour growth and
               immune activation, the expression of which can be predicted from
               the histopathology images at a resolution of 100 µm. We also
               show that the algorithm generalizes well to The Cancer Genome
               Atlas and to other breast cancer gene expression datasets
               without the need for re-training. Predicting the spatially
               resolved transcriptome of a tissue directly from tissue images
               may enable image-based screening for molecular biomarkers with
               spatial variation.",
  journal   = "Nat. Biomed. Eng.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  4,
  number    =  8,
  pages     = "827--834",
  month     =  aug,
  year      =  2020,
  copyright = "https://www.springernature.com/gp/researchers/text-and-data-mining",
  language  = "en"
}

@ARTICLE{Stahl2016-zf,
  title     = "Visualization and analysis of gene expression in tissue sections
               by spatial transcriptomics",
  author    = "St{\aa}hl, Patrik L and Salm{\'e}n, Fredrik and Vickovic, Sanja
               and Lundmark, Anna and Navarro, Jos{\'e} Fern{\'a}ndez and
               Magnusson, Jens and Giacomello, Stefania and Asp, Michaela and
               Westholm, Jakub O and Huss, Mikael and Mollbrink, Annelie and
               Linnarsson, Sten and Codeluppi, Simone and Borg, {\AA}ke and
               Pont{\'e}n, Fredrik and Costea, Paul Igor and Sahl{\'e}n, Pelin
               and Mulder, Jan and Bergmann, Olaf and Lundeberg, Joakim and
               Fris{\'e}n, Jonas",
  abstract  = "Spatial structure of RNA expression RNA-seq and similar methods
               can record gene expression within and among cells. Current
               methods typically lose positional information and many require
               arduous single-cell isolation and sequencing. St{\aa}hl et al.
               have developed a way of measuring the spatial distribution of
               transcripts by annealing fixed brain or cancer tissue samples
               directly to bar-coded reverse transcriptase primers, performing
               reverse transcription followed by sequencing and computational
               reconstruction, and they can do so for multiple genes. Science ,
               this issue p. 78",
  journal   = "Science",
  publisher = "American Association for the Advancement of Science (AAAS)",
  volume    =  353,
  number    =  6294,
  pages     = "78--82",
  month     =  jul,
  year      =  2016,
  copyright = "http://www.sciencemag.org/about/science-licenses-journal-article-reuse",
  language  = "en"
}

@ARTICLE{Asp2019-ga,
  title     = "A spatiotemporal organ-wide gene expression and cell atlas of
               the developing human heart",
  author    = "Asp, Michaela and Giacomello, Stefania and Larsson, Ludvig and
               Wu, Chenglin and F{\"u}rth, Daniel and Qian, Xiaoyan and
               W{\"a}rdell, Eva and Custodio, Joaquin and Reimeg{\aa}rd, Johan
               and Salm{\'e}n, Fredrik and {\"O}sterholm, Cecilia and
               St{\aa}hl, Patrik L and Sundstr{\"o}m, Erik and {\AA}kesson,
               Elisabet and Bergmann, Olaf and Bienko, Magda and
               M{\aa}nsson-Broberg, Agneta and Nilsson, Mats and Sylv{\'e}n,
               Christer and Lundeberg, Joakim",
  abstract  = "The process of cardiac morphogenesis in humans is incompletely
               understood. Its full characterization requires a deep
               exploration of the organ-wide orchestration of gene expression
               with a single-cell spatial resolution. Here, we present a
               molecular approach that reveals the comprehensive
               transcriptional landscape of cell types populating the embryonic
               heart at three developmental stages and that maps
               cell-type-specific gene expression to specific anatomical
               domains. Spatial transcriptomics identified unique gene profiles
               that correspond to distinct anatomical regions in each
               developmental stage. Human embryonic cardiac cell types
               identified by single-cell RNA sequencing confirmed and enriched
               the spatial annotation of embryonic cardiac gene expression. In
               situ sequencing was then used to refine these results and create
               a spatial subcellular map for the three developmental phases.
               Finally, we generated a publicly available web resource of the
               human developing heart to facilitate future studies on human
               cardiogenesis.",
  journal   = "Cell",
  publisher = "Elsevier BV",
  volume    =  179,
  number    =  7,
  pages     = "1647--1660.e19",
  month     =  dec,
  year      =  2019,
  keywords  = "gene expression; heart development; human development; human
               developmental cell atlas; in situ sequencing; single-cell
               RNA-sequencing; spatial transcriptomics; spatially resolved
               transcriptomics",
  copyright = "http://www.elsevier.com/open-access/userlicense/1.0/",
  language  = "en"
}

@ARTICLE{Hasel2021-pg,
  title     = "Neuroinflammatory astrocyte subtypes in the mouse brain",
  author    = "Hasel, Philip and Rose, Indigo V L and Sadick, Jessica S and
               Kim, Rachel D and Liddelow, Shane A",
  abstract  = "Astrocytes undergo an inflammatory transition after infections,
               acute injuries and chronic neurodegenerative diseases. How this
               transition is affected by time and sex, its heterogeneity at the
               single-cell level and how sub-states are spatially distributed
               in the brain remains unclear. In this study, we investigated
               transcriptome changes of mouse cortical astrocytes after an
               acute inflammatory stimulus using the bacterial cell wall
               endotoxin lipopolysaccharide. We identified fast transcriptomic
               changes in astrocytes occurring within hours that drastically
               change over time. By sequencing ~80,000 astrocytes at
               single-cell resolution, we show that inflammation causes a
               widespread response with subtypes of astrocytes undergoing
               distinct inflammatory transitions with defined transcriptomic
               profiles. We also attribute key sub-states of
               inflammation-induced reactive astrocytes to specific brain
               regions using spatial transcriptomics and in situ hybridization.
               Together, our datasets provide a powerful resource for profiling
               astrocyte heterogeneity and will be useful for understanding the
               biological importance of regionally constrained reactive
               astrocyte sub-states.",
  journal   = "Nat. Neurosci.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  24,
  number    =  10,
  pages     = "1475--1487",
  month     =  oct,
  year      =  2021,
  copyright = "https://www.springernature.com/gp/researchers/text-and-data-mining",
  language  = "en"
}

@ARTICLE{Ratz2022-fl,
  title     = "Clonal relations in the mouse brain revealed by single-cell and
               spatial transcriptomics",
  author    = "Ratz, Michael and von Berlin, Leonie and Larsson, Ludvig and
               Martin, Marcel and Westholm, Jakub Orzechowski and La Manno,
               Gioele and Lundeberg, Joakim and Fris{\'e}n, Jonas",
  abstract  = "The mammalian brain contains many specialized cells that develop
               from a thin sheet of neuroepithelial progenitor cells.
               Single-cell transcriptomics revealed hundreds of molecularly
               diverse cell types in the nervous system, but the lineage
               relationships between mature cell types and progenitor cells are
               not well understood. Here we show in vivo barcoding of early
               progenitors to simultaneously profile cell phenotypes and clonal
               relations in the mouse brain using single-cell and spatial
               transcriptomics. By reconstructing thousands of clones, we
               discovered fate-restricted progenitor cells in the mouse
               hippocampal neuroepithelium and show that microglia are derived
               from few primitive myeloid precursors that massively expand to
               generate widely dispersed progeny. We combined spatial
               transcriptomics with clonal barcoding and disentangled migration
               patterns of clonally related cells in densely labeled tissue
               sections. Our approach enables high-throughput dense
               reconstruction of cell phenotypes and clonal relations at the
               single-cell and tissue level in individual animals and provides
               an integrated approach for understanding tissue architecture.",
  journal   = "Nat. Neurosci.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  25,
  number    =  3,
  pages     = "285--294",
  month     =  mar,
  year      =  2022,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Lebrigand2023-im,
  title     = "The spatial landscape of gene expression isoforms in tissue
               sections",
  author    = "Lebrigand, Kevin and Bergenstr{\aa}hle, Joseph and Thrane, Kim
               and Mollbrink, Annelie and Meletis, Konstantinos and Barbry,
               Pascal and Waldmann, Rainer and Lundeberg, Joakim",
  abstract  = "In situ capturing technologies add tissue context to gene
               expression data, with the potential of providing a greater
               understanding of complex biological systems. However, splicing
               variants and full-length sequence heterogeneity cannot be
               characterized at spatial resolution with current transcriptome
               profiling methods. To that end, we introduce spatial isoform
               transcriptomics (SiT), an explorative method for characterizing
               spatial isoform variation and sequence heterogeneity using
               long-read sequencing. We show in mouse brain how SiT can be used
               to profile isoform expression and sequence heterogeneity in
               different areas of the tissue. SiT reveals regional isoform
               switching of Plp1 gene between different layers of the olfactory
               bulb, and the use of external single-cell data allows the
               nomination of cell types expressing each isoform. Furthermore,
               SiT identifies differential isoform usage for several major
               genes implicated in brain function (Snap25, Bin1, Gnas) that are
               independently validated by in situ sequencing. SiT also provides
               for the first time an in-depth A-to-I RNA editing map of the
               adult mouse brain. Data exploration can be performed through an
               online resource (https://www.isomics.eu), where isoform
               expression and RNA editing can be visualized in a spatial
               context.",
  journal   = "Nucleic Acids Res.",
  publisher = "Oxford University Press (OUP)",
  volume    =  51,
  number    =  8,
  pages     = "e47",
  month     =  may,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by-nc/4.0/",
  language  = "en"
}

@ARTICLE{Joglekar2021-xs,
  title     = "A spatially resolved brain region- and cell type-specific
               isoform atlas of the postnatal mouse brain",
  author    = "Joglekar, Anoushka and Prjibelski, Andrey and Mahfouz, Ahmed and
               Collier, Paul and Lin, Susan and Schlusche, Anna Katharina and
               Marrocco, Jordan and Williams, Stephen R and Haase, Bettina and
               Hayes, Ashley and Chew, Jennifer G and Weisenfeld, Neil I and
               Wong, Man Ying and Stein, Alexander N and Hardwick, Simon A and
               Hunt, Toby and Wang, Qi and Dieterich, Christoph and Bent,
               Zachary and Fedrigo, Olivier and Sloan, Steven A and Risso,
               Davide and Jarvis, Erich D and Flicek, Paul and Luo, Wenjie and
               Pitt, Geoffrey S and Frankish, Adam and Smit, August B and Ross,
               M Elizabeth and Tilgner, Hagen U",
  abstract  = "Splicing varies across brain regions, but the single-cell
               resolution of regional variation is unclear. We present a
               single-cell investigation of differential isoform expression
               (DIE) between brain regions using single-cell long-read
               sequencing in mouse hippocampus and prefrontal cortex in 45 cell
               types at postnatal day 7 ( www.isoformAtlas.com ). Isoform tests
               for DIE show better performance than exon tests. We detect
               hundreds of DIE events traceable to cell types, often
               corresponding to functionally distinct protein isoforms. Mostly,
               one cell type is responsible for brain-region specific DIE.
               However, for fewer genes, multiple cell types influence DIE.
               Thus, regional identity can, although rarely, override cell-type
               specificity. Cell types indigenous to one anatomic structure
               display distinctive DIE, e.g. the choroid plexus epithelium
               manifests distinct transcription-start-site usage. Spatial
               transcriptomics and long-read sequencing yield a spatially
               resolved splicing map. Our methods quantify isoform expression
               with cell-type and spatial resolution and it contributes to
               further our understanding of how the brain integrates molecular
               and cellular complexity.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  12,
  number    =  1,
  pages     = "463",
  month     =  jan,
  year      =  2021,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Mikheenko2022-ql,
  title     = "Sequencing of individual barcoded {cDNAs} using Pacific
               Biosciences and Oxford Nanopore Technologies reveals
               platform-specific error patterns",
  author    = "Mikheenko, Alla and Prjibelski, Andrey D and Joglekar, Anoushka
               and Tilgner, Hagen U",
  abstract  = "Long-read transcriptomics require understanding error sources
               inherent to technologies. Current approaches cannot compare
               methods for an individual RNA molecule. Here, we present a novel
               platform-comparison method that combines barcoding strategies
               and long-read sequencing to sequence cDNA copies representing an
               individual RNA molecule on both Pacific Biosciences (PacBio) and
               Oxford Nanopore Technologies (ONT). We compare these long-read
               pairs in terms of sequence content and isoform patterns.
               Although individual read pairs show high similarity, we find
               differences in (1) aligned length, (2) transcription start site
               (TSS), (3) polyadenylation site (poly(A)-site) assignment, and
               (4) exon-intron structures. Overall, 25\% of read pairs disagree
               on either TSS, poly(A)-site, or splice site. Intron-chain
               disagreement typically arises from alignment errors of
               microexons and complicated splice sites. Our single-molecule
               technology comparison reveals that inconsistencies are often
               caused by sequencing error-induced inaccurate ONT alignments,
               especially to downstream GUNNGU donor motifs. However,
               annotation-disagreeing upstream shifts in NAGNAG acceptors in
               ONT are often confirmed by PacBio and are thus likely real. In
               both barcoded and nonbarcoded ONT reads, we find that intron
               number and proximity of GU/AGs better predict inconsistencies
               with the annotation than read quality alone. We summarize these
               findings in an annotation-based algorithm for spliced alignment
               correction that improves subsequent transcript construction with
               ONT reads.",
  journal   = "Genome Res.",
  publisher = "Cold Spring Harbor Laboratory",
  volume    =  32,
  number    =  4,
  pages     = "726--737",
  month     =  apr,
  year      =  2022,
  language  = "en"
}

@ARTICLE{Stein2022-ia,
  title     = "{ScisorWiz}: visualizing differential isoform expression in
               single-cell long-read data",
  author    = "Stein, Alexander N and Joglekar, Anoushka and Poon, Chi-Lam and
               Tilgner, Hagen U",
  abstract  = "SUMMARY: RNA isoforms contribute to the diverse functionality of
               the proteins they encode within the cell. Visualizing how
               isoform expression differs across cell types and brain regions
               can inform our understanding of disease and gain or loss of
               functionality caused by alternative splicing with potential
               negative impacts. However, the extent to which this occurs in
               specific cell types and brain regions is largely unknown. This
               is the kind of information that ScisorWiz plots can provide in
               an informative and easily communicable manner. ScisorWiz affords
               its user the opportunity to visualize specific genes across any
               number of cell types, and provides various sorting options for
               the user to gain different ways to understand their data.
               ScisorWiz provides a clear picture of differential isoform
               expression through various clustering methods and highlights
               features such as alternative exons and single-nucleotide
               variants. Tools like ScisorWiz are key for interpreting
               single-cell isoform sequencing data. This tool applies to any
               single-cell long-read RNA sequencing data in any cell type,
               tissue or species. AVAILABILITY AND IMPLEMENTATION: Source code
               is available at http://github.com/ans4013/ScisorWiz. No new data
               were generated for this publication. Data used to generate
               figures was sourced from GEO accession token GSE158450 and
               available on GitHub as example data.",
  journal   = "Bioinformatics",
  publisher = "Oxford University Press (OUP)",
  volume    =  38,
  number    =  13,
  pages     = "3474--3476",
  month     =  jun,
  year      =  2022,
  keywords  = "Computational Neuroscience; Differential Isoform Expression;
               Genetics; RNA Splicing",
  copyright = "https://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Prjibelski2023-dl,
  title     = "Accurate isoform discovery with {IsoQuant} using long reads",
  author    = "Prjibelski, Andrey D and Mikheenko, Alla and Joglekar, Anoushka
               and Smetanin, Alexander and Jarroux, Julien and Lapidus, Alla L
               and Tilgner, Hagen U",
  abstract  = "Annotating newly sequenced genomes and determining alternative
               isoforms from long-read RNA data are complex and incompletely
               solved problems. Here we present IsoQuant-a computational tool
               using intron graphs that accurately reconstructs transcripts
               both with and without reference genome annotation. For novel
               transcript discovery, IsoQuant reduces the false-positive rate
               fivefold and 2.5-fold for Oxford Nanopore reference-based or
               reference-free mode, respectively. IsoQuant also improves
               performance for Pacific Biosciences data.",
  journal   = "Nat. Biotechnol.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  41,
  number    =  7,
  pages     = "915--918",
  month     =  jul,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Bashkirova2023-mr,
  title    = "Opposing, spatially-determined epigenetic forces impose
              restrictions on stochastic olfactory receptor choice",
  author   = "Bashkirova, Elizaveta V and Klimpert, Nell and Monahan, Kevin and
              Campbell, Christine E and Osinski, Jason M and Tan, Longzhi and
              Schieren, Ira and Pourmorady, Ariel and Stecky, Beka and Barnea,
              Gilad and Xie, X Sunnie and Abdus-Saboor, Ishmail and Shykind,
              Benjamin and Jones-Marlin, Bianca and Gronostajski, Richard M and
              Fleischmann, Alexander and Lomvardas, Stavros",
  abstract = "Olfactory receptor (OR) choice represents an example of
              genetically hardwired stochasticity, where every olfactory neuron
              expresses one out of ~2000 OR alleles in a probabilistic, yet
              stereotypic fashion. Here, we propose that topographic
              restrictions in OR expression are established in neuronal
              progenitors by two opposing forces: polygenic transcription and
              genomic silencing, both of which are influenced by dorsoventral
              gradients of transcription factors NFIA, B, and X. Polygenic
              transcription of OR genes may define spatially constrained OR
              repertoires, among which one OR allele is selected for singular
              expression later in development. Heterochromatin assembly and
              genomic compartmentalization of OR alleles also vary across the
              axes of the olfactory epithelium and may preferentially eliminate
              ectopically expressed ORs with more dorsal expression
              destinations from this ``privileged'' repertoire. Our experiments
              identify early transcription as a potential ``epigenetic''
              contributor to future developmental patterning and reveal how two
              spatially responsive probabilistic processes may act in concert
              to establish deterministic, precise, and reproducible territories
              of stochastic gene expression.",
  journal  = "bioRxivorg",
  month    =  sep,
  year     =  2023,
  language = "en"
}

@ARTICLE{Sanchez-Ferras2021-yo,
  title     = "A coordinated progression of progenitor cell states initiates
               urinary tract development",
  author    = "Sanchez-Ferras, Oraly and Pacis, Alain and Sotiropoulou, Maria
               and Zhang, Yuhong and Wang, Yu Chang and Bourgey, Mathieu and
               Bourque, Guillaume and Ragoussis, Jiannis and Bouchard, Maxime",
  abstract  = "The kidney and upper urinary tract develop through reciprocal
               interactions between the ureteric bud and the surrounding
               mesenchyme. Ureteric bud branching forms the arborized
               collecting duct system of the kidney, while ureteric tips
               promote nephron formation from dedicated progenitor cells. While
               nephron progenitor cells are relatively well characterized, the
               origin of ureteric bud progenitors has received little attention
               so far. It is well established that the ureteric bud is induced
               from the nephric duct, an epithelial duct derived from the
               intermediate mesoderm of the embryo. However, the cell state
               transitions underlying the progression from intermediate
               mesoderm to nephric duct and ureteric bud remain unknown. Here
               we show that nephric duct morphogenesis results from the
               coordinated organization of four major progenitor cell
               populations. Using single cell RNA-seq and Cluster RNA-seq, we
               show that these progenitors emerge in time and space according
               to a stereotypical pattern. We identify the transcription
               factors Tfap2a/b and Gata3 as critical coordinators of this
               progenitor cell progression. This study provides a better
               understanding of the cellular origin of the renal collecting
               duct system and associated urinary tract developmental diseases,
               which may inform guided differentiation of functional kidney
               tissue.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  12,
  number    =  1,
  pages     = "2627",
  month     =  may,
  year      =  2021,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Parigi2022-mo,
  title     = "The spatial transcriptomic landscape of the healing mouse
               intestine following damage",
  author    = "Parigi, Sara M and Larsson, Ludvig and Das, Srustidhar and
               Ramirez Flores, Ricardo O and Frede, Annika and Tripathi, Kumar
               P and Diaz, Oscar E and Selin, Katja and Morales, Rodrigo A and
               Luo, Xinxin and Monasterio, Gustavo and Engblom, Camilla and
               Gagliani, Nicola and Saez-Rodriguez, Julio and Lundeberg, Joakim
               and Villablanca, Eduardo J",
  abstract  = "The intestinal barrier is composed of a complex cell network
               defining highly compartmentalized and specialized structures.
               Here, we use spatial transcriptomics to define how the
               transcriptomic landscape is spatially organized in the steady
               state and healing murine colon. At steady state conditions, we
               demonstrate a previously unappreciated molecular regionalization
               of the colon, which dramatically changes during mucosal healing.
               Here, we identified spatially-organized transcriptional programs
               defining compartmentalized mucosal healing, and regions with
               dominant wired pathways. Furthermore, we showed that decreased
               p53 activation defined areas with increased presence of
               proliferating epithelial stem cells. Finally, we mapped
               transcriptomics modules associated with human diseases
               demonstrating the translational potential of our dataset.
               Overall, we provide a publicly available resource defining
               principles of transcriptomic regionalization of the colon during
               mucosal healing and a framework to develop and progress further
               hypotheses.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  13,
  number    =  1,
  pages     = "828",
  month     =  feb,
  year      =  2022,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Tower2021-yy,
  title     = "Spatial transcriptomics reveals a role for sensory nerves in
               preserving cranial suture patency through modulation of
               {BMP/TGF-$\beta$} signaling",
  author    = "Tower, Robert J and Li, Zhu and Cheng, Yu-Hao and Wang, Xue-Wei
               and Rajbhandari, Labchan and Zhang, Qian and Negri, Stefano and
               Uytingco, Cedric R and Venkatesan, Arun and Zhou, Feng-Quan and
               Cahan, Patrick and James, Aaron W and Clemens, Thomas L",
  abstract  = "The patterning and ossification of the mammalian skeleton
               requires the coordinated actions of both intrinsic bone
               morphogens and extrinsic neurovascular signals, which function
               in a temporal and spatial fashion to control mesenchymal
               progenitor cell (MPC) fate. Here, we show the genetic inhibition
               of tropomyosin receptor kinase A (TrkA) sensory nerve
               innervation of the developing cranium results in premature
               calvarial suture closure, associated with a decrease in suture
               MPC proliferation and increased mineralization. In vitro, axons
               from peripheral afferent neurons derived from dorsal root
               ganglions (DRGs) of wild-type mice induce MPC proliferation in a
               spatially restricted manner via a soluble factor when cocultured
               in microfluidic chambers. Comparative spatial transcriptomic
               analysis of the cranial sutures in vivo confirmed a positive
               association between sensory axons and proliferative MPCs.
               SpatialTime analysis across the developing suture revealed
               regional-specific alterations in bone morphogenetic protein
               (BMP) and TGF-$\beta$ signaling pathway transcripts in response
               to TrkA inhibition. RNA sequencing of DRG cell bodies, following
               direct, axonal coculture with MPCs, confirmed the alterations in
               BMP/TGF-$\beta$ signaling pathway transcripts. Among these, the
               BMP inhibitor follistatin-like 1 (FSTL1) replicated key features
               of the neural-to-bone influence, including mitogenic and
               anti-osteogenic effects via the inhibition of BMP/TGF-$\beta$
               signaling. Taken together, our results demonstrate that sensory
               nerve-derived signals, including FSTL1, function to coordinate
               cranial bone patterning by regulating MPC proliferation and
               differentiation in the suture mesenchyme.",
  journal   = "Proc. Natl. Acad. Sci. U. S. A.",
  publisher = "Proceedings of the National Academy of Sciences",
  volume    =  118,
  number    =  42,
  pages     = "e2103087118",
  month     =  oct,
  year      =  2021,
  keywords  = "TrkA; calvarial bone; cranial suture; skeletal innervation;
               spatial transcriptomics",
  copyright = "https://www.pnas.org/site/aboutpnas/licenses.xhtml",
  language  = "en"
}

@ARTICLE{Meylan2022-wt,
  title     = "Tertiary lymphoid structures generate and propagate anti-tumor
               antibody-producing plasma cells in renal cell cancer",
  author    = "Meylan, Maxime and Petitprez, Florent and Becht, Etienne and
               Bougo{\"u}in, Antoine and Pupier, Guilhem and Calvez, Anne and
               Giglioli, Ilenia and Verkarre, Virginie and Lacroix, Guillaume
               and Verneau, Johanna and Sun, Chen-Ming and Laurent-Puig, Pierre
               and Vano, Yann-Alexandre and Ela{\"\i}di, Reza and M{\'e}jean,
               Arnaud and Sanchez-Salas, Rafa{\"e}l and Barret, Eric and
               Cathelineau, Xavier and Oudard, Stephane and Reynaud,
               Claude-Agn{\`e}s and de Reyni{\`e}s, Aur{\'e}lien and
               Saut{\`e}s-Fridman, Catherine and Fridman, Wolf Herman",
  abstract  = "The presence of intratumoral tertiary lymphoid structures (TLS)
               is associated with positive clinical outcomes and responses to
               immunotherapy in cancer. Here, we used spatial transcriptomics
               to examine the nature of B cell responses within TLS in renal
               cell carcinoma (RCC). B cells were enriched in TLS, and therein,
               we could identify all B cell maturation stages toward plasma
               cell (PC) formation. B cell repertoire analysis revealed clonal
               diversification, selection, expansion in TLS, and the presence
               of fully mature clonotypes at distance. In TLS+ tumors, IgG- and
               IgA-producing PCs disseminated into the tumor beds along
               fibroblastic tracks. TLS+ tumors exhibited high frequencies of
               IgG-producing PCs and IgG-stained and apoptotic malignant cells,
               suggestive of anti-tumor effector activity. Therapeutic
               responses and progression-free survival correlated with
               IgG-stained tumor cells in RCC patients treated with immune
               checkpoint inhibitors. Thus, intratumoral TLS sustains B cell
               maturation and antibody production that is associated with
               response to immunotherapy, potentially via direct anti-tumor
               effects.",
  journal   = "Immunity",
  publisher = "Elsevier BV",
  volume    =  55,
  number    =  3,
  pages     = "527--541.e5",
  month     =  mar,
  year      =  2022,
  keywords  = "B cell maturation; B cell repertoire; Visium; anti-tumor IgG;
               fibroblasts; plasma cells; renal cell cancer; response to immune
               check point inhibition; spatial transcriptomics; tertiary
               lymphoid structures; tumor microenvironment",
  copyright = "http://www.elsevier.com/open-access/userlicense/1.0/",
  language  = "en"
}

@ARTICLE{Ni2022-ap,
  title     = "{SpotClean} adjusts for spot swapping in spatial transcriptomics
               data",
  author    = "Ni, Zijian and Prasad, Aman and Chen, Shuyang and Halberg,
               Richard B and Arkin, Lisa M and Drolet, Beth A and Newton,
               Michael A and Kendziorski, Christina",
  abstract  = "Spatial transcriptomics is a powerful and widely used approach
               for profiling the gene expression landscape across a tissue with
               emerging applications in molecular medicine and tumor
               diagnostics. Recent spatial transcriptomics experiments utilize
               slides containing thousands of spots with spot-specific barcodes
               that bind RNA. Ideally, unique molecular identifiers (UMIs) at a
               spot measure spot-specific expression, but this is often not the
               case in practice due to bleed from nearby spots, an artifact we
               refer to as spot swapping. To improve the power and precision of
               downstream analyses in spatial transcriptomics experiments, we
               propose SpotClean, a probabilistic model that adjusts for spot
               swapping to provide more accurate estimates of gene-specific UMI
               counts. SpotClean provides substantial improvements in marker
               gene analyses and in clustering, especially when tissue regions
               are not easily separated. As demonstrated in multiple studies of
               cancer, SpotClean improves tumor versus normal tissue
               delineation and improves tumor burden estimation thus increasing
               the potential for clinical and diagnostic applications of
               spatial transcriptomics technologies.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  13,
  number    =  1,
  pages     = "2971",
  month     =  may,
  year      =  2022,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Kadur_Lakshminarasimha_Murthy2022-ch,
  title     = "Human distal lung maps and lineage hierarchies reveal a bipotent
               progenitor",
  author    = "Kadur Lakshminarasimha Murthy, Preetish and Sontake, Vishwaraj
               and Tata, Aleksandra and Kobayashi, Yoshihiko and Macadlo,
               Lauren and Okuda, Kenichi and Conchola, Ansley S and Nakano,
               Satoko and Gregory, Simon and Miller, Lisa A and Spence, Jason R
               and Engelhardt, John F and Boucher, Richard C and Rock, Jason R
               and Randell, Scott H and Tata, Purushothama Rao",
  abstract  = "Mapping the spatial distribution and molecular identity of
               constituent cells is essential for understanding tissue dynamics
               in health and disease. We lack a comprehensive map of human
               distal airways, including the terminal and respiratory
               bronchioles (TRBs), which are implicated in respiratory
               diseases1-4. Here, using spatial transcriptomics and single-cell
               profiling of microdissected distal airways, we identify
               molecularly distinct TRB cell types that have not-to our
               knowledge-been previously characterized. These include
               airway-associated LGR5+ fibroblasts and TRB-specific alveolar
               type-0 (AT0) cells and TRB secretory cells (TRB-SCs). Connectome
               maps and organoid-based co-cultures reveal that LGR5+
               fibroblasts form a signalling hub in the airway niche. AT0 cells
               and TRB-SCs are conserved in primates and emerge dynamically
               during human lung development. Using a non-human primate model
               of lung injury, together with human organoids and tissue
               specimens, we show that alveolar type-2 cells in regenerating
               lungs transiently acquire an AT0 state from which they can
               differentiate into either alveolar type-1 cells or TRB-SCs. This
               differentiation programme is distinct from that identified in
               the mouse lung5-7. Our study also reveals mechanisms that drive
               the differentiation of the bipotent AT0 cell state into normal
               or pathological states. In sum, our findings revise human lung
               cell maps and lineage trajectories, and implicate an epithelial
               transitional state in primate lung regeneration and disease.",
  journal   = "Nature",
  publisher = "Springer Science and Business Media LLC",
  volume    =  604,
  number    =  7904,
  pages     = "111--119",
  month     =  apr,
  year      =  2022,
  language  = "en"
}

@ARTICLE{Foster2021-br,
  title     = "Integrated spatial multiomics reveals fibroblast fate during
               tissue repair",
  author    = "Foster, Deshka S and Januszyk, Michael and Yost, Kathryn E and
               Chinta, Malini S and Gulati, Gunsagar S and Nguyen, Alan T and
               Burcham, Austin R and Salhotra, Ankit and Ransom, R Chase and
               Henn, Dominic and Chen, Kellen and Mascharak, Shamik and
               Tolentino, Karen and Titan, Ashley L and Jones, R Ellen and da
               Silva, Oscar and Leavitt, W Tripp and Marshall, Clement D and
               des Jardins-Park, Heather E and Hu, Michael S and Wan, Derrick C
               and Wernig, Gerlinde and Wagh, Dhananjay and Coller, John and
               Norton, Jeffrey A and Gurtner, Geoffrey C and Newman, Aaron M
               and Chang, Howard Y and Longaker, Michael T",
  abstract  = "In the skin, tissue injury results in fibrosis in the form of
               scars composed of dense extracellular matrix deposited by
               fibroblasts. The therapeutic goal of regenerative wound healing
               has remained elusive, in part because principles of fibroblast
               programming and adaptive response to injury remain incompletely
               understood. Here, we present a multimodal -omics platform for
               the comprehensive study of cell populations in complex tissue,
               which has allowed us to characterize the cells involved in wound
               healing across both time and space. We employ a stented wound
               model that recapitulates human tissue repair kinetics and
               multiple Rainbow transgenic lines to precisely track fibroblast
               fate during the physiologic response to skin injury. Through
               integrated analysis of single cell chromatin landscapes and gene
               expression states, coupled with spatial transcriptomic
               profiling, we are able to impute fibroblast epigenomes with
               temporospatial resolution. This has allowed us to reveal
               potential mechanisms controlling fibroblast fate during
               migration, proliferation, and differentiation following skin
               injury, and thereby reexamine the canonical phases of wound
               healing. These findings have broad implications for the study of
               tissue repair in complex organ systems.",
  journal   = "Proc. Natl. Acad. Sci. U. S. A.",
  publisher = "Proceedings of the National Academy of Sciences",
  volume    =  118,
  number    =  41,
  pages     = "e2110025118",
  month     =  oct,
  year      =  2021,
  keywords  = "chromatin accessibility; fibrosis; multiomics; spatial
               epigenomics; spatial transcriptomics",
  copyright = "https://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Sudmeier2022-nf,
  title     = "Distinct phenotypic states and spatial distribution of {CD8+}
               {T} cell clonotypes in human brain metastases",
  author    = "Sudmeier, Lisa J and Hoang, Kimberly B and Nduom, Edjah K and
               Wieland, Andreas and Neill, Stewart G and Schniederjan, Matthew
               J and Ramalingam, Suresh S and Olson, Jeffrey J and Ahmed, Rafi
               and Hudson, William H",
  abstract  = "Metastatic disease in the brain is difficult to control and
               predicts poor prognosis. Here, we analyze human brain metastases
               and demonstrate their robust infiltration by CD8+ T cell subsets
               with distinct antigen specificities, phenotypic states, and
               spatial localization within the tumor microenvironment. Brain
               metastases are densely infiltrated by T cells; the majority of
               infiltrating CD8+ T cells express PD-1. Single-cell RNA
               sequencing shows significant clonal overlap between
               proliferating and exhausted CD8+ T cells, but these subsets have
               minimal clonal overlap with circulating and other
               tumor-infiltrating CD8+ T cells, including bystander CD8+ T
               cells specific for microbial antigens. Using spatial
               transcriptomics and spatial T cell receptor (TCR) sequencing, we
               show these clonally unrelated, phenotypically distinct CD8+ T
               cell populations occupy discrete niches within the brain
               metastasis tumor microenvironment. Together, our work identifies
               signaling pathways within CD8+ T cells and in their surrounding
               environment that may be targeted for immunotherapy of brain
               metastases.",
  journal   = "Cell Rep. Med.",
  publisher = "Elsevier BV",
  volume    =  3,
  number    =  5,
  pages     = "100620",
  month     =  may,
  year      =  2022,
  keywords  = "CD8(+) T cells; TCR-sequencing; brain metastases; bystander;
               exhaustion; spatial transcriptomics",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Hudson2022-mz,
  title     = "Localization of {T} cell clonotypes using the Visium spatial
               transcriptomics platform",
  author    = "Hudson, William H and Sudmeier, Lisa J",
  abstract  = "We present a protocol to localize T cell receptor clones using
               the Visium spatial transcriptomics platform. This approach
               permits simultaneous localization of both gene expression and T
               cell clonotypes in situ within tissue sections. T cell receptor
               sequences identified by this protocol are readily recapitulated
               by single-cell sequencing. This technique enables detailed
               studies of the spatial organization of the human T cell
               repertoire, such as the localization of infiltrating T cell
               clones within the tumor microenvironment. For complete details
               on the use and execution of this protocol, please refer to
               Sudmeier et al. (2022).",
  journal   = "STAR Protoc.",
  publisher = "Elsevier BV",
  volume    =  3,
  number    =  2,
  pages     = "101391",
  month     =  jun,
  year      =  2022,
  keywords  = "Immunology; Molecular Biology; Sequence analysis",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Tower2022-fi,
  title     = "Spatial transcriptomics reveals metabolic changes underly
               age-dependent declines in digit regeneration",
  author    = "Tower, Robert J and Busse, Emily and Jaramillo, Josue and Lacey,
               Michelle and Hoffseth, Kevin and Guntur, Anyonya R and Simkin,
               Jennifer and Sammarco, Mimi C",
  abstract  = "De novo limb regeneration after amputation is restricted in
               mammals to the distal digit tip. Central to this regenerative
               process is the blastema, a heterogeneous population of
               lineage-restricted, dedifferentiated cells that ultimately
               orchestrates regeneration of the amputated bone and surrounding
               soft tissue. To investigate skeletal regeneration, we made use
               of spatial transcriptomics to characterize the transcriptional
               profile specifically within the blastema. Using this technique,
               we generated a gene signature with high specificity for the
               blastema in both our spatial data, as well as other previously
               published single-cell RNA-sequencing transcriptomic studies. To
               elucidate potential mechanisms distinguishing regenerative from
               non-regenerative healing, we applied spatial transcriptomics to
               an aging model. Consistent with other forms of repair, our digit
               amputation mouse model showed a significant impairment in
               regeneration in aged mice. Contrasting young and aged mice,
               spatial analysis revealed a metabolic shift in aged blastema
               associated with an increased bioenergetic requirement. This
               enhanced metabolic turnover was associated with increased
               hypoxia and angiogenic signaling, leading to excessive
               vascularization and altered regenerated bone architecture in
               aged mice. Administration of the metabolite oxaloacetate
               decreased the oxygen consumption rate of the aged blastema and
               increased WNT signaling, leading to enhanced in vivo bone
               regeneration. Thus, targeting cell metabolism may be a promising
               strategy to mitigate aging-induced declines in tissue
               regeneration.",
  journal   = "Elife",
  publisher = "eLife Sciences Publications, Ltd",
  volume    =  11,
  month     =  may,
  year      =  2022,
  keywords  = "aging; bone regeneration; cell biology; cell metabolism; digit
               regeneration; mouse; oxaloacetate; spatial transcriptomics",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Rustagi2022-io,
  title     = "Endothelial phospholipase {C$\gamma$2} improves outcomes of
               diabetic ischemic limb rescue following {VEGF} therapy",
  author    = "Rustagi, Yashika and Abouhashem, Ahmed S and Verma, Priyanka and
               Verma, Sumit S and Hernandez, Edward and Liu, Sheng and Kumar,
               Manishekhar and Guda, Poornachander R and Srivastava, Rajneesh
               and Mohanty, Sujit K and Kacar, Sedat and Mahajan, Sanskruti and
               Wanczyk, Kristen E and Khanna, Savita and Murphy, Michael P and
               Gordillo, Gayle M and Roy, Sashwati and Wan, Jun and Sen,
               Chandan K and Singh, Kanhaiya",
  abstract  = "Therapeutic vascular endothelial growth factor (VEGF)
               replenishment has met with limited success for the management of
               critical limb-threatening ischemia. To improve outcomes of VEGF
               therapy, we applied single-cell RNA sequencing (scRNA-seq)
               technology to study the endothelial cells of the human diabetic
               skin. Single-cell suspensions were generated from the human skin
               followed by cDNA preparation using the Chromium Next GEM
               Single-cell 3' Kit v3.1. Using appropriate quality control
               measures, 36,487 cells were chosen for downstream analysis.
               scRNA-seq studies identified that although VEGF signaling was
               not significantly altered in diabetic versus nondiabetic skin,
               phospholipase C$\gamma$2 (PLC$\gamma$2) was downregulated. The
               significance of PLC$\gamma$2 in VEGF-mediated increase in
               endothelial cell metabolism and function was assessed in
               cultured human microvascular endothelial cells. In these cells,
               VEGF enhanced mitochondrial function, as indicated by elevation
               in oxygen consumption rate and extracellular acidification rate.
               The VEGF-dependent increase in cell metabolism was blunted in
               response to PLC$\gamma$2 inhibition. Follow-up rescue studies
               therefore focused on understanding the significance of VEGF
               therapy in presence or absence of endothelial PLC$\gamma$2 in
               type 1 (streptozotocin-injected) and type 2 (db/db) diabetic
               ischemic tissue. Nonviral topical tissue nanotransfection
               technology (TNT) delivery of CDH5 promoter-driven PLC$\gamma$2
               open reading frame promoted the rescue of hindlimb ischemia in
               diabetic mice. Improvement of blood flow was also associated
               with higher abundance of VWF+/CD31+ and VWF+/SMA+
               immunohistochemical staining. TNT-based gene delivery was not
               associated with tissue edema, a commonly noted complication
               associated with proangiogenic gene therapies. Taken together,
               our study demonstrates that TNT-mediated delivery of endothelial
               PLC$\gamma$2, as part of combination gene therapy, is effective
               in diabetic ischemic limb rescue.",
  journal   = "Diabetes",
  publisher = "American Diabetes Association",
  volume    =  71,
  number    =  5,
  pages     = "1149--1165",
  month     =  may,
  year      =  2022,
  copyright = "https://www.diabetesjournals.org/journals/pages/license",
  language  = "en"
}

@ARTICLE{Dixon2022-ew,
  title     = "Spatially resolved transcriptomic analysis of acute kidney
               injury in a female Murine model",
  author    = "Dixon, Eryn E and Wu, Haojia and Muto, Yoshiharu and Wilson,
               Parker C and Humphreys, Benjamin D",
  abstract  = "BACKGROUND: Single-cell sequencing technologies have advanced
               our understanding of kidney biology and disease, but the loss of
               spatial information in these datasets hinders our interpretation
               of intercellular communication networks and regional gene
               expression patterns. New spatial transcriptomic sequencing
               platforms make it possible to measure the topography of gene
               expression at genome depth. METHODS: We optimized and validated
               a female bilateral ischemia-reperfusion injury model. Using the
               10$\times$ Genomics Visium Spatial Gene Expression solution, we
               generated spatial maps of gene expression across the injury and
               repair time course, and applied two open-source computational
               tools, Giotto and SPOTlight, to increase resolution and measure
               cell-cell interaction dynamics. RESULTS: An ischemia time of 34
               minutes in a female murine model resulted in comparable injury
               to 22 minutes for males. We report a total of 16,856 unique
               genes mapped across our injury and repair time course. Giotto, a
               computational toolbox for spatial data analysis, enabled
               increased resolution mapping of genes and cell types. Using a
               seeded nonnegative matrix regression (SPOTlight) to deconvolute
               the dynamic landscape of cell-cell interactions, we found that
               injured proximal tubule cells were characterized by increasing
               macrophage and lymphocyte interactions even 6 weeks after
               injury, potentially reflecting the AKI to CKD transition.
               CONCLUSIONS: In this transcriptomic atlas, we defined
               region-specific and injury-induced loss of differentiation
               markers and their re-expression during repair, as well as
               region-specific injury and repair transcriptional responses.
               Lastly, we created an interactive data visualization application
               for the scientific community to explore these results
               (http://humphreyslab.com/SingleCell/).",
  journal   = "J. Am. Soc. Nephrol.",
  publisher = "Ovid Technologies (Wolters Kluwer Health)",
  volume    =  33,
  number    =  2,
  pages     = "279--289",
  month     =  feb,
  year      =  2022,
  keywords  = "AKI; spatial; transcriptomics",
  language  = "en"
}

@ARTICLE{Lake2023-mf,
  title    = "An atlas of healthy and injured cell states and niches in the
              human kidney",
  author   = "Lake, Blue B and Menon, Rajasree and Winfree, Seth and Hu, Qiwen
              and Melo Ferreira, Ricardo and Kalhor, Kian and Barwinska, Daria
              and Otto, Edgar A and Ferkowicz, Michael and Diep, Dinh and
              Plongthongkum, Nongluk and Knoten, Amanda and Urata, Sarah and
              Mariani, Laura H and Naik, Abhijit S and Eddy, Sean and Zhang, Bo
              and Wu, Yan and Salamon, Diane and Williams, James C and Wang,
              Xin and Balderrama, Karol S and Hoover, Paul J and Murray, Evan
              and Marshall, Jamie L and Noel, Teia and Vijayan, Anitha and
              Hartman, Austin and Chen, Fei and Waikar, Sushrut S and Rosas,
              Sylvia E and Wilson, Francis P and Palevsky, Paul M and Kiryluk,
              Krzysztof and Sedor, John R and Toto, Robert D and Parikh, Chirag
              R and Kim, Eric H and Satija, Rahul and Greka, Anna and Macosko,
              Evan Z and Kharchenko, Peter V and Gaut, Joseph P and Hodgin,
              Jeffrey B and {KPMP Consortium} and Eadon, Michael T and Dagher,
              Pierre C and El-Achkar, Tarek M and Zhang, Kun and Kretzler,
              Matthias and Jain, Sanjay",
  abstract = "Understanding kidney disease relies on defining the complexity of
              cell types and states, their associated molecular profiles and
              interactions within tissue neighbourhoods1. Here we applied
              multiple single-cell and single-nucleus assays (>400,000 nuclei
              or cells) and spatial imaging technologies to a broad spectrum of
              healthy reference kidneys (45 donors) and diseased kidneys (48
              patients). This has provided a high-resolution cellular atlas of
              51 main cell types, which include rare and previously undescribed
              cell populations. The multi-omic approach provides detailed
              transcriptomic profiles, regulatory factors and spatial
              localizations spanning the entire kidney. We also define 28
              cellular states across nephron segments and interstitium that
              were altered in kidney injury, encompassing cycling, adaptive
              (successful or maladaptive repair), transitioning and
              degenerative states. Molecular signatures permitted the
              localization of these states within injury neighbourhoods using
              spatial transcriptomics, while large-scale 3D imaging analysis
              (around 1.2 million neighbourhoods) provided corresponding
              linkages to active immune responses. These analyses defined
              biological pathways that are relevant to injury time-course and
              niches, including signatures underlying epithelial repair that
              predicted maladaptive states associated with a decline in kidney
              function. This integrated multimodal spatial cell atlas of
              healthy and diseased human kidneys represents a comprehensive
              benchmark of cellular states, neighbourhoods, outcome-associated
              signatures and publicly available interactive visualizations.",
  journal  = "Nature",
  volume   =  619,
  number   =  7970,
  pages    = "585--594",
  month    =  jul,
  year     =  2023,
  language = "en"
}

@ARTICLE{Mohammadi2023-uv,
  title     = "Size matters: the impact of nucleus size on results from spatial
               transcriptomics",
  author    = "Mohammadi, Elyas and Chojnowska, Katarzyna and Bie{\'n}kowski,
               Micha{\l} and Kostecka, Anna and Koczkowska, Magdalena and
               {\.Z}mijewski, Micha{\l} A and J{\k a}kalski, Marcin and
               Ingelsson, Martin and Filipowicz, Natalia and Olszewski,
               Pawe{\l} and Davies, Hanna and Wierzbicka, Justyna M and Hyman,
               Bradley T and Dumanski, Jan P and Piotrowski, Arkadiusz and
               Mieczkowski, Jakub",
  abstract  = "BACKGROUND: Visium Spatial Gene Expression (ST) is a method
               combining histological spatial information with transcriptomics
               profiles directly from tissue sections. The use of spatial
               information has made it possible to discover new modes of gene
               expression regulations. However, in the ST experiment, the
               nucleus size of cells may exceed the thickness of a tissue
               slice. This may, in turn, negatively affect comprehensive
               capturing the transcriptomics profile in a single slice,
               especially for tissues having large differences in the size of
               nuclei. METHODS: Here, we defined the effect of Consecutive
               Slices Data Integration (CSDI) on unveiling accurate spot
               clustering and deconvolution of spatial transcriptomic spots in
               human postmortem brains. By considering the histological
               information as reference, we assessed the improvement of
               unsupervised clustering and single nuclei RNA-seq and ST data
               integration before and after CSDI. RESULTS: Apart from the
               escalated number of defined clusters representing neuronal
               layers, the pattern of clusters in consecutive sections was
               concordant only after CSDI. Besides, the assigned cell labels to
               spots matches the histological pattern of tissue sections after
               CSDI. CONCLUSION: CSDI can be applied to investigate consecutive
               sections studied with ST in the human cerebral cortex, avoiding
               misinterpretation of spot clustering and annotation, increasing
               accuracy of cell recognition as well as improvement in
               uncovering the layers of grey matter in the human brain.",
  journal   = "J. Transl. Med.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  21,
  number    =  1,
  pages     = "270",
  month     =  apr,
  year      =  2023,
  keywords  = "Cerebral cortex; Consecutive tissue sections; Data integration;
               Neuronal nuclei; Spatial transcriptomics",
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Yamasaki2022-bq,
  title     = "{MEK} inhibition suppresses metastatic progression of
               {KRAS-mutated} gastric cancer",
  author    = "Yamasaki, Juntaro and Hirata, Yuki and Otsuki, Yuji and Suina,
               Kentaro and Saito, Yoshiyuki and Masuda, Kenta and Okazaki,
               Shogo and Ishimoto, Takatsugu and Saya, Hideyuki and Nagano,
               Osamu",
  abstract  = "Metastatic progression of tumors is driven by genetic
               alterations and tumor-stroma interaction. To elucidate the
               mechanism underlying the oncogene-induced gastric tumor
               progression, we have developed an organoid-based model of
               gastric cancer from GAstric Neoplasia (GAN) mice, which express
               Wnt1 and the enzymes COX2 and microsomal prostaglandin E
               synthase 1 in the stomach. Both p53 knockout (GAN-p53KO)
               organoids and KRASG12V -expressing GAN-p53KO (GAN-KP) organoids
               were generated by genetic manipulation of GAN mouse-derived
               tumor (GAN wild-type [WT]) organoids. In contrast with GAN-WT
               and GAN-p53KO organoids, which manifested Wnt addiction, GAN-KP
               organoids showed a Wnt-independent phenotype and the ability to
               proliferate without formation of a Wnt-regulated
               three-dimensional epithelial architecture. After transplantation
               in syngeneic mouse stomach, GAN-p53KO cells formed only small
               tumors, whereas GAN-KP cells gave rise to invasive tumors
               associated with the development of hypoxia as well as to liver
               metastasis. Spatial transcriptomics analysis suggested that
               hypoxia signaling contributes to the metastatic progression of
               GAN-KP tumors. In particular, such analysis identified a cluster
               of stromal cells located at the tumor invasive front that
               expressed genes related to hypoxia signaling, angiogenesis, and
               cell migration. These cells were also positive for
               phosphorylated extracellular signal-regulated kinase (ERK),
               suggesting that mitogen-activated protein kinase (MAPK)
               signaling promotes development of both tumor and
               microenvironment. The MEK (MAPK kinase) inhibitor trametinib
               suppressed the development of GAN-KP gastric tumors, formation
               of a hypoxic microenvironment, tumor angiogenesis, and liver
               metastasis. Our findings therefore establish a rationale for
               application of trametinib to suppress metastatic progression of
               KRAS-mutated gastric cancer.",
  journal   = "Cancer Sci.",
  publisher = "Wiley",
  volume    =  113,
  number    =  3,
  pages     = "916--925",
  month     =  mar,
  year      =  2022,
  keywords  = "MEK; epithelial-mesenchymal transition (EMT); gastric cancer;
               hypoxia; mouse model",
  copyright = "http://creativecommons.org/licenses/by-nc/4.0/",
  language  = "en"
}

@ARTICLE{Chen2022-en,
  title     = "Prostaglandin {E2} synchronizes lunar-regulated beach spawning
               in grass puffers",
  author    = "Chen, Junfeng and Katada, Yuma and Okimura, Kousuke and
               Yamaguchi, Taiki and Guh, Ying-Jey and Nakayama, Tomoya and
               Maruyama, Michiyo and Furukawa, Yuko and Nakane, Yusuke and
               Yamamoto, Naoyuki and Sato, Yoshikatsu and Ando, Hironori and
               Sugimura, Asako and Tabata, Kazufumi and Sato, Ayato and
               Yoshimura, Takashi",
  abstract  = "Many organisms living along the coastlines synchronize their
               reproduction with the lunar cycle. At the time of spring tide,
               thousands of grass puffers (Takifugu alboplumbeus) aggregate and
               vigorously tremble their bodies at the water's edge to spawn. To
               understand the mechanisms underlying this spectacular semilunar
               beach spawning, we collected the hypothalamus and pituitary from
               male grass puffers every week for 2 months. RNA sequencing
               (RNA-seq) analysis identified 125 semilunar genes, including
               genes crucial for reproduction (e.g., gonadotropin-releasing
               hormone 1 [gnrh1], luteinizing hormone $\beta$ subunit [lhb])
               and receptors for pheromone prostaglandin E (PGE). PGE2 is
               secreted into the seawater during the spawning, and its
               administration activates olfactory sensory neurons and triggers
               trembling behavior of surrounding individuals. These results
               suggest that PGE2 synchronizes lunar-regulated beach-spawning
               behavior in grass puffers. To further explore the mechanism that
               regulates the lunar-synchronized transcription of semilunar
               genes, we searched for semilunar transcription factors. Spatial
               transcriptomics and multiplex fluorescent in situ hybridization
               showed co-localization of the semilunar transcription factor
               CCAAT/enhancer-binding protein $\delta$ (cebpd) and gnrh1, and
               cebpd induced the promoter activity of gnrh1. Taken together,
               our study demonstrates semilunar genes that mediate
               lunar-synchronized beach-spawning behavior. VIDEO ABSTRACT.",
  journal   = "Curr. Biol.",
  publisher = "Elsevier BV",
  volume    =  32,
  number    =  22,
  pages     = "4881--4889.e5",
  month     =  nov,
  year      =  2022,
  keywords  = "beach spawning; biological clock; circalunar rhythms; grass
               puffer; lunar cycle; neap tide; pheromone; seasonal
               reproduction; semilunar rhythm; spring tide",
  language  = "en"
}

@ARTICLE{Russ2022-sy,
  title     = "Spatially resolved transcriptomic profiling of ovarian aging in
               mice",
  author    = "Russ, Jennifer E and Haywood, Mary E and Lane, Sydney L and
               Schoolcraft, William B and Katz-Jaffe, Mandy G",
  abstract  = "Ovarian aging precedes that of any other mammalian organ and is
               the primary cause of female age-related infertility. The
               biological mechanisms responsible for ovarian aging remain
               unclear. Previous studies have been limited by their use of bulk
               RNA-sequencing, which masks the dynamic and heterogeneous nature
               of the ovary. In this study, we spatially resolved the
               transcriptomic landscape of ovaries from young and aged outbred
               mice. In total, we defined eight main ovarian cell populations,
               all of which were characterized by significant transcriptomic
               changes between young and aged samples. Further sub-cluster
               analysis revealed separate transcriptomes for distinct granulosa
               cell populations found in young versus aged mice, in addition to
               an oocyte sub-cluster population completely absent from aged
               mouse ovaries. This study provides a new perspective on
               mammalian ovarian aging using spatial transcriptomics to achieve
               deeper understanding of the localization and
               cell-population-specific mechanisms underlying age-related
               fertility decline.",
  journal   = "iScience",
  publisher = "Elsevier BV",
  volume    =  25,
  number    =  8,
  pages     = "104819",
  month     =  aug,
  year      =  2022,
  keywords  = "Cellular physiology; Omics; Physiology; Transcriptomics",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Misra2021-pr,
  title     = "Characterizing neonatal heart maturation, regeneration, and scar
               resolution using spatial transcriptomics",
  author    = "Misra, Adwiteeya and Baker, Cameron D and Pritchett, Elizabeth M
               and Burgos Villar, Kimberly N and Ashton, John M and Small, Eric
               M",
  abstract  = "The neonatal mammalian heart exhibits a remarkable regenerative
               potential, which includes fibrotic scar resolution and the
               generation of new cardiomyocytes. To investigate the mechanisms
               facilitating heart repair after apical resection in neonatal
               mice, we conducted bulk and spatial transcriptomic analyses at
               regenerative and non-regenerative timepoints. Importantly,
               spatial transcriptomics provided near single-cell resolution,
               revealing distinct domains of atrial and ventricular myocardium
               that exhibit dynamic phenotypic alterations during postnatal
               heart maturation. Spatial transcriptomics also defined the
               cardiac scar, which transitions from a proliferative to
               secretory phenotype as the heart loses regenerative potential.
               The resolving scar is characterized by spatially and temporally
               restricted programs of inflammation, epicardium expansion and
               extracellular matrix production, metabolic reprogramming,
               lipogenic scar extrusion, and cardiomyocyte restoration.
               Finally, this study revealed the emergence of a regenerative
               border zone defined by immature cardiomyocyte markers and the
               robust expression of Sprr1a. Taken together, our study defines
               the spatially and temporally restricted gene programs that
               underlie neonatal heart regeneration and provides insight into
               cardio-restorative mechanisms supporting scar resolution.",
  journal   = "J. Cardiovasc. Dev. Dis.",
  publisher = "MDPI AG",
  volume    =  9,
  number    =  1,
  pages     = "1",
  month     =  dec,
  year      =  2021,
  keywords  = "fibroblast; heart; mouse; regeneration; scar; spatial
               transcriptomics",
  copyright = "https://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Guilliams2022-kd,
  title     = "Spatial proteogenomics reveals distinct and evolutionarily
               conserved hepatic macrophage niches",
  author    = "Guilliams, Martin and Bonnardel, Johnny and Haest, Birthe and
               Vanderborght, Bart and Wagner, Camille and Remmerie, Anneleen
               and Bujko, Anna and Martens, Liesbet and Thon{\'e}, Tinne and
               Browaeys, Robin and De Ponti, Federico F and Vanneste, Bavo and
               Zwicker, Christian and Svedberg, Freya R and Vanhalewyn, Tineke
               and Gon{\c c}alves, Amanda and Lippens, Saskia and Devriendt,
               Bert and Cox, Eric and Ferrero, Giuliano and Wittamer, Valerie
               and Willaert, Andy and Kaptein, Suzanne J F and Neyts, Johan and
               Dallmeier, Kai and Geldhof, Peter and Casaert, Stijn and
               Deplancke, Bart and Ten Dijke, Peter and Hoorens, Anne and
               Vanlander, Aude and Berrevoet, Frederik and Van Nieuwenhove,
               Yves and Saeys, Yvan and Saelens, Wouter and Van Vlierberghe,
               Hans and Devisscher, Lindsey and Scott, Charlotte L",
  abstract  = "The liver is the largest solid organ in the body, yet it remains
               incompletely characterized. Here we present a spatial
               proteogenomic atlas of the healthy and obese human and murine
               liver combining single-cell CITE-seq, single-nuclei sequencing,
               spatial transcriptomics, and spatial proteomics. By integrating
               these multi-omic datasets, we provide validated strategies to
               reliably discriminate and localize all hepatic cells, including
               a population of lipid-associated macrophages (LAMs) at the bile
               ducts. We then align this atlas across seven species, revealing
               the conserved program of bona fide Kupffer cells and LAMs. We
               also uncover the respective spatially resolved cellular niches
               of these macrophages and the microenvironmental circuits driving
               their unique transcriptomic identities. We demonstrate that LAMs
               are induced by local lipid exposure, leading to their induction
               in steatotic regions of the murine and human liver, while
               Kupffer cell development crucially depends on their cross-talk
               with hepatic stellate cells via the evolutionarily conserved
               ALK1-BMP9/10 axis.",
  journal   = "Cell",
  publisher = "Elsevier BV",
  volume    =  185,
  number    =  2,
  pages     = "379--396.e38",
  month     =  jan,
  year      =  2022,
  keywords  = "CITE-seq; Kupffer cell; NAFLD; across species; atlas;
               lipid-associated macrophage; liver; multi-omic; proteogenomic;
               spatial transcriptomics",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Habenicht2022-ae,
  title     = "The {C1q-ApoE} complex: A new hallmark pathology of viral
               hepatitis and nonalcoholic fatty liver disease",
  author    = "Habenicht, Livia K L and Wang, Zhihua and Zhang, Xi and Li,
               Yuanfang and Mogler, Carolin and Huspenina, Julia Slotta and
               Schmid, Roland M and Weber, Christian and Mohanta, Sarajo K and
               Ma, Zhe and Yin, Changjun",
  abstract  = "We recently identified a high-affinity C1q-ApoE complex in human
               artery atherosclerotic intima lesions and in human amyloid
               plaques of Alzheimer's Disease brains defining a common
               pathogenetic pathway of two diverse diseases, i.e.
               atherosclerosis and dementia. C1q is the initiating and
               controlling protein of the classical complement cascade (CCC),
               which occupies a key role in multiple acute and chronic
               inflammatory tissue responses. C1q is largely produced by
               myeloid cells including Kupffer cells (KCs) and subsequently
               secreted into the circulation as an inactive preprotein. Its
               binding partner, Apolipoprotein E (ApoE), is produced by KCs and
               hepatocytes and it is also secreted into the circulation, where
               it regulates essential steps of lipid transport. In addition to
               its major source, ApoE can be produced by non-liver cells
               including immune cells and multiple other cells depending on
               local tissue contexts. To initiate the CCC cascade, C1q must be
               activated by molecules as varied as oxidized lipids, amyloid
               fibrils, and immune complexes. However, ApoE is mute towards
               inactive C1q but binds at high-affinity to its activated form.
               Specifically, our studies revealed that ApoE is a CCC-specific
               checkpoint inhibitor via the formation of the C1q-ApoE complex.
               We proposed that it may arise in multiple if not all
               CCC-associated diseases and that its presence indicates ongoing
               CCC activity. Here, we turned to the liver to examine C1q-ApoE
               complexes in human B- and C-viral hepatitis and nonalcoholic
               fatty liver disease (NAFLD). In addition, we used
               multidrug-resistance-2 gene-knockout (Mdr2-KO) mice as a model
               for inflammatory liver disease and hepatocellular carcinoma
               (HCC) pathogenesis. In normal murine and human livers, KCs were
               the major C1q-producing cell type while hepatocytes were the
               primary ApoE-forming cell type though the C1q-ApoE complex was
               rare or nonexistent. However, significant numbers of C1q-ApoE
               complexes formed in both Mdr2-KO, human viral hepatitis, and
               NAFLD around portal triads where immune cells had infiltrated
               the liver. Additionally, high numbers of C1q-ApoE complexes
               emerged in human livers in areas of extracellular lipid droplets
               across the entire liver parenchyma in NAFLD-affected patients.
               Thus, the C1q-ApoE complex is a new pathological hallmark of
               viral hepatitis B and C and NAFLD.",
  journal   = "Front. Immunol.",
  publisher = "Frontiers Media SA",
  volume    =  13,
  pages     = "970938",
  month     =  oct,
  year      =  2022,
  keywords  = "C1q-ApoE complex; classical complement cascade (CCC);
               hepatocellular carcinoma (HCC); nonalcoholic fatty liver disease
               (NAFLD); viral hepatitis",
  copyright = "https://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Dhainaut2022-ck,
  title     = "Spatial {CRISPR} genomics identifies regulators of the tumor
               microenvironment",
  author    = "Dhainaut, Maxime and Rose, Samuel A and Akturk, Guray and
               Wroblewska, Aleksandra and Nielsen, Sebastian R and Park, Eun
               Sook and Buckup, Mark and Roudko, Vladimir and Pia, Luisanna and
               Sweeney, Robert and Le Berichel, Jessica and Wilk, C Matthias
               and Bektesevic, Anela and Lee, Brian H and Bhardwaj, Nina and
               Rahman, Adeeb H and Baccarini, Alessia and Gnjatic, Sacha and
               Pe'er, Dana and Merad, Miriam and Brown, Brian D",
  abstract  = "While CRISPR screens are helping uncover genes regulating many
               cell-intrinsic processes, existing approaches are suboptimal for
               identifying extracellular gene functions, particularly in the
               tissue context. Here, we developed an approach for spatial
               functional genomics called Perturb-map. We applied Perturb-map
               to knock out dozens of genes in parallel in a mouse model of
               lung cancer and simultaneously assessed how each knockout
               influenced tumor growth, histopathology, and immune composition.
               Moreover, we paired Perturb-map and spatial transcriptomics for
               unbiased analysis of CRISPR-edited tumors. We found that in
               Tgfbr2 knockout tumors, the tumor microenvironment (TME) was
               converted to a fibro-mucinous state, and T cells excluded,
               concomitant with upregulated TGF$\beta$ and TGF$\beta$-mediated
               fibroblast activation, indicating that TGF$\beta$-receptor loss
               on cancer cells increased TGF$\beta$ bioavailability and its
               immunosuppressive effects on the TME. These studies establish
               Perturb-map for functional genomics within the tissue at
               single-cell resolution with spatial architecture preserved and
               provide insight into how TGF$\beta$ responsiveness of cancer
               cells can affect the TME.",
  journal   = "Cell",
  publisher = "Elsevier BV",
  volume    =  185,
  number    =  7,
  pages     = "1223--1239.e20",
  month     =  mar,
  year      =  2022,
  keywords  = "CRISPR screens; Socs1; TGF beta; cancer immunology; interferon
               gamma; lung cancer; spatial genomics; spatial transcriptomics;
               tumor clonality; tumor microenvironment",
  language  = "en"
}

@ARTICLE{Ren2023-cv,
  title    = "Spatial transcriptomics reveals niche-specific enrichment and
              vulnerabilities of radial glial stem-like cells in malignant
              gliomas",
  author   = "Ren, Yanming and Huang, Zongyao and Zhou, Lingling and Xiao, Peng
              and Song, Junwei and He, Ping and Xie, Chuanxing and Zhou, Ran
              and Li, Menghan and Dong, Xiangqun and Mao, Qing and You, Chao
              and Xu, Jianguo and Liu, Yanhui and Lan, Zhigang and Zhang,
              Tiejun and Gan, Qi and Yang, Yuan and Chen, Tengyun and Huang,
              Bowen and Yang, Xiang and Xiao, Anqi and Ou, Yun and Su,
              Zhengzheng and Chen, Lu and Zhang, Yan and Ju, Yan and Zhang,
              Yuekang and Wang, Yuan",
  abstract = "Diffuse midline glioma-H3K27M mutant (DMG) and glioblastoma (GBM)
              are the most lethal brain tumors that primarily occur in
              pediatric and adult patients, respectively. Both tumors exhibit
              significant heterogeneity, shaped by distinct genetic/epigenetic
              drivers, transcriptional programs including RNA splicing, and
              microenvironmental cues in glioma niches. However, the spatial
              organization of cellular states and niche-specific regulatory
              programs remain to be investigated. Here, we perform a spatial
              profiling of DMG and GBM combining short- and long-read spatial
              transcriptomics, and single-cell transcriptomic datasets. We
              identify clinically relevant transcriptional programs, RNA
              isoform diversity, and multi-cellular ecosystems across different
              glioma niches. We find that while the tumor core enriches for
              oligodendrocyte precursor-like cells, radial glial stem-like
              (RG-like) cells are enriched in the neuron-rich invasive niche in
              both DMG and GBM. Further, we identify niche-specific regulatory
              programs for RG-like cells, and functionally confirm that FAM20C
              mediates invasive growth of RG-like cells in a neuron-rich
              microenvironment in a human neural stem cell derived orthotopic
              DMG model. Together, our results provide a blueprint for
              understanding the spatial architecture and niche-specific
              vulnerabilities of DMG and GBM.",
  journal  = "Nat. Commun.",
  volume   =  14,
  number   =  1,
  pages    = "1028",
  month    =  feb,
  year     =  2023,
  language = "en"
}

@ARTICLE{Kenney2023-tj,
  title    = "Multi-omics analysis identifies {IgG2b} class-switching with
              {ALCAM-CD6} co-stimulation in joint-draining lymph nodes during
              advanced inflammatory-erosive arthritis",
  author   = "Kenney, H Mark and Rangel-Moreno, Javier and Peng, Yue and Chen,
              Kiana L and Bruno, Jennifer and Embong, Abdul and Pritchett,
              Elizabeth and Fox, Jeffrey I and Becerril-Villanueva, Enrique and
              Gamboa-Dom{\'\i}nguez, Armando and Quataert, Sally and
              Muthukrishnan, Gowrishankar and Wood, Ronald W and Korman,
              Benjamin D and Anolik, Jennifer H and Xing, Lianping and
              Ritchlin, Christopher T and Schwarz, Edward M and Wu, Chia-Lung",
  abstract = "Introduction: Defective lymphatic drainage and translocation of
              B-cells in inflamed (Bin) joint-draining lymph node sinuses are
              pathogenic phenomena in patients with severe rheumatoid arthritis
              (RA). However, the molecular mechanisms underlying this lymphatic
              dysfunction remain poorly understood. Herein, we utilized
              multi-omic spatial and single-cell transcriptomics to evaluate
              altered cellular composition (including lymphatic endothelial
              cells, macrophages, B-cells, and T-cells) in the joint-draining
              lymph node sinuses and their associated phenotypic changes and
              cell-cell interactions during RA development using the tumor
              necrosis factor transgenic (TNF-Tg) mouse model. Methods:
              Popliteal lymph nodes (PLNs) from wild-type (n=10) and TNF-Tg
              male mice with ``Early'' (5 to 6-months of age; n=6) and
              ``Advanced'' (>8-months of age; n=12) arthritis were harvested
              and processed for spatial transcriptomics. Single-cell RNA
              sequencing (scRNAseq) was performed in PLNs from the TNF-Tg
              cohorts (n=6 PLNs pooled/cohort). PLN histopathology and ELISPOT
              along with ankle histology and micro-CT were evaluated.
              Histopathology of human lymph nodes and synovia was performed for
              clinical correlation. Results: Advanced PLN sinuses exhibited an
              increased Ighg2b/Ighm expression ratio (Early 0.5 $\pm$ 0.1 vs
              Advanced 1.4 $\pm$ 0.5 counts/counts; p<0.001) that significantly
              correlated with reduced talus bone volumes in the afferent ankle
              (R2 = 0.54, p<0.001). Integration of single-cell and spatial
              transcriptomics revealed the increased IgG2b+ plasma cells
              localized in MARCO+ peri-follicular medullary sinuses. A
              concomitant decreased Fth1 expression (Early 2.5 $\pm$ 0.74 vs
              Advanced 1.0 $\pm$ 0.50 counts, p<0.001) within Advanced PLN
              sinuses was associated with accumulation of iron-laden Prussian
              blue positive macrophages in lymph nodes and synovium of Advanced
              TNF-Tg mice, and further validated in RA clinical samples.
              T-cells were increased 8-fold in Advanced PLNs, and bioinformatic
              pathway assessment identified the interaction between ALCAM+
              macrophages and CD6+ T-cells as a plausible co-stimulatory
              mechanism to promote IgG2b class-switching. Discussion:
              Collectively, these data support a model of flare in chronic
              TNF-induced arthritis in which loss of lymphatic flow through
              affected joint-draining lymph nodes facilitates the interaction
              between effluxing macrophages and T-cells via ALCAM-CD6
              co-stimulation, initiating IgG2b class-switching and plasma cell
              differentiation of the expanded Bin population. Future work is
              warranted to investigate immunoglobulin clonality and potential
              autoimmune consequences, as well as the efficacy of anti-CD6
              therapy to prevent these pathogenic events.",
  journal  = "Front. Immunol.",
  volume   =  14,
  pages    = "1237498",
  month    =  aug,
  year     =  2023,
  keywords = "B-cells; arthritis; lymph node; lymphatics; plasma cells;
              single-cell RNA sequencing; spatial transcriptomics",
  language = "en"
}

@ARTICLE{Mitamura2023-pp,
  title     = "Spatial transcriptomics combined with single-cell
               {RNA-sequencing} unravels the complex inflammatory cell network
               in atopic dermatitis",
  author    = "Mitamura, Yasutaka and Reiger, Matthias and Kim, Juno and Xiao,
               Yi and Zhakparov, Damir and Tan, Ge and R{\"u}ckert, Beate and
               Rinaldi, Arturo O and Baerenfaller, Katja and Akdis,
               M{\"u}beccel and Br{\"u}ggen, Marie-Charlotte and Nadeau, Kari C
               and Brunner, Patrick M and Roqueiro, Damian and Traidl-Hoffmann,
               Claudia and Akdis, Cezmi A",
  abstract  = "BACKGROUND: Atopic dermatitis (AD) is the most common chronic
               inflammatory skin disease with complex pathogenesis for which
               the cellular and molecular crosstalk in AD skin has not been
               fully understood. METHODS: Skin tissues examined for spatial
               gene expression were derived from the upper arm of 6 healthy
               control (HC) donors and 7 AD patients (lesion and nonlesion). We
               performed spatial transcriptomics sequencing to characterize the
               cellular infiltrate in lesional skin. For single-cell analysis,
               we analyzed the single-cell data from suction blister material
               from AD lesions and HC skin at the antecubital fossa skin (4 ADs
               and 5 HCs) and full-thickness skin biopsies (4 ADs and 2 HCs).
               The multiple proximity extension assays were performed in the
               serum samples from 36 AD patients and 28 HCs. RESULTS: The
               single-cell analysis identified unique clusters of fibroblasts,
               dendritic cells, and macrophages in the lesional AD skin.
               Spatial transcriptomics analysis showed the upregulation of
               COL6A5, COL4A1, TNC, and CCL19 in COL18A1-expressing fibroblasts
               in the leukocyte-infiltrated areas in AD skin. CCR7-expressing
               dendritic cells (DCs) showed a similar distribution in the
               lesions. Additionally, M2 macrophages expressed CCL13 and CCL18
               in this area. Ligand-receptor interaction analysis of the
               spatial transcriptome identified neighboring infiltration and
               interaction between activated COL18A1-expressing fibroblasts,
               CCL13- and CCL18-expressing M2 macrophages, CCR7- and
               LAMP3-expressing DCs, and T cells. As observed in skin lesions,
               serum levels of TNC and CCL18 were significantly elevated in AD,
               and correlated with clinical disease severity. CONCLUSION: In
               this study, we show the unknown cellular crosstalk in
               leukocyte-infiltrated area in lesional skin. Our findings
               provide a comprehensive in-depth knowledge of the nature of AD
               skin lesions to guide the development of better treatments.",
  journal   = "Allergy",
  publisher = "Wiley",
  volume    =  78,
  number    =  8,
  pages     = "2215--2231",
  month     =  aug,
  year      =  2023,
  keywords  = "atopic dermatitis; single-cell transcriptomics; spatial
               transcriptomics; targeted proteomics",
  copyright = "http://creativecommons.org/licenses/by-nc/4.0/",
  language  = "en"
}

@ARTICLE{Olaniru2023-dl,
  title     = "Single-cell transcriptomic and spatial landscapes of the
               developing human pancreas",
  author    = "Olaniru, Oladapo Edward and Kadolsky, Ulrich and Kannambath,
               Shichina and Vaikkinen, Heli and Fung, Kathy and Dhami, Pawan
               and Persaud, Shanta J",
  abstract  = "Current differentiation protocols have not been successful in
               reproducibly generating fully functional human beta cells in
               vitro, partly due to incomplete understanding of human pancreas
               development. Here, we present detailed transcriptomic analysis
               of the various cell types of the developing human pancreas,
               including their spatial gene patterns. We integrated single-cell
               RNA sequencing with spatial transcriptomics at multiple
               developmental time points and revealed distinct temporal-spatial
               gene cascades. Cell trajectory inference identified endocrine
               progenitor populations and branch-specific genes as the
               progenitors differentiate toward alpha or beta cells. Spatial
               differentiation trajectories indicated that Schwann cells are
               spatially co-located with endocrine progenitors, and cell-cell
               connectivity analysis predicted that they may interact via
               L1CAM-EPHB2 signaling. Our integrated approach enabled us to
               identify heterogeneity and multiple lineage dynamics within the
               mesenchyme, showing that it contributed to the exocrine acinar
               cell state. Finally, we have generated an interactive web
               resource for investigating human pancreas development for the
               research community.",
  journal   = "Cell Metab.",
  publisher = "Elsevier BV",
  volume    =  35,
  number    =  1,
  pages     = "184--199.e5",
  month     =  jan,
  year      =  2023,
  keywords  = "Schwann cells; Visium; beta cell development; endocrine
               progenitors; human fetal pancreas; scRNA-seq; spatial
               transcriptomics; trajectory inference",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Heezen2023-oj,
  title     = "Spatial transcriptomics reveal markers of histopathological
               changes in Duchenne muscular dystrophy mouse models",
  author    = "Heezen, L G M and Abdelaal, T and van Putten, M and Aartsma-Rus,
               A and Mahfouz, A and Spitali, P",
  abstract  = "Duchenne muscular dystrophy is caused by mutations in the DMD
               gene, leading to lack of dystrophin. Chronic muscle damage
               eventually leads to histological alterations in skeletal
               muscles. The identification of genes and cell types driving
               tissue remodeling is a key step to developing effective
               therapies. Here we use spatial transcriptomics in two Duchenne
               muscular dystrophy mouse models differing in disease severity to
               identify gene expression signatures underlying skeletal muscle
               pathology and to directly link gene expression to muscle
               histology. We perform deconvolution analysis to identify cell
               types contributing to histological alterations. We show
               increased expression of specific genes in areas of muscle
               regeneration (Myl4, Sparc, Hspg2), fibrosis (Vim, Fn1, Thbs4)
               and calcification (Bgn, Ctsk, Spp1). These findings are
               confirmed by smFISH. Finally, we use differentiation dynamic
               analysis in the D2-mdx muscle to identify muscle fibers in the
               present state that are predicted to become affected in the
               future state.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "4909",
  month     =  aug,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Topchyan2022-vc,
  title     = "Spatial transcriptomics demonstrates the role of {CD4} {T} cells
               in effector {CD8} {T} cell differentiation during chronic viral
               infection",
  author    = "Topchyan, Paytsar and Zander, Ryan and Kasmani, Moujtaba Y and
               Nguyen, Christine and Brown, Ashley and Lin, Siying and Burns,
               Robert and Cui, Weiguo",
  abstract  = "CD4 T cell help is critical to sustain effector CD8 T cell
               responses during chronic infection, notably via T follicular
               helper (Tfh)-derived interleukin-21 (IL-21). Conversely, CD4
               depletion results in severe CD8 T cell dysfunction and lifelong
               viremia despite CD4 T cell reemergence following transient
               depletion. These observations suggest that repopulating CD4
               subsets are functionally or numerically insufficient to
               orchestrate a robust CD8 response. We utilize spatial
               transcriptomics and single-cell RNA sequencing (scRNA-seq) to
               investigate CD4 T cell heterogeneity under CD4-replete and
               -deplete conditions and explore cellular interactions during
               chronic infection. Although IL-21-producing Tfh cells repopulate
               following transient CD4 depletion, they are outnumbered by
               immunomodulatory CD4 T cells. Moreover, the splenic architecture
               appears perturbed, with decreases in white pulp regions,
               coinciding with germinal center losses. These disruptions in
               splenic architecture are associated with diminished Tfh and
               progenitor CD8 T cell colocalization, providing a potential
               mechanism for impaired progenitor-to-effector CD8 T cell
               differentiation during ``un-helped'' conditions.",
  journal   = "Cell Rep.",
  publisher = "Elsevier BV",
  volume    =  41,
  number    =  9,
  pages     = "111736",
  month     =  nov,
  year      =  2022,
  keywords  = "CD4 T cells; CD8 T cells; CP: Immunology; IL-21; LCMV; T
               follicular helper cells; single-cell RNA sequencing; spatial
               transcriptomics",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Filipescu2023-tl,
  title     = "{MacroH2A} restricts inflammatory gene expression in melanoma
               cancer-associated fibroblasts by coordinating chromatin looping",
  author    = "Filipescu, Dan and Carcamo, Saul and Agarwal, Aman and Tung,
               Navpreet and Humblin, {\'E}tienne and Goldberg, Matthew S and
               Vyas, Nikki S and Beaumont, Kristin G and Demircioglu, Deniz and
               Sridhar, Subhasree and Ghiraldini, Flavia G and Capparelli,
               Claudia and Aplin, Andrew E and Salmon, H{\'e}l{\`e}ne and
               Sebra, Robert and Kamphorst, Alice O and Merad, Miriam and
               Hasson, Dan and Bernstein, Emily",
  abstract  = "MacroH2A has established tumour suppressive functions in
               melanoma and other cancers, but an unappreciated role in the
               tumour microenvironment. Using an autochthonous, immunocompetent
               mouse model of melanoma, we demonstrate that mice devoid of
               macroH2A variants exhibit increased tumour burden compared with
               wild-type counterparts. MacroH2A-deficient tumours accumulate
               immunosuppressive monocytes and are depleted of functional
               cytotoxic T cells, characteristics consistent with a compromised
               anti-tumour response. Single cell and spatial transcriptomics
               identify increased dedifferentiation along the neural crest
               lineage of the tumour compartment and increased frequency and
               activation of cancer-associated fibroblasts following macroH2A
               loss. Mechanistically, macroH2A-deficient cancer-associated
               fibroblasts display increased myeloid chemoattractant activity
               as a consequence of hyperinducible expression of inflammatory
               genes, which is enforced by increased chromatin looping of their
               promoters to enhancers that gain H3K27ac. In summary, we reveal
               a tumour suppressive role for macroH2A variants through the
               regulation of chromatin architecture in the tumour stroma with
               potential implications for human melanoma.",
  journal   = "Nat. Cell Biol.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  25,
  number    =  9,
  pages     = "1332--1345",
  month     =  sep,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Vanrobaeys2023-zc,
  title     = "Mapping the spatial transcriptomic signature of the hippocampus
               during memory consolidation",
  author    = "Vanrobaeys, Yann and Mukherjee, Utsav and Langmack, Lucy and
               Beyer, Stacy E and Bahl, Ethan and Lin, Li-Chun and Michaelson,
               Jacob J and Abel, Ted and Chatterjee, Snehajyoti",
  abstract  = "Memory consolidation involves discrete patterns of
               transcriptional events in the hippocampus. Despite the emergence
               of single-cell transcriptomic profiling techniques, mapping the
               transcriptomic signature across subregions of the hippocampus
               has remained challenging. Here, we utilized unbiased spatial
               sequencing to delineate transcriptome-wide gene expression
               changes across subregions of the dorsal hippocampus of male mice
               following learning. We find that each subregion of the
               hippocampus exhibits distinct yet overlapping transcriptomic
               signatures. The CA1 region exhibited increased expression of
               genes related to transcriptional regulation, while the DG showed
               upregulation of genes associated with protein folding.
               Importantly, our approach enabled us to define the
               transcriptomic signature of learning within two less-defined
               hippocampal subregions, CA1 stratum radiatum, and oriens. We
               demonstrated that CA1 subregion-specific expression of a
               transcription factor subfamily has a critical functional role in
               the consolidation of long-term memory. This work demonstrates
               the power of spatial molecular approaches to reveal simultaneous
               transcriptional events across the hippocampus during memory
               consolidation.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "6100",
  month     =  sep,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Kasmani2023-bp,
  title     = "A spatial sequencing atlas of age-induced changes in the lung
               during influenza infection",
  author    = "Kasmani, Moujtaba Y and Topchyan, Paytsar and Brown, Ashley K
               and Brown, Ryan J and Wu, Xiaopeng and Chen, Yao and Khatun,
               Achia and Alson, Donia and Wu, Yue and Burns, Robert and Lin,
               Chien-Wei and Kudek, Matthew R and Sun, Jie and Cui, Weiguo",
  abstract  = "Influenza virus infection causes increased morbidity and
               mortality in the elderly. Aging impairs the immune response to
               influenza, both intrinsically and because of altered
               interactions with endothelial and pulmonary epithelial cells. To
               characterize these changes, we performed single-cell RNA
               sequencing (scRNA-seq), spatial transcriptomics, and bulk RNA
               sequencing (bulk RNA-seq) on lung tissue from young and aged
               female mice at days 0, 3, and 9 post-influenza infection. Our
               analyses identified dozens of key genes differentially expressed
               in kinetic, age-dependent, and cell type-specific manners. Aged
               immune cells exhibited altered inflammatory, memory, and
               chemotactic profiles. Aged endothelial cells demonstrated
               characteristics of reduced vascular wound healing and a
               prothrombotic state. Spatial transcriptomics identified novel
               profibrotic and antifibrotic markers expressed by epithelial and
               non-epithelial cells, highlighting the complex networks that
               promote fibrosis in aged lungs. Bulk RNA-seq generated a
               timeline of global transcriptional activity, showing increased
               expression of genes involved in inflammation and coagulation in
               aged lungs. Our work provides an atlas of high-throughput
               sequencing methodologies that can be used to investigate
               age-related changes in the response to influenza virus, identify
               novel cell-cell interactions for further study, and ultimately
               uncover potential therapeutic targets to improve health outcomes
               in the elderly following influenza infection.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "6597",
  month     =  oct,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Castranio2023-gp,
  title     = "Microglial {INPP5D} limits plaque formation and glial reactivity
               in the {PSAPP} mouse model of Alzheimer's disease",
  author    = "Castranio, Emilie L and Hasel, Philip and Haure-Mirande,
               Jean-Vianney and Ramirez Jimenez, Angie V and Hamilton, B Wade
               and Kim, Rachel D and Glabe, Charles G and Wang, Minghui and
               Zhang, Bin and Gandy, Sam and Liddelow, Shane A and Ehrlich,
               Michelle E",
  abstract  = "INTRODUCTION: The inositol polyphosphate-5-phosphatase D
               (INPP5D) gene encodes a dual-specificity phosphatase that can
               dephosphorylate both phospholipids and phosphoproteins. Single
               nucleotide polymorphisms in INPP5D impact risk for developing
               late onset sporadic Alzheimer's disease (LOAD). METHODS: To
               assess the consequences of inducible Inpp5d knockdown in
               microglia of APPKM670/671NL /PSEN1$\Delta$exon9 (PSAPP) mice, we
               injected 3-month-old Inpp5dfl/fl /Cx3cr1CreER/+ and
               PSAPP/Inpp5dfl/fl /Cx3cr1CreER/+ mice with either tamoxifen
               (TAM) or corn oil (CO) to induce recombination. RESULTS: At age
               6 months, we found that the percent area of 6E10+ deposits and
               plaque-associated microglia in Inpp5d knockdown mice were
               increased compared to controls. Spatial transcriptomics
               identified a plaque-specific expression profile that was
               extensively altered by Inpp5d knockdown. DISCUSSION: These
               results demonstrate that conditional Inpp5d downregulation in
               the PSAPP mouse increases plaque burden and recruitment of
               microglia to plaques. Spatial transcriptomics highlighted an
               extended gene expression signature associated with plaques and
               identified CST7 (cystatin F) as a novel marker of plaques.
               HIGHLIGHTS: Inpp5d knockdown increases plaque burden and
               plaque-associated microglia number. Spatial transcriptomics
               identifies an expanded plaque-specific gene expression profile.
               Plaque-induced gene expression is altered by Inpp5d knockdown in
               microglia. Our plaque-associated gene signature overlaps with
               human Alzheimer's disease gene networks.",
  journal   = "Alzheimers. Dement.",
  publisher = "Wiley",
  volume    =  19,
  number    =  6,
  pages     = "2239--2252",
  month     =  jun,
  year      =  2023,
  keywords  = "Alzheimer's disease; Inpp5d; SHIP1; cystatin F; microglia;
               oligomer; spatial transcriptomics",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Barkley2022-wm,
  title     = "Cancer cell states recur across tumor types and form specific
               interactions with the tumor microenvironment",
  author    = "Barkley, Dalia and Moncada, Reuben and Pour, Maayan and
               Liberman, Deborah A and Dryg, Ian and Werba, Gregor and Wang,
               Wei and Baron, Maayan and Rao, Anjali and Xia, Bo and Fran{\c
               c}a, Gustavo S and Weil, Alejandro and Delair, Deborah F and
               Hajdu, Cristina and Lund, Amanda W and Osman, Iman and Yanai,
               Itai",
  abstract  = "Transcriptional heterogeneity among malignant cells of a tumor
               has been studied in individual cancer types and shown to be
               organized into cancer cell states; however, it remains unclear
               to what extent these states span tumor types, constituting
               general features of cancer. Here, we perform a pan-cancer
               single-cell RNA-sequencing analysis across 15 cancer types and
               identify a catalog of gene modules whose expression defines
               recurrent cancer cell states including 'stress', 'interferon
               response', 'epithelial-mesenchymal transition', 'metal
               response', 'basal' and 'ciliated'. Spatial transcriptomic
               analysis linked the interferon response in cancer cells to T
               cells and macrophages in the tumor microenvironment. Using mouse
               models, we further found that induction of the interferon
               response module varies by tumor location and is diminished upon
               elimination of lymphocytes. Our work provides a framework for
               studying how cancer cell states interact with the tumor
               microenvironment to form organized systems capable of immune
               evasion, drug resistance and metastasis.",
  journal   = "Nat. Genet.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  54,
  number    =  8,
  pages     = "1192--1201",
  month     =  aug,
  year      =  2022,
  language  = "en"
}

@ARTICLE{Eum2024-gk,
  title    = "Single-cell {RNA} sequencing reveals myeloid and {T} cell
              co-stimulation mediated by {IL-7} anti-cancer immunotherapy",
  author   = "Eum, Hye Hyeon and Jeong, Dasom and Kim, Nayoung and Jo, Areum
              and Na, Minsu and Kang, Huiram and Hong, Yourae and Kong, Jin-Sun
              and Jeong, Gi Heon and Yoo, Seung-Ah and Lee, Hae-Ock",
  abstract = "BACKGROUND: Immune checkpoint inhibitors unleash inhibitory
              signals on T cells conferred by tumors and surrounding stromal
              cells. Despite the clinical efficacy of checkpoint inhibitors,
              the lack of target expression and persistence of
              immunosuppressive cells limit the pervasive effectiveness of the
              therapy. These limitations may be overcome by alternative
              approaches that co-stimulate T cells and the immune
              microenvironment. METHODS: We analyzed single-cell RNA sequencing
              data from multiple human cancers and a mouse tumor transplant
              model to discover the pleiotropic expression of the Interleukin 7
              (IL-7) receptor on T cells, macrophages, and dendritic cells.
              RESULTS: Our experiment on the mouse model demonstrated that
              recombinant IL-7 therapy induces tumor regression, expansion of
              effector CD8 T cells, and pro-inflammatory activation of
              macrophages. Moreover, spatial transcriptomic data support
              immunostimulatory interactions between macrophages and T cells.
              CONCLUSION: These results indicate that IL-7 therapy induces
              anti-tumor immunity by activating T cells and pro-inflammatory
              myeloid cells, which may have diverse therapeutic applicability.",
  journal  = "Br. J. Cancer",
  month    =  feb,
  year     =  2024,
  language = "en"
}

@ARTICLE{Canela2023-sa,
  title    = "A spatially anchored transcriptomic atlas of the human kidney
              papilla identifies significant immune injury in patients with
              stone disease",
  author   = "Canela, Victor Hugo and Bowen, William S and Ferreira, Ricardo
              Melo and Syed, Farooq and Lingeman, James E and Sabo, Angela R
              and Barwinska, Daria and Winfree, Seth and Lake, Blue B and
              Cheng, Ying-Hua and Gaut, Joseph P and Ferkowicz, Michael and
              LaFavers, Kaice A and Zhang, Kun and Coe, Fredric L and
              Worcester, Elaine and {Kidney Precision Medicine Project} and
              Jain, Sanjay and Eadon, Michael T and Williams, Jr, James C and
              El-Achkar, Tarek M",
  abstract = "Kidney stone disease causes significant morbidity and increases
              health care utilization. In this work, we decipher the cellular
              and molecular niche of the human renal papilla in patients with
              calcium oxalate (CaOx) stone disease and healthy subjects. In
              addition to identifying cell types important in papillary
              physiology, we characterize collecting duct cell subtypes and an
              undifferentiated epithelial cell type that was more prevalent in
              stone patients. Despite the focal nature of mineral deposition in
              nephrolithiasis, we uncover a global injury signature
              characterized by immune activation, oxidative stress and
              extracellular matrix remodeling. We also identify the association
              of MMP7 and MMP9 expression with stone disease and mineral
              deposition, respectively. MMP7 and MMP9 are significantly
              increased in the urine of patients with CaOx stone disease, and
              their levels correlate with disease activity. Our results define
              the spatial molecular landscape and specific pathways
              contributing to stone-mediated injury in the human papilla and
              identify associated urinary biomarkers.",
  journal  = "Nat. Commun.",
  volume   =  14,
  number   =  1,
  pages    = "4140",
  month    =  jul,
  year     =  2023,
  language = "en"
}

@ARTICLE{Garbarino2023-uw,
  title    = "Spatial resolution of cellular senescence dynamics in human
              colorectal liver metastasis",
  author   = "Garbarino, Ombretta and Lambroia, Luca and Basso, Gianluca and
              Marrella, Veronica and Franceschini, Barbara and Soldani,
              Cristiana and Pasqualini, Fabio and Giuliano, Desiree and Costa,
              Guido and Peano, Clelia and Barbarossa, Davide and Annarita,
              Destro and Salvati, Andreina and Terracciano, Luigi and Torzilli,
              Guido and Donadon, Matteo and Faggioli, Francesca",
  abstract = "Hepatic metastasis is a clinical challenge for colorectal cancer
              (CRC). Senescent cancer cells accumulate in CRC favoring tumor
              dissemination. Whether this mechanism progresses also in
              metastasis is unexplored. Here, we integrated spatial
              transcriptomics, 3D-microscopy, and multicellular transcriptomics
              to study the role of cellular senescence in human colorectal
              liver metastasis (CRLM). We discovered two distinct senescent
              metastatic cancer cell (SMCC) subtypes, transcriptionally located
              at the opposite pole of epithelial (e) to mesenchymal (m)
              transition. SMCCs differ in chemotherapy susceptibility,
              biological program, and prognostic roles. Mechanistically,
              epithelial (e)SMCC initiation relies on nucleolar stress, whereby
              c-myc dependent oncogene hyperactivation induces ribosomal RPL11
              accumulation and DNA damage response. In a 2D pre-clinical model,
              we demonstrated that RPL11 co-localized with HDM2, a p53-specific
              ubiquitin ligase, leading to senescence activation in (e)SMCCs.
              On the contrary, mesenchymal (m)SMCCs undergo TGF$\beta$
              paracrine activation of NOX4-p15 effectors. SMCCs display
              opposing effects also in the immune regulation of neighboring
              cells, establishing an immunosuppressive environment or leading
              to an active immune workflow. Both SMCC signatures are predictive
              biomarkers whose unbalanced ratio determined the clinical outcome
              in CRLM and CRC patients. Altogether, we provide a comprehensive
              new understanding of the role of SMCCs in CRLM and highlight
              their potential as new therapeutic targets to limit CRLM
              progression.",
  journal  = "Aging Cell",
  volume   =  22,
  number   =  7,
  pages    = "e13853",
  month    =  jul,
  year     =  2023,
  keywords = "EMT; cellular senescence; colorectal cancer liver metastasis;
              prognostic role; senescence-associated secretory phenotype;
              spatial transcriptomics",
  language = "en"
}

@ARTICLE{Caetano2023-kj,
  title     = "Spatially resolved transcriptomics reveals pro-inflammatory
               fibroblast involved in lymphocyte recruitment through {CXCL8}
               and {CXCL10}",
  author    = "Caetano, Ana J and Redhead, Yushi and Karim, Farah and Dhami,
               Pawan and Kannambath, Shichina and Nuamah, Rosamond and Volponi,
               Ana A and Nibali, Luigi and Booth, Veronica and D'Agostino,
               Eleanor M and Sharpe, Paul T",
  abstract  = "The interplay among different cells in a tissue is essential for
               maintaining homeostasis. Although disease states have been
               traditionally attributed to individual cell types, increasing
               evidence and new therapeutic options have demonstrated the
               primary role of multicellular functions to understand health and
               disease, opening new avenues to understand pathogenesis and
               develop new treatment strategies. We recently described the
               cellular composition and dynamics of the human oral mucosa;
               however, the spatial arrangement of cells is needed to better
               understand a morphologically complex tissue. Here, we link
               single-cell RNA sequencing, spatial transcriptomics, and
               high-resolution multiplex fluorescence in situ hybridisation to
               characterise human oral mucosa in health and oral chronic
               inflammatory disease. We deconvolved expression for resolution
               enhancement of spatial transcriptomic data and defined highly
               specialised epithelial and stromal compartments describing
               location-specific immune programs. Furthermore, we spatially
               mapped a rare pathogenic fibroblast population localised in a
               highly immunogenic region, responsible for lymphocyte
               recruitment through CXCL8 and CXCL10 and with a possible role in
               pathological angiogenesis through ALOX5AP. Collectively, our
               study provides a comprehensive reference for the study of oral
               chronic disease pathogenesis.",
  journal   = "Elife",
  publisher = "eLife Sciences Publications, Ltd",
  volume    =  12,
  month     =  jan,
  year      =  2023,
  keywords  = "cell biology; fibroblast; gingiva; human; immunology;
               inflammation; oral mucosa; periodontal disease; spatial genomics",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Tung2023-oi,
  title    = "Spatiotemporal signaling underlies progressive vascular
              rarefaction in myocardial infarction",
  author   = "Tung, Lin Wei and Groppa, Elena and Soliman, Hesham and Lin,
              Bruce and Chang, Chihkai and Cheung, Chun Wai and Ritso, Morten
              and Guo, David and Rempel, Lucas and Sinha, Sarthak and Eisner,
              Christine and Brassard, Julyanne and McNagny, Kelly and
              Biernaskie, Jeff and Rossi, Fabio",
  abstract = "Therapeutic angiogenesis represents a promising avenue to
              revascularize the ischemic heart. Its limited success is partly
              due to our poor understanding of the cardiac stroma, specifically
              mural cells, and their response to ischemic injury. Here, we
              combine single-cell and positional transcriptomics to assess the
              behavior of mural cells within the healing heart. In response to
              myocardial infarction, mural cells adopt an altered state closely
              associated with the infarct and retain a distinct lineage from
              fibroblasts. This response is concurrent with vascular
              rarefaction and reduced vascular coverage by mural cells.
              Positional transcriptomics reveals that the infarcted heart is
              governed by regional-dependent and temporally regulated programs.
              While the remote zone acts as an important source of
              pro-angiogenic signals, the infarct zone is accentuated by
              chronic activation of anti-angiogenic, pro-fibrotic, and
              inflammatory cues. Together, our work unveils the spatiotemporal
              programs underlying cardiac repair and establishes an association
              between vascular deterioration and mural cell dysfunction.",
  journal  = "Nat. Commun.",
  volume   =  14,
  number   =  1,
  pages    = "8498",
  month    =  dec,
  year     =  2023,
  language = "en"
}

% The entry below contains non-ASCII chars that could not be converted
% to a LaTeX equivalent.
@ARTICLE{Heimli2022-lj,
  title    = "Multimodal human thymic profiling reveals trajectories and
              cellular milieu for {T} agonist selection",
  author   = "Heimli, Marte and Fl{\aa}m, Siri Tenneb{\o} and Hjorthaug, Hanne
              Sagsveen and Trinh, Don and Frisk, Michael and Dumont,
              Karl-Andreas and Ribarska, Teodora and Tekpli, Xavier and Saare,
              Mario and Lie, Benedicte Alexandra",
  abstract = "To prevent autoimmunity, thymocytes expressing self-reactive T
              cell receptors (TCRs) are negatively selected, however,
              divergence into tolerogenic, agonist selected lineages represent
              an alternative fate. As thymocyte development, selection, and
              lineage choices are dependent on spatial context and cell-to-cell
              interactions, we have performed Cellular Indexing of
              Transcriptomes and Epitopes by sequencing (CITE-seq) and spatial
              transcriptomics on paediatric human thymu​​s. Thymocytes
              expressing markers of strong TCR signalling diverged from the
              conventional developmental trajectory prior to CD4+ or CD8+
              lineage commitment, while markers of different agonist selected T
              cell populations (CD8$\alpha$$\alpha$(I),
              CD8$\alpha$$\alpha$(II), T(agonist), Treg(diff), and Treg)
              exhibited variable timing of induction. Expression profiles of
              chemokines and co-stimulatory molecules, together with spatial
              localisation, supported that dendritic cells, B cells, and
              stromal cells contribute to agonist selection, with different
              subsets influencing thymocytes at specific developmental stages
              within distinct spatial niches. Understanding factors influencing
              agonist T cells is needed to benefit from their immunoregulatory
              effects in clinical use.",
  journal  = "Front. Immunol.",
  volume   =  13,
  pages    = "1092028",
  year     =  2022,
  keywords = "T agonist selection; T cell development; antigen-presenting
              cells; autoimmunity; human thymus; multi-modal; single-cell RNA
              sequencing; spatial transcriptomics",
  language = "en"
}

@ARTICLE{Arora2023-px,
  title     = "Spatial transcriptomics reveals distinct and conserved tumor
               core and edge architectures that predict survival and targeted
               therapy response",
  author    = "Arora, Rohit and Cao, Christian and Kumar, Mehul and Sinha,
               Sarthak and Chanda, Ayan and McNeil, Reid and Samuel, Divya and
               Arora, Rahul K and Matthews, T Wayne and Chandarana, Shamir and
               Hart, Robert and Dort, Joseph C and Biernaskie, Jeff and Neri,
               Paola and Hyrcza, Martin D and Bose, Pinaki",
  abstract  = "The spatial organization of the tumor microenvironment has a
               profound impact on biology and therapy response. Here, we
               perform an integrative single-cell and spatial transcriptomic
               analysis on HPV-negative oral squamous cell carcinoma (OSCC) to
               comprehensively characterize malignant cells in tumor core (TC)
               and leading edge (LE) transcriptional architectures. We show
               that the TC and LE are characterized by unique transcriptional
               profiles, neighboring cellular compositions, and ligand-receptor
               interactions. We demonstrate that the gene expression profile
               associated with the LE is conserved across different cancers
               while the TC is tissue specific, highlighting common mechanisms
               underlying tumor progression and invasion. Additionally, we find
               our LE gene signature is associated with worse clinical outcomes
               while TC gene signature is associated with improved prognosis
               across multiple cancer types. Finally, using an in silico
               modeling approach, we describe spatially-regulated patterns of
               cell development in OSCC that are predictably associated with
               drug response. Our work provides pan-cancer insights into TC and
               LE biology and interactive spatial atlases (
               http://www.pboselab.ca/spatial\_OSCC/ ;
               http://www.pboselab.ca/dynamo\_OSCC/ ) that can be foundational
               for developing novel targeted therapies.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "5029",
  month     =  aug,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Chen2023-ci,
  title    = "Human neural stem cells restore spatial memory in a transgenic
              Alzheimer's disease mouse model by an immunomodulating mechanism",
  author   = "Chen, Kevin S and Noureldein, Mohamed H and McGinley, Lisa M and
              Hayes, John M and Rigan, Diana M and Kwentus, Jacquelin F and
              Mason, Shayna N and Mendelson, Faye E and Savelieff, Masha G and
              Feldman, Eva L",
  abstract = "Introduction: Stem cells are a promising therapeutic in
              Alzheimer's disease (AD) given the complex pathophysiologic
              pathways involved. However, the therapeutic mechanisms of stem
              cells remain unclear. Here, we used spatial transcriptomics to
              elucidate therapeutic mechanisms of human neural stem cells
              (hNSCs) in an animal model of AD. Methods: hNSCs were
              transplanted into the fimbria fornix of the hippocampus using the
              5XFAD mouse model. Spatial memory was assessed by Morris water
              maze. Amyloid plaque burden was quantified. Spatial
              transcriptomics was performed and differentially expressed genes
              (DEGs) identified both globally and within the hippocampus.
              Subsequent pathway enrichment and ligand-receptor network
              analysis was performed. Results: hNSC transplantation restored
              learning curves of 5XFAD mice. However, there were no changes in
              amyloid plaque burden. Spatial transcriptomics showed 1,061 DEGs
              normalized in hippocampal subregions. Plaque induced genes in
              microglia, along with populations of stage 1 and stage 2 disease
              associated microglia (DAM), were normalized upon hNSC
              transplantation. Pathologic signaling between hippocampus and DAM
              was also restored. Discussion: hNSCs normalized many dysregulated
              genes, although this was not mediated by a change in amyloid
              plaque levels. Rather, hNSCs appear to exert beneficial effects
              in part by modulating microglia-mediated neuroinflammation and
              signaling in AD.",
  journal  = "Front. Aging Neurosci.",
  volume   =  15,
  pages    = "1306004",
  month    =  dec,
  year     =  2023,
  keywords = "Alzheimer's disease; cell communication; disease-associated
              microglia; immunomodulation; microglia; neural stem cell; spatial
              transcriptomics; stem cell therapy",
  language = "en"
}

@ARTICLE{Mauduit2022-hu,
  title     = "Spatial transcriptomics of the lacrimal gland features
               macrophage activity and epithelium metabolism as key alterations
               during chronic inflammation",
  author    = "Mauduit, Olivier and Delcroix, Vanessa and Umazume, Takeshi and
               de Paiva, Cintia S and Dartt, Darlene A and Makarenkova, Helen P",
  abstract  = "The lacrimal gland (LG) is an exocrine gland that produces the
               watery part of the tear film that lubricates the ocular surface.
               Chronic inflammation, such as Sj{\"o}gren's syndrome (SS), is
               one of the leading causes of aqueous-deficiency dry eye (ADDE)
               disease worldwide. In this study we analyzed the chronic
               inflammation in the LGs of the NOD.B10Sn-H2b/J (NOD.H-2b) mice,
               a mouse model of SS, utilizing bulk RNAseq and Visium spatial
               gene expression. With Seurat we performed unsupervised
               clustering and analyzed the spatial cell distribution and gene
               expression changes in all cell clusters within the LG sections.
               Moreover, for the first time, we analyzed and validated specific
               pathways defined by bulk RNAseq using Visium technology to
               determine activation of these pathways within the LG sections.
               This analysis suggests that altered metabolism and the hallmarks
               of inflammatory responses from both epithelial and immune cells
               drive inflammation. The most significant pathway enriched in
               upregulated DEGs was the ``TYROBP Causal Network'', that has not
               been described previously in SS. We also noted a significant
               decrease in lipid metabolism in the LG of the NOD.H-2b mice. Our
               data suggests that modulation of these pathways can provide a
               therapeutic strategy to treat ADDE.",
  journal   = "Front. Immunol.",
  publisher = "Frontiers Media SA",
  volume    =  13,
  pages     = "1011125",
  month     =  oct,
  year      =  2022,
  keywords  = "RNA sequencing; TYROBP; chronic inflammation; lacrimal gland;
               lipid metabolism; macrophages; spatial transcriptomics; visium",
  copyright = "https://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Bassiouni2023-ls,
  title     = "Spatial transcriptomic analysis of a diverse patient cohort
               reveals a conserved architecture in triple-negative breast
               cancer",
  author    = "Bassiouni, Rania and Idowu, Michael O and Gibbs, Lee D and
               Robila, Valentina and Grizzard, Pamela J and Webb, Michelle G
               and Song, Jiarong and Noriega, Ashley and Craig, David W and
               Carpten, John D",
  abstract  = "Triple-negative breast cancer (TNBC) is an aggressive disease
               that disproportionately affects African American (AA) women.
               Limited targeted therapeutic options exist for patients with
               TNBC. Here, we employ spatial transcriptomics to interrogate
               tissue from a racially diverse TNBC cohort to comprehensively
               annotate the transcriptional states of spatially resolved
               cellular populations. A total of 38,706 spatial features from a
               cohort of 28 sections from 14 patients were analyzed.
               Intratumoral analysis of spatial features from individual
               sections revealed heterogeneous transcriptional substructures.
               However, integrated analysis of all samples resulted in nine
               transcriptionally distinct clusters that mapped across all
               individual sections. Furthermore, novel use of join count
               analysis demonstrated nonrandom directional spatial dependencies
               of the transcriptionally defined shared clusters, supporting a
               conserved spatio-transcriptional architecture in TNBC. These
               findings were substantiated in an independent validation cohort
               comprising 17,861 spatial features representing 15 samples from
               8 patients. Stratification of samples by race revealed
               race-associated differences in hypoxic tumor content and regions
               of immune-rich infiltrate. Overall, this study combined spatial
               and functional molecular analyses to define the tumor
               architecture of TNBC, with potential implications in
               understanding TNBC disparities. SIGNIFICANCE: Spatial
               transcriptomics profiling of a diverse cohort of triple-negative
               breast cancers and innovative informatics approaches reveal a
               conserved cellular architecture across cancers and identify
               proportional differences in tumor cell composition by race.",
  journal   = "Cancer Res.",
  publisher = "American Association for Cancer Research (AACR)",
  volume    =  83,
  number    =  1,
  pages     = "34--48",
  month     =  jan,
  year      =  2023,
  language  = "en"
}

@ARTICLE{Lyubetskaya2022-yl,
  title     = "Assessment of spatial transcriptomics for oncology discovery",
  author    = "Lyubetskaya, Anna and Rabe, Brian and Fisher, Andrew and Lewin,
               Anne and Neuhaus, Isaac and Brett, Constance and Brett, Todd and
               Pereira, Ethel and Golhar, Ryan and Kebede, Sami and Font-Tello,
               Alba and Mosure, Kathy and Van Wittenberghe, Nicholas and
               Mavrakis, Konstantinos J and MacIsaac, Kenzie and Chen, Benjamin
               J and Drokhlyansky, Eugene",
  abstract  = "Tumor heterogeneity is a major challenge for oncology drug
               discovery and development. Understanding of the spatial tumor
               landscape is key to identifying new targets and impactful model
               systems. Here, we test the utility of spatial transcriptomics
               (ST) for oncology discovery by profiling 40 tissue sections and
               80,024 capture spots across a diverse set of tissue types,
               sample formats, and RNA capture chemistries. We verify the
               accuracy and fidelity of ST by leveraging matched pathology
               analysis, which provides a ground truth for tissue section
               composition. We then use spatial data to demonstrate the capture
               of key tumor depth features, identifying hypoxia, necrosis,
               vasculature, and extracellular matrix variation. We also
               leverage spatial context to identify relative cell-type
               locations showing the anti-correlation of tumor and immune cells
               in syngeneic cancer models. Lastly, we demonstrate target
               identification approaches in clinical pancreatic adenocarcinoma
               samples, highlighting tumor intrinsic biomarkers and paracrine
               signaling.",
  journal   = "Cell Rep. Methods",
  publisher = "Elsevier BV",
  volume    =  2,
  number    =  11,
  pages     = "100340",
  month     =  nov,
  year      =  2022,
  keywords  = "biomarkers; cancer biology; cancer genomics; digital pathology;
               genomics; oncology; pancreatic cancer; spatial genomics; spatial
               transcriptomics; tumors",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Lee2023-ng,
  title     = "{APOE} modulates microglial immunometabolism in response to age,
               amyloid pathology, and inflammatory challenge",
  author    = "Lee, Sangderk and Devanney, Nicholas A and Golden, Lesley R and
               Smith, Cathryn T and Schwartz, James L and Walsh, Adeline E and
               Clarke, Harrison A and Goulding, Danielle S and Allenger,
               Elizabeth J and Morillo-Segovia, Gabriella and Friday, Cassi M
               and Gorman, Amy A and Hawkinson, Tara R and MacLean, Steven M
               and Williams, Holden C and Sun, Ramon C and Morganti, Josh M and
               Johnson, Lance A",
  abstract  = "The E4 allele of Apolipoprotein E (APOE) is associated with both
               metabolic dysfunction and a heightened pro-inflammatory
               response: two findings that may be intrinsically linked through
               the concept of immunometabolism. Here, we combined bulk,
               single-cell, and spatial transcriptomics with cell-specific and
               spatially resolved metabolic analyses in mice expressing human
               APOE to systematically address the role of APOE across age,
               neuroinflammation, and AD pathology. RNA sequencing (RNA-seq)
               highlighted immunometabolic changes across the APOE4 glial
               transcriptome, specifically in subsets of metabolically distinct
               microglia enriched in the E4 brain during aging or following an
               inflammatory challenge. E4 microglia display increased
               Hif1$\alpha$ expression and a disrupted tricarboxylic acid (TCA)
               cycle and are inherently pro-glycolytic, while spatial
               transcriptomics and mass spectrometry imaging highlight an
               E4-specific response to amyloid that is characterized by
               widespread alterations in lipid metabolism. Taken together, our
               findings emphasize a central role for APOE in regulating
               microglial immunometabolism and provide valuable, interactive
               resources for discovery and validation research.",
  journal   = "Cell Rep.",
  publisher = "Elsevier BV",
  volume    =  42,
  number    =  3,
  pages     = "112196",
  month     =  mar,
  year      =  2023,
  keywords  = "APOE; Apolipoprotein E; CP: Neuroscience; DAM; LPS; aging;
               amyloid; immunometabolism; microglia; scRNA-seq; spatial
               transcriptomics",
  copyright = "http://creativecommons.org/licenses/by/4.0/",
  language  = "en"
}

@ARTICLE{Foster2022-uy,
  title     = "Multiomic analysis reveals conservation of cancer-associated
               fibroblast phenotypes across species and tissue of origin",
  author    = "Foster, Deshka S and Januszyk, Michael and Delitto, Daniel and
               Yost, Kathryn E and Griffin, Michelle and Guo, Jason and
               Guardino, Nicholas and Delitto, Andrea E and Chinta, Malini and
               Burcham, Austin R and Nguyen, Alan T and Bauer-Rowe, Khristian E
               and Titan, Ashley L and Salhotra, Ankit and Jones, R Ellen and
               da Silva, Oscar and Lindsay, Hunter G and Berry, Charlotte E and
               Chen, Kellen and Henn, Dominic and Mascharak, Shamik and
               Talbott, Heather E and Kim, Alexia and Nosrati, Fatemeh and
               Sivaraj, Dharshan and Ransom, R Chase and Matthews, Michael and
               Khan, Anum and Wagh, Dhananjay and Coller, John and Gurtner,
               Geoffrey C and Wan, Derrick C and Wapnir, Irene L and Chang,
               Howard Y and Norton, Jeffrey A and Longaker, Michael T",
  abstract  = "Cancer-associated fibroblasts (CAFs) are integral to the solid
               tumor microenvironment. CAFs were once thought to be a
               relatively uniform population of matrix-producing cells, but
               single-cell RNA sequencing has revealed diverse CAF phenotypes.
               Here, we further probed CAF heterogeneity with a comprehensive
               multiomics approach. Using paired, same-cell chromatin
               accessibility and transcriptome analysis, we provided an
               integrated analysis of CAF subpopulations over a complex spatial
               transcriptomic and proteomic landscape to identify three
               superclusters: steady state-like (SSL), mechanoresponsive (MR),
               and immunomodulatory (IM) CAFs. These superclusters are
               recapitulated across multiple tissue types and species.
               Selective disruption of underlying mechanical force or immune
               checkpoint inhibition therapy results in shifts in CAF
               subpopulation distributions and affected tumor growth. As such,
               the balance among CAF superclusters may have considerable
               translational implications. Collectively, this research expands
               our understanding of CAF biology, identifying regulatory
               pathways in CAF differentiation and elucidating therapeutic
               targets in a species- and tumor-agnostic manner.",
  journal   = "Cancer Cell",
  publisher = "Elsevier BV",
  volume    =  40,
  number    =  11,
  pages     = "1392--1406.e7",
  month     =  nov,
  year      =  2022,
  keywords  = "ATAC-seq; CODEX; RNA-seq; cancer; fibroblasts;
               mechanotransduction; multi-omics; single cell; spatial
               transcriptomics",
  copyright = "http://www.elsevier.com/open-access/userlicense/1.0/",
  language  = "en"
}

@ARTICLE{Subramanian2024-ov,
  title    = "Sarcoma microenvironment cell states and ecosystems are
              associated with prognosis and predict response to immunotherapy",
  author   = "Subramanian, Ajay and Nemat-Gorgani, Neda and Ellis-Caleo,
              Timothy J and van IJzendoorn, David G P and Sears, Timothy J and
              Somani, Anish and Luca, Bogdan A and Zhou, Maggie Y and Bradic,
              Martina and Torres, Ileana A and Oladipo, Eniola and New,
              Christin and Kenney, Deborah E and Avedian, Raffi S and Steffner,
              Robert J and Binkley, Michael S and Mohler, David G and Tap,
              William D and D'Angelo, Sandra P and van de Rijn, Matt and
              Ganjoo, Kristen N and Bui, Nam Q and Charville, Gregory W and
              Newman, Aaron M and Moding, Everett J",
  abstract = "Characterization of the diverse malignant and stromal cell states
              that make up soft tissue sarcomas and their correlation with
              patient outcomes has proven difficult using fixed clinical
              specimens. Here, we employed EcoTyper, a machine-learning
              framework, to identify the fundamental cell states and cellular
              ecosystems that make up sarcomas on a large scale using bulk
              transcriptomes with clinical annotations. We identified and
              validated 23 sarcoma-specific, transcriptionally defined cell
              states, many of which were highly prognostic of patient outcomes
              across independent datasets. We discovered three conserved
              cellular communities or ecotypes associated with underlying
              genomic alterations and distinct clinical outcomes. We show that
              one ecotype defined by tumor-associated macrophages and
              epithelial-like malignant cells predicts response to
              immune-checkpoint inhibition but not chemotherapy and validate
              our findings in an independent cohort. Our results may enable
              identification of patients with soft tissue sarcomas who could
              benefit from immunotherapy and help develop new therapeutic
              strategies.",
  journal  = "Nat. Cancer",
  month    =  mar,
  year     =  2024,
  language = "en"
}

@ARTICLE{Gu2022-wz,
  title     = "Multi-omics profiling visualizes dynamics of cardiac development
               and functions",
  author    = "Gu, Yayun and Zhou, Yan and Ju, Sihan and Liu, Xiaofei and
               Zhang, Zicheng and Guo, Jia and Gao, Jimiao and Zang, Jie and
               Sun, Hao and Chen, Qi and Wang, Jinghan and Xu, Jiani and Xu,
               Yiqun and Chen, Yingjia and Guo, Yueshuai and Dai, Juncheng and
               Ma, Hongxia and Wang, Cheng and Jin, Guangfu and Li, Chaojun and
               Xia, Yankai and Shen, Hongbing and Yang, Yang and Guo, Xuejiang
               and Hu, Zhibin",
  abstract  = "Cardiogenesis is a tightly regulated dynamic process through a
               continuum of differentiation and proliferation events. Key
               factors and pathways governing this process remain incompletely
               understood. Here, we investigate mice hearts from embryonic day
               10.5 to postnatal week 8 and dissect developmental changes in
               phosphoproteome-, proteome-, metabolome-, and
               transcriptome-encompassing cardiogenesis and cardiac maturation.
               We identify mitogen-activated protein kinases as core kinases
               involved in transcriptional regulation by mediating the
               phosphorylation of chromatin remodeling proteins during early
               cardiogenesis. We construct the reciprocal regulatory network of
               transcription factors (TFs) and identify a series of TFs
               controlling early cardiogenesis involved in cycling-dependent
               proliferation. After birth, we identify cardiac resident
               macrophages with high arachidonic acid metabolism activities
               likely involved in the clearance of injured apoptotic
               cardiomyocytes. Together, our comprehensive multi-omics data
               offer a panoramic view of cardiac development and maturation
               that provides a resource for further in-depth functional
               exploration.",
  journal   = "Cell Rep.",
  publisher = "Elsevier BV",
  volume    =  41,
  number    =  13,
  pages     = "111891",
  month     =  dec,
  year      =  2022,
  keywords  = "CP: Developmental biology; cardiac maturation; cardiogenesis;
               efferocytosis; macrophages; multi-omics; protein
               phosphorylation; transcriptional regulation",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Coutant2023-jt,
  title     = "Spatial transcriptomics reveal pitfalls and opportunities for
               the detection of rare high-plasticity breast cancer subtypes",
  author    = "Coutant, Ang{\`e}le and Cockenpot, Vincent and Muller, Lauriane
               and Degletagne, Cyril and Pommier, Roxane and Tonon, Laurie and
               Ardin, Maude and Michallet, Marie-C{\'e}cile and Caux,
               Christophe and Laurent, Marie and Morel, Anne-Pierre and
               Saintigny, Pierre and Puisieux, Alain and Ouzounova, Maria and
               Martinez, Pierre",
  abstract  = "Breast cancer is one of the most prominent types of cancers, in
               which therapeutic resistance is a major clinical concern.
               Specific subtypes, such as claudin-low and metaplastic breast
               carcinoma (MpBC), have been associated with high nongenetic
               plasticity, which can facilitate resistance. The similarities
               and differences between these orthogonal subtypes, identified by
               molecular and histopathological analyses, respectively, remain
               insufficiently characterized. Furthermore, adequate methods to
               identify high-plasticity tumors to better anticipate resistance
               are lacking. Here, we analyzed 11 triple-negative breast tumors,
               including 3 claudin-low and 4 MpBC, via high-resolution spatial
               transcriptomics. We combined pathological annotations and
               deconvolution approaches to precisely identify tumor spots, on
               which we performed signature enrichment, differential
               expression, and copy number analyses. We used The Cancer Genome
               Atlas and Cancer Cell Line Encyclopedia public databases for
               external validation of expression markers. By focusing our
               spatial transcriptomic analyses on tumor cells in MpBC samples,
               we bypassed the negative impact of stromal contamination and
               identified specific markers that are neither expressed in other
               breast cancer subtypes nor expressed in stromal cells. Three
               markers (BMPER, POPDC3, and SH3RF3) were validated in external
               expression databases encompassing bulk tumor material and
               stroma-free cell lines. We unveiled that existing bulk
               expression signatures of high-plasticity breast cancers are
               relevant in mesenchymal transdifferentiated compartments but can
               be hindered by abundant stromal cells in tumor samples,
               negatively impacting their clinical applicability. Spatial
               transcriptomic analyses constitute powerful tools to identify
               specific expression markers and could thus enhance diagnosis and
               clinical care of rare high-plasticity breast cancers.",
  journal   = "Lab. Invest.",
  publisher = "Elsevier BV",
  volume    =  103,
  number    =  12,
  pages     = "100258",
  month     =  dec,
  year      =  2023,
  keywords  = "diagnostic markers; integrative approaches; plasticity; rare
               subtypes; spatial transcriptomics",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Sanders2022-wz,
  title     = "Small cell carcinoma of the ovary hypercalcemic type ({SCCOHT)}:
               A review and novel case with dual germline {SMARCA4} and {BRCA2}
               mutations",
  author    = "Sanders, Brooke E and Wolsky, Rebecca and Doughty, Elizabeth S
               and Wells, Kristen L and Ghosh, Debashis and Ku, Lisa and
               Pressey, Joseph G and Bitler, Benjamin B and Brubaker, Lindsay W",
  abstract  = "Small cell carcinoma of the ovary hypercalcemic type (SCCOHT) is
               a rare and aggressive disease. While classically linked to
               mutations in SMARCA4, we describe a case in a patient with both
               SMARCA4 and BRCA2 germline mutations. We describe her disease
               presentation, histopathology and treatment with adjuvant
               systemic chemotherapy, interval hyperthermic intraperitoneal
               chemotherapy, high dose chemotherapy with stem cell rescue, and
               maintenance with a poly-ADP-ribose polymerase inhibitor (PARPi).
               Additionally, we share spatial transcriptomics completed on
               original tumor.",
  journal   = "Gynecol. Oncol. Rep.",
  publisher = "Elsevier BV",
  volume    =  44,
  number    =  101077,
  pages     = "101077",
  month     =  dec,
  year      =  2022,
  keywords  = "PARP inhibitor; Small cell carcinoma of the ovary;
               Transcriptomics",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Akiyama2023-oh,
  title     = "Stromal reprogramming through dual {PDGFR$\alpha$/$\beta$}
               blockade boosts the efficacy of {anti-PD-1} immunotherapy in
               fibrotic tumors",
  author    = "Akiyama, Takahiko and Yasuda, Tadahito and Uchihara, Tomoyuki
               and Yasuda-Yoshihara, Noriko and Tan, Benjy J Y and Yonemura,
               Atsuko and Semba, Takashi and Yamasaki, Juntaro and Komohara,
               Yoshihiro and Ohnishi, Koji and Wei, Feng and Fu, Lingfeng and
               Zhang, Jun and Kitamura, Fumimasa and Yamashita, Kohei and Eto,
               Kojiro and Iwagami, Shiro and Tsukamoto, Hirotake and Umemoto,
               Terumasa and Masuda, Mari and Nagano, Osamu and Satou, Yorifumi
               and Saya, Hideyuki and Tan, Patrick and Baba, Hideo and
               Ishimoto, Takatsugu",
  abstract  = "Excess stroma and cancer-associated fibroblasts (CAF) enhance
               cancer progression and facilitate immune evasion. Insights into
               the mechanisms by which the stroma manipulates the immune
               microenvironment could help improve cancer treatment. Here, we
               aimed to elucidate potential approaches for stromal
               reprogramming and improved cancer immunotherapy.
               Platelet-derived growth factor C (PDGFC) and D expression were
               significantly associated with a poor prognosis in patients with
               gastric cancer, and PDGF receptor beta (PDGFR$\beta$) was
               predominantly expressed in diffuse-type gastric cancer stroma.
               CAFs stimulated with PDGFs exhibited markedly increased
               expression of CXCL1, CXCL3, CXCL5, and CXCL8, which are involved
               in polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC)
               recruitment. Fibrotic gastric cancer xenograft tumors exhibited
               increased PMN-MDSC accumulation and decreased lymphocyte
               infiltration, as well as resistance to anti-PD-1. Single-cell
               RNA sequencing and spatial transcriptomics revealed that
               PDGFR$\alpha$/$\beta$ blockade reversed the immunosuppressive
               microenvironment through stromal modification. Finally,
               combining PDGFR$\alpha$/$\beta$ blockade and anti-PD-1 treatment
               synergistically suppressed the growth of fibrotic tumors. These
               findings highlight the impact of stromal reprogramming on immune
               reactivation and the potential for combined immunotherapy for
               patients with fibrotic cancer. SIGNIFICANCE: Stromal targeting
               with PDGFR$\alpha$/$\beta$ dual blockade reverses the
               immunosuppressive microenvironment and enhances the efficacy of
               immune checkpoint inhibitors in fibrotic cancer. See related
               commentary by Tauriello, p. 655.",
  journal   = "Cancer Res.",
  publisher = "American Association for Cancer Research (AACR)",
  volume    =  83,
  number    =  5,
  pages     = "753--770",
  month     =  mar,
  year      =  2023,
  language  = "en"
}

@ARTICLE{Yoshitake2024-qi,
  title    = "Molecular features of luminal breast cancer defined through
              spatial and single-cell transcriptomics",
  author   = "Yoshitake, Ryohei and Mori, Hitomi and Ha, Desiree and Wu, Xiwei
              and Wang, Jinhui and Wang, Xiaoqiang and Saeki, Kohei and Chang,
              Gregory and Shim, Hyun Jeong and Chan, Yin and Chen, Shiuan",
  abstract = "BACKGROUND: Intratumour heterogeneity is a hallmark of most solid
              tumours, including breast cancers. We applied spatial
              transcriptomics and single-cell RNA-sequencing on patient-derived
              xenografts (PDXs) to profile spatially resolved cell populations
              within oestrogen receptor-positive (ER+ ) breast cancer and to
              elucidate their importance in oestrogen-dependent tumour growth.
              METHODS: Two PDXs of 'ER-high' breast cancers with opposite
              oestrogen-mediated growth responses were investigated:
              oestrogen-suppressed GS3 (80-100\% ER) and oestrogen-dependent
              SC31 (40-90\% ER) models. The observation was validated via
              single-cell analyses on an 'ER-low' PDX, GS1 (5\% ER). The
              results from our spatial and single-cell analyses were further
              supported by a public ER+ breast cancer single-cell dataset and
              protein-based dual immunohistochemistry (IHC) of SC31 examining
              important luminal cancer markers (i.e., ER, progesterone receptor
              and Ki67). The translational implication of our findings was
              assessed by clinical outcome analyses on publicly available
              cohorts. RESULTS: Our space-gene-function study revealed four
              spatially distinct compartments within ER+ breast cancers. These
              compartments showed functional diversity (oestrogen-responsive,
              proliferative, hypoxia-induced and inflammation-related). The
              'proliferative' population, rather than the
              'oestrogen-responsive' compartment, was crucial for
              oestrogen-dependent tumour growth, leading to the acquisition of
              luminal B-like features. The cells expressing typical
              oestrogen-responsive genes like PGR were not directly linked to
              oestrogen-dependent proliferation. Dual IHC analyses demonstrated
              the distinct contribution of the Ki67+ proliferative cells toward
              oestrogen-mediated growth and their response to a CDK4/6
              inhibitor. The gene signatures derived from the proliferative,
              hypoxia-induced and inflammation-related compartments were
              significantly correlated with worse clinical outcomes, while
              patients with the oestrogen-responsive signature showed better
              prognoses, suggesting that this compartment would not be directly
              associated with oestrogen-dependent tumour progression.
              CONCLUSIONS: Our study identified the gene signature in our
              'proliferative' compartment as an important determinant of
              luminal cancer subtypes. This 'proliferative' cell population is
              a causative feature of luminal B breast cancer, contributing
              toward its aggressive behaviours.",
  journal  = "Clin. Transl. Med.",
  volume   =  14,
  number   =  1,
  pages    = "e1548",
  month    =  jan,
  year     =  2024,
  keywords = "breast cancer; intratumour heterogeneity; oestrogen receptor;
              single-cell RNA-sequencing; spatial transcriptomics",
  language = "en"
}

@ARTICLE{Ballester_Roig2023-hb,
  title    = "Probing pathways by which rhynchophylline modifies sleep using
              spatial transcriptomics",
  author   = "Ballester Roig, Maria Neus and Leduc, Tanya and Dufort-Gervais,
              Julien and Maghmoul, Yousra and Tastet, Olivier and Mongrain,
              Val{\'e}rie",
  abstract = "BACKGROUND: Rhynchophylline (RHY) is an alkaloid component of
              Uncaria, which are plants extensively used in traditional Asian
              medicines. Uncaria treatments increase sleep time and quality in
              humans, and RHY induces sleep in rats. However, like many
              traditional natural treatments, the mechanisms of action of RHY
              and Uncaria remain evasive. Moreover, it is unknown whether RHY
              modifies key brain oscillations during sleep. We thus aimed at
              defining the effects of RHY on sleep architecture and
              oscillations throughout a 24-h cycle, as well as identifying the
              underlying molecular mechanisms. Mice received systemic RHY
              injections at two times of the day (beginning and end of the
              light period), and vigilance states were studied by
              electrocorticographic recordings. RESULTS: RHY enhanced slow wave
              sleep (SWS) after both injections, suppressed paradoxical sleep
              (PS) in the light but enhanced PS in the dark period.
              Furthermore, RHY modified brain oscillations during both
              wakefulness and SWS (including delta activity dynamics) in a
              time-dependent manner. Interestingly, most effects were larger in
              females. A brain spatial transcriptomic analysis showed that RHY
              modifies the expression of genes linked to cell movement,
              apoptosis/necrosis, and transcription/translation in a brain
              region-independent manner, and changes those linked to sleep
              regulation (e.g., Hcrt, Pmch) in a brain region-specific manner
              (e.g., in the hypothalamus). CONCLUSIONS: The findings provide
              support to the sleep-inducing effect of RHY, expose the relevance
              to shape wake/sleep oscillations, and highlight its effects on
              the transcriptome with a high spatial resolution. The exposed
              molecular mechanisms underlying the effect of a natural compound
              should benefit sleep- and brain-related medicine.",
  journal  = "Biol. Direct",
  volume   =  18,
  number   =  1,
  pages    = "21",
  month    =  may,
  year     =  2023,
  keywords = "Electrocorticographic oscillations; Hypothalamus; Molecular
              profiling; Sex; Sleep induction; Slow wave sleep",
  language = "en"
}

% The entry below contains non-ASCII chars that could not be converted
% to a LaTeX equivalent.
@ARTICLE{Villemin2023-ck,
  title     = "Inferring ligand-receptor cellular networks from bulk and
               spatial transcriptomic datasets with {BulkSignalR}",
  author    = "Villemin, Jean-Philippe and Bassaganyas, Laia and Pourquier,
               Didier and Boissi{\`e}re, Florence and Cabello-Aguilar, Simon
               and Crapez, Evelyne and Tanos, Rita and Cornillot, Emmanuel and
               Turtoi, Andrei and Colinge, Jacques",
  abstract  = "The study of cellular networks mediated by ligand-receptor
               interactions has attracted much attention recently owing to
               single-cell omics. However, rich collections of bulk data
               accompanied with clinical information exists and continue to be
               generated with no equivalent in single-cell so far. In parallel,
               spatial transcriptomic (ST) analyses represent a revolutionary
               tool in biology. A large number of ST projects rely on
               multicellular resolution, for instance the Visium™ platform,
               where several cells are analyzed at each location, thus
               producing localized bulk data. Here, we describe BulkSignalR, a
               R package to infer ligand-receptor networks from bulk data.
               BulkSignalR integrates ligand-receptor interactions with
               downstream pathways to estimate statistical significance. A
               range of visualization methods complement the statistics,
               including functions dedicated to spatial data. We demonstrate
               BulkSignalR relevance using different datasets, including new
               Visium liver metastasis ST data, with experimental validation of
               protein colocalization. A comparison with other ST packages
               shows the significantly higher quality of BulkSignalR
               inferences. BulkSignalR can be applied to any species thanks to
               its built-in generic ortholog mapping functionality.",
  journal   = "Nucleic Acids Res.",
  publisher = "Oxford University Press (OUP)",
  volume    =  51,
  number    =  10,
  pages     = "4726--4744",
  month     =  may,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by-nc/4.0/",
  language  = "en"
}

@ARTICLE{Caronni2023-pe,
  title     = "{IL-1$\beta$+} macrophages fuel pathogenic inflammation in
               pancreatic cancer",
  author    = "Caronni, Nicoletta and La Terza, Federica and Vittoria,
               Francesco M and Barbiera, Giulia and Mezzanzanica, Luca and
               Cuzzola, Vincenzo and Barresi, Simona and Pellegatta, Marta and
               Canevazzi, Paolo and Dunsmore, Garett and Leonardi, Carlo and
               Montaldo, Elisa and Lusito, Eleonora and Dugnani, Erica and
               Citro, Antonio and Ng, Melissa S F and Schiavo Lena, Marco and
               Drago, Denise and Andolfo, Annapaola and Brugiapaglia, Silvia
               and Scagliotti, Alessandro and Mortellaro, Alessandra and Corbo,
               Vincenzo and Liu, Zhaoyuan and Mondino, Anna and Dellabona,
               Paolo and Piemonti, Lorenzo and Taveggia, Carla and Doglioni,
               Claudio and Cappello, Paola and Novelli, Francesco and
               Iannacone, Matteo and Ng, Lai Guan and Ginhoux, Florent and
               Crippa, Stefano and Falconi, Massimo and Bonini, Chiara and
               Naldini, Luigi and Genua, Marco and Ostuni, Renato",
  abstract  = "Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with
               high resistance to therapies1. Inflammatory and immunomodulatory
               signals co-exist in the pancreatic tumour microenvironment,
               leading to dysregulated repair and cytotoxic responses.
               Tumour-associated macrophages (TAMs) have key roles in PDAC2,
               but their diversity has prevented therapeutic exploitation. Here
               we combined single-cell and spatial genomics with functional
               experiments to unravel macrophage functions in pancreatic
               cancer. We uncovered an inflammatory loop between tumour cells
               and interleukin-1$\beta$ (IL-1$\beta$)-expressing TAMs, a subset
               of macrophages elicited by a local synergy between prostaglandin
               E2 (PGE2) and tumour necrosis factor (TNF). Physical proximity
               with IL-1$\beta$+ TAMs was associated with inflammatory
               reprogramming and acquisition of pathogenic properties by a
               subset of PDAC cells. This occurrence was an early event in
               pancreatic tumorigenesis and led to persistent transcriptional
               changes associated with disease progression and poor outcomes
               for patients. Blocking PGE2 or IL-1$\beta$ activity elicited TAM
               reprogramming and antagonized tumour cell-intrinsic and
               -extrinsic inflammation, leading to PDAC control in vivo.
               Targeting the PGE2-IL-1$\beta$ axis may enable preventive or
               therapeutic strategies for reprogramming of immune dynamics in
               pancreatic cancer.",
  journal   = "Nature",
  publisher = "Springer Science and Business Media LLC",
  volume    =  623,
  number    =  7986,
  pages     = "415--422",
  month     =  nov,
  year      =  2023,
  copyright = "https://www.springernature.com/gp/researchers/text-and-data-mining",
  language  = "en"
}

@ARTICLE{Sukhanov2023-ja,
  title    = "Insulin-like growth factor 1 reduces coronary atherosclerosis in
              pigs with familial hypercholesterolemia",
  author   = "Sukhanov, Sergiy and Higashi, Yusuke and Yoshida, Tadashi and
              Danchuk, Svitlana and Alfortish, Mitzi and Goodchild, Traci and
              Scarborough, Amy and Sharp, Thomas and Jenkins, James S and
              Garcia, Daniel and Ivey, Jan and Tharp, Darla L and Schumacher,
              Jeffrey and Rozenbaum, Zach and Kolls, Jay K and Bowles, Douglas
              and Lefer, David and Delafontaine, Patrice",
  abstract = "Although murine models of coronary atherosclerotic disease have
              been used extensively to determine mechanisms, limited new
              therapeutic options have emerged. Pigs with familial
              hypercholesterolemia (FH pigs) develop complex coronary atheromas
              that are almost identical to human lesions. We reported
              previously that insulin-like growth factor 1 (IGF-1) reduced
              aortic atherosclerosis and promoted features of stable plaque in
              a murine model. We administered human recombinant IGF-1 or saline
              (control) in atherosclerotic FH pigs for 6 months. IGF-1
              decreased relative coronary atheroma in vivo (intravascular
              ultrasound) and reduced lesion cross-sectional area (postmortem
              histology). IGF-1 increased plaque's fibrous cap thickness, and
              reduced necrotic core, macrophage content, and cell apoptosis,
              consistent with promotion of a stable plaque phenotype. IGF-1
              reduced circulating triglycerides, markers of systemic oxidative
              stress, and CXCL12 chemokine levels. We used spatial
              transcriptomics (ST) to identify global transcriptome changes in
              advanced plaque compartments and to obtain mechanistic insights
              into IGF-1 effects. ST analysis showed that IGF-1 suppressed
              FOS/FOSB factors and gene expression of MMP9 and CXCL14 in plaque
              macrophages, suggesting possible involvement of these molecules
              in IGF-1's effect on atherosclerosis. Thus, IGF-1 reduced
              coronary plaque burden and promoted features of stable plaque in
              a pig model, providing support for consideration of clinical
              trials.",
  journal  = "JCI Insight",
  volume   =  8,
  number   =  4,
  month    =  feb,
  year     =  2023,
  keywords = "Atherosclerosis; Cardiology; Growth factors; Plaque formation;
              Vascular Biology",
  language = "en"
}

@ARTICLE{Zhi2024-hz,
  title    = "Spatial transcriptomic and metabolomic landscapes of oral
              submucous fibrosis-derived oral squamous cell carcinoma and its
              tumor microenvironment",
  author   = "Zhi, Yuan and Wang, Qian and Zi, Moxin and Zhang, Shanshan and
              Ge, Junshang and Liu, Keyue and Lu, Linsong and Fan, Chunmei and
              Yan, Qijia and Shi, Lei and Chen, Pan and Fan, Songqing and Liao,
              Qianjin and Guo, Can and Wang, Fuyan and Gong, Zhaojian and
              Xiong, Wei and Zeng, Zhaoyang",
  abstract = "In South and Southeast Asia, the habit of chewing betel nuts is
              prevalent, which leads to oral submucous fibrosis (OSF). OSF is a
              well-established precancerous lesion, and a portion of OSF cases
              eventually progress to oral squamous cell carcinoma (OSCC).
              However, the specific molecular mechanisms underlying the
              malignant transformation of OSCC from OSF are poorly understood.
              In this study, the leading-edge techniques of Spatial
              Transcriptomics (ST) and Spatial Metabolomics (SM) are integrated
              to obtain spatial location information of cancer cells,
              fibroblasts, and immune cells, as well as the transcriptomic and
              metabolomic landscapes in OSF-derived OSCC tissues. This work
              reveals for the first time that some OSF-derived OSCC cells
              undergo partial epithelial-mesenchymal transition (pEMT) within
              the in situ carcinoma (ISC) region, eventually acquiring
              fibroblast-like phenotypes and participating in collagen
              deposition. Complex interactions among epithelial cells,
              fibroblasts, and immune cells in the tumor microenvironment are
              demonstrated. Most importantly, significant metabolic
              reprogramming in OSF-derived OSCC, including abnormal polyamine
              metabolism, potentially playing a pivotal role in promoting
              tumorigenesis and immune evasion is discovered. The ST and SM
              data in this study shed new light on deciphering the mechanisms
              of OSF-derived OSCC. The work also offers invaluable clues for
              the prevention and treatment of OSCC.",
  journal  = "Adv. Sci. (Weinh.)",
  volume   =  11,
  number   =  12,
  pages    = "e2306515",
  month    =  mar,
  year     =  2024,
  keywords = "oral squamous cell carcinoma (OSCC); oral submucous fibrosis
              (OSF); polyamine metabolism; spatial metabolomics; spatial
              transcriptomics; tumor microenvironment",
  language = "en"
}

@ARTICLE{Kerzel2023-fn,
  title     = "In vivo macrophage engineering reshapes the tumor
               microenvironment leading to eradication of liver metastases",
  author    = "Kerzel, Thomas and Giacca, Giovanna and Beretta, Stefano and
               Bresesti, Chiara and Notaro, Marco and Scotti, Giulia Maria and
               Balestrieri, Chiara and Canu, Tamara and Redegalli, Miriam and
               Pedica, Federica and Genua, Marco and Ostuni, Renato and
               Kajaste-Rudnitski, Anna and Oshima, Masanobu and Tonon, Giovanni
               and Merelli, Ivan and Aldrighetti, Luca and Dellabona, Paolo and
               Coltella, Nadia and Doglioni, Claudio and Rancoita, Paola M V
               and Sanvito, Francesca and Naldini, Luigi and Squadrito, Mario
               Leonardo",
  abstract  = "Liver metastases are associated with poor response to current
               pharmacological treatments, including immunotherapy. We describe
               a lentiviral vector (LV) platform to selectively engineer liver
               macrophages, including Kupffer cells and tumor-associated
               macrophages (TAMs), to deliver type I interferon (IFN$\alpha$)
               to liver metastases. Gene-based IFN$\alpha$ delivery delays the
               growth of colorectal and pancreatic ductal adenocarcinoma liver
               metastases in mice. Response to IFN$\alpha$ is associated with
               TAM immune activation, enhanced MHC-II-restricted antigen
               presentation and reduced exhaustion of CD8+ T cells. Conversely,
               increased IL-10 signaling, expansion of Eomes CD4+ T cells, a
               cell type displaying features of type I regulatory T (Tr1)
               cells, and CTLA-4 expression are associated with resistance to
               therapy. Targeting regulatory T cell functions by combinatorial
               CTLA-4 immune checkpoint blockade and IFN$\alpha$ LV delivery
               expands tumor-reactive T cells, attaining complete response in
               most mice. These findings support a promising therapeutic
               strategy with feasible translation to patients with unmet
               medical need.",
  journal   = "Cancer Cell",
  publisher = "Elsevier BV",
  volume    =  41,
  number    =  11,
  pages     = "1892--1910.e10",
  month     =  nov,
  year      =  2023,
  keywords  = "Colorectal cancer (CRC); EOMES; Gene therapy; Immunotherapy;
               Interferon-alpha; Interleukin-10 (IL-10); Liver metastases;
               Pancreatic cancer; Tumor-associated macrophages (TAMs); Type 1
               regulatory T cells (Tr1)",
  copyright = "http://creativecommons.org/licenses/by-nc-nd/4.0/",
  language  = "en"
}

@ARTICLE{Mirzazadeh2023-ql,
  title     = "Spatially resolved transcriptomic profiling of degraded and
               challenging fresh frozen samples",
  author    = "Mirzazadeh, Reza and Andrusivova, Zaneta and Larsson, Ludvig and
               Newton, Phillip T and Galicia, Leire Alonso and Abalo, Xes{\'u}s
               M and Avijgan, Mahtab and Kvastad, Linda and Denadai-Souza,
               Alexandre and Stakenborg, Nathalie and Firsova, Alexandra B and
               Shamikh, Alia and Jurek, Aleksandra and Schultz, Niklas and
               Nist{\'e}r, Monica and Samakovlis, Christos and Boeckxstaens,
               Guy and Lundeberg, Joakim",
  abstract  = "Spatially resolved transcriptomics has enabled precise
               genome-wide mRNA expression profiling within tissue sections.
               The performance of methods targeting the polyA tails of mRNA
               relies on the availability of specimens with high RNA quality.
               Moreover, the high cost of currently available spatial resolved
               transcriptomics assays requires a careful sample screening
               process to increase the chance of obtaining high-quality data.
               Indeed, the upfront analysis of RNA quality can show
               considerable variability due to sample handling, storage, and/or
               intrinsic factors. We present RNA-Rescue Spatial Transcriptomics
               (RRST), a workflow designed to improve mRNA recovery from fresh
               frozen specimens with moderate to low RNA quality. First, we
               provide a benchmark of RRST against the standard Visium spatial
               gene expression protocol on high RNA quality samples represented
               by mouse brain and prostate cancer samples. Then, we test the
               RRST protocol on tissue sections collected from five challenging
               tissue types, including human lung, colon, small intestine,
               pediatric brain tumor, and mouse bone/cartilage. In total, we
               analyze 52 tissue sections and demonstrate that RRST is a
               versatile, powerful, and reproducible protocol for fresh frozen
               specimens of different qualities and origins.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "509",
  month     =  jan,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Vanrobaeys2023-bw,
  title     = "Spatial transcriptomics reveals unique gene expression changes
               in different brain regions after sleep deprivation",
  author    = "Vanrobaeys, Yann and Peterson, Zeru J and Walsh, Emily N and
               Chatterjee, Snehajyoti and Lin, Li-Chun and Lyons, Lisa C and
               Nickl-Jockschat, Thomas and Abel, Ted",
  abstract  = "Sleep deprivation has far-reaching consequences on the brain and
               behavior, impacting memory, attention, and metabolism. Previous
               research has focused on gene expression changes in individual
               brain regions, such as the hippocampus or cortex. Therefore, it
               is unclear how uniformly or heterogeneously sleep loss affects
               the brain. Here, we use spatial transcriptomics to define the
               impact of a brief period of sleep deprivation across the brain
               in male mice. We find that sleep deprivation induced pronounced
               differences in gene expression across the brain, with the
               greatest changes in the hippocampus, neocortex, hypothalamus,
               and thalamus. Both the differentially expressed genes and the
               direction of regulation differed markedly across regions.
               Importantly, we developed bioinformatic tools to register tissue
               sections and gene expression data into a common anatomical
               space, allowing a brain-wide comparison of gene expression
               patterns between samples. Our results suggest that distinct
               molecular mechanisms acting in discrete brain regions underlie
               the biological effects of sleep deprivation.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "7095",
  month     =  nov,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Liu2023-tk,
  title    = "Moxibustion improves hypothalamus Aqp4 polarization in {APP/PS1}
              mice: Evidence from spatial transcriptomics",
  author   = "Liu, Shuqing and Li, Hongying and Shen, Yuan and Zhu, Weikang and
              Wang, Yong and Wang, Junmeng and Zhang, Ning and Li, Chenyu and
              Xie, Lushuang and Wu, Qiaofeng",
  abstract = "Aquaporin-4 (AQP4) is highly polarized to perivascular astrocytic
              endfeet. Loss of AQP4 polarization is associated with many
              diseases. In Alzheimer's disease (AD), AQP4 loses its normal
              location and thus reduces the clearance of amyloid-$\beta$
              plaques and tau protein. Clinical and experimental studies showed
              that moxibustion can improve the learning and memory abilities of
              AD. To explore whether moxibustion can affect the polarization of
              AQP4 around the blood-brain barrier (BBB), we used spatial
              transcriptomics (ST) to analyze the expression and polarization
              of Aqp4 in wild-type mice, APP/PS1 mice, and APP/PS1 mice
              intervened by moxibustion. The results showed that moxibustion
              improved the loss of abnormal polarization of AQP4 in APP/PS1
              mice, especially in the hypothalamic BBB. Besides, the other 31
              genes with Aqp4 as the core have similar depolarization in
              APP/PS1 mice, most of which are also membrane proteins. The
              majority of them have been reversed by moxibustion. At the same
              time, we employed the cerebrospinal fluid circulation gene set,
              which was found to be at a higher level in the group of APP/PS1
              mice with moxibustion treatment. Finally, to further explore its
              mechanism, we analyzed the mitochondrial respiratory chain
              complex enzymes closely related to energy metabolism and found
              that moxibustion can significantly increase the expression of
              mitochondrial respiratory chain enzymes such as Cox6a2 in the
              hypothalamus, which could provide energy for mRNA transport. Our
              research shows that increasing the polarization of hypothalamic
              Aqp4 through mitochondrial energy supply may be an important
              target for moxibustion to improve cognitive impairment in APP/PS1
              mice.",
  journal  = "Front. Aging Neurosci.",
  volume   =  15,
  pages    = "1069155",
  month    =  feb,
  year     =  2023,
  keywords = "Alzheimer's disease; aquaporin-4; hypothalamus; mitochondrial
              respiratory chain; moxibustion; spatial transcriptomics",
  language = "en"
}

@ARTICLE{Chaker2023-cj,
  title    = "Pregnancy-responsive pools of adult neural stem cells for
              transient neurogenesis in mothers",
  author   = "Chaker, Zayna and Segalada, Corina and Kretz, Jonas A and Acar,
              Ilhan E and Delgado, Ana C and Crotet, Valerie and Moor, Andreas
              E and Doetsch, Fiona",
  abstract = "Adult neural stem cells (NSCs) contribute to lifelong brain
              plasticity. In the adult mouse ventricular-subventricular zone,
              NSCs are heterogeneous and, depending on their location in the
              niche, give rise to different subtypes of olfactory bulb (OB)
              interneurons. Here, we show that multiple regionally distinct
              NSCs, including domains that are usually quiescent, are recruited
              on different gestation days during pregnancy. Synchronized
              activation of these adult NSC pools generates transient waves of
              short-lived OB interneurons, especially in layers with less
              neurogenesis under homeostasis. Using spatial transcriptomics, we
              identified molecular markers of pregnancy-associated interneurons
              and showed that some subsets are temporarily needed for own pup
              recognition. Thus, pregnancy triggers transient yet behaviorally
              relevant neurogenesis, highlighting the physiological relevance
              of adult stem cell heterogeneity.",
  journal  = "Science",
  volume   =  382,
  number   =  6673,
  pages    = "958--963",
  month    =  nov,
  year     =  2023,
  language = "en"
}

@ARTICLE{Deshpande2023-eo,
  title     = "Uncovering the spatial landscape of molecular interactions
               within the tumor microenvironment through latent spaces",
  author    = "Deshpande, Atul and Loth, Melanie and Sidiropoulos, Dimitrios N
               and Zhang, Shuming and Yuan, Long and Bell, Alexander T F and
               Zhu, Qingfeng and Ho, Won Jin and Santa-Maria, Cesar and Gilkes,
               Daniele M and Williams, Stephen R and Uytingco, Cedric R and
               Chew, Jennifer and Hartnett, Andrej and Bent, Zachary W and
               Favorov, Alexander V and Popel, Aleksander S and Yarchoan, Mark
               and Kiemen, Ashley and Wu, Pei-Hsun and Fujikura, Kohei and
               Wirtz, Denis and Wood, Laura D and Zheng, Lei and Jaffee,
               Elizabeth M and Anders, Robert A and Danilova, Ludmila and
               Stein-O'Brien, Genevieve and Kagohara, Luciane T and Fertig,
               Elana J",
  abstract  = "Recent advances in spatial transcriptomics (STs) enable gene
               expression measurements from a tissue sample while retaining its
               spatial context. This technology enables unprecedented in situ
               resolution of the regulatory pathways that underlie the
               heterogeneity in the tumor as well as the tumor microenvironment
               (TME). The direct characterization of cellular co-localization
               with spatial technologies facilities quantification of the
               molecular changes resulting from direct cell-cell interaction,
               as it occurs in tumor-immune interactions. We present
               SpaceMarkers, a bioinformatics algorithm to infer molecular
               changes from cell-cell interactions from latent space analysis
               of ST data. We apply this approach to infer the molecular
               changes from tumor-immune interactions in Visium spatial
               transcriptomics data of metastasis, invasive and precursor
               lesions, and immunotherapy treatment. Further transfer learning
               in matched scRNA-seq data enabled further quantification of the
               specific cell types in which SpaceMarkers are enriched.
               Altogether, SpaceMarkers can identify the location and
               context-specific molecular interactions within the TME from ST
               data.",
  journal   = "Cell Syst.",
  publisher = "Elsevier BV",
  volume    =  14,
  number    =  4,
  pages     = "285--301.e4",
  month     =  apr,
  year      =  2023,
  keywords  = "cell-cell interactions; latent space factorization; single-cell
               transcriptomics; spatial analysis; spatial transcriptomics;
               transfer learning; tumor microenvironment",
  language  = "en"
}

@ARTICLE{Deshpande2023-bt,
  title    = "Uncovering the spatial landscape of molecular interactions within
              the tumor microenvironment through latent spaces",
  author   = "Deshpande, Atul and Loth, Melanie and Sidiropoulos, Dimitrios N
              and Zhang, Shuming and Yuan, Long and Bell, Alexander T F and
              Zhu, Qingfeng and Ho, Won Jin and Santa-Maria, Cesar and Gilkes,
              Daniele M and Williams, Stephen R and Uytingco, Cedric R and
              Chew, Jennifer and Hartnett, Andrej and Bent, Zachary W and
              Favorov, Alexander V and Popel, Aleksander S and Yarchoan, Mark
              and Kiemen, Ashley and Wu, Pei-Hsun and Fujikura, Kohei and
              Wirtz, Denis and Wood, Laura D and Zheng, Lei and Jaffee,
              Elizabeth M and Anders, Robert A and Danilova, Ludmila and
              Stein-O'Brien, Genevieve and Kagohara, Luciane T and Fertig,
              Elana J",
  journal  = "Cell Syst.",
  volume   =  14,
  number   =  8,
  pages    = "722",
  month    =  aug,
  year     =  2023,
  language = "en"
}

@ARTICLE{Stec2023-md,
  title    = "A cellular and molecular spatial atlas of dystrophic muscle",
  author   = "Stec, Michael J and Su, Qi and Adler, Christina and Zhang, Lance
              and Golann, David R and Khan, Naveen P and Panagis, Lampros and
              Villalta, S Armando and Ni, Min and Wei, Yi and Walls, Johnathon
              R and Murphy, Andrew J and Yancopoulos, George D and Atwal,
              Gurinder S and Kleiner, Sandra and Halasz, Gabor and Sleeman,
              Mark W",
  abstract = "Asynchronous skeletal muscle degeneration/regeneration is a
              hallmark feature of Duchenne muscular dystrophy (DMD); however,
              traditional -omics technologies that lack spatial context make it
              difficult to study the biological mechanisms of how asynchronous
              regeneration contributes to disease progression. Here, using the
              severely dystrophic D2-mdx mouse model, we generated a
              high-resolution cellular and molecular spatial atlas of
              dystrophic muscle by integrating spatial transcriptomics and
              single-cell RNAseq datasets. Unbiased clustering revealed
              nonuniform distribution of unique cell populations throughout
              D2-mdx muscle that were associated with multiple regenerative
              timepoints, demonstrating that this model faithfully
              recapitulates the asynchronous regeneration observed in human DMD
              muscle. By probing spatiotemporal gene expression signatures, we
              found that propagation of inflammatory and fibrotic signals from
              locally damaged areas contributes to widespread pathology and
              that querying expression signatures within discrete
              microenvironments can identify targetable pathways for DMD
              therapy. Overall, this spatial atlas of dystrophic muscle
              provides a valuable resource for studying DMD disease biology and
              therapeutic target discovery.",
  journal  = "Proc. Natl. Acad. Sci. U. S. A.",
  volume   =  120,
  number   =  29,
  pages    = "e2221249120",
  month    =  jul,
  year     =  2023,
  keywords = "Duchenne muscular dystrophy; asynchronous regeneration; skeletal
              muscle; spatial transcriptomics",
  language = "en"
}

@ARTICLE{Chitturi2023-tv,
  title    = "Tripterygium wilfordii derivative celastrol, a {YAP} inhibitor,
              has antifibrotic effects in systemic sclerosis",
  author   = "Chitturi, Pratyusha and Xu, Shiwen and Ahmed Abdi, Bahja and
              Nguyen, John and Carter, David E and Sinha, Sartak and Arora,
              Rohit and Biernaskie, Jeff and Stratton, Richard J and Leask,
              Andrew",
  abstract = "OBJECTIVES: Systemic sclerosis (SSc) is characterised by
              extensive tissue fibrosis maintained by
              mechanotranductive/proadhesive signalling. Drugs targeting this
              pathway are therefore of likely therapeutic benefit. The
              mechanosensitive transcriptional co-activator, yes activated
              protein-1 (YAP1), is activated in SSc fibroblasts. The terpenoid
              celastrol is a YAP1 inhibitor; however, if celastrol can
              alleviate SSc fibrosis is unknown. Moreover, the cell niches
              required for skin fibrosis are unknown. METHODS: Human dermal
              fibroblasts from healthy individuals and patients with diffuse
              cutaneous SSc were treated with or without transforming growth
              factor $\beta$1 (TGF$\beta$1), with or without celastrol. Mice
              were subjected to the bleomycin-induced model of skin SSc, in the
              presence or absence of celastrol. Fibrosis was assessed using RNA
              Sequencing, real-time PCR, spatial transcriptomic analyses,
              Western blot, ELISA and histological analyses. RESULTS: In dermal
              fibroblasts, celastrol impaired the ability of TGF$\beta$1 to
              induce an SSc-like pattern of gene expression, including that of
              cellular communication network factor 2, collagen I and
              TGF$\beta$1. Celastrol alleviated the persistent fibrotic
              phenotype of dermal fibroblasts cultured from lesions of SSc
              patients. In the bleomycin-induced model of skin SSc, increased
              expression of genes associated with reticular fibroblast and
              hippo/YAP clusters was observed; conversely, celastrol inhibited
              these bleomycin-induced changes and blocked nuclear localisation
              of YAP. CONCLUSIONS: Our data clarify niches within the skin
              activated in fibrosis and suggest that compounds, such as
              celastrol, that antagonise the YAP pathway may be potential
              treatments for SSc skin fibrosis.",
  journal  = "Ann. Rheum. Dis.",
  volume   =  82,
  number   =  9,
  pages    = "1191--1204",
  month    =  sep,
  year     =  2023,
  keywords = "Arthritis, Experimental; Fibroblasts; Scleroderma, Systemic;
              Therapeutics",
  language = "en"
}

@ARTICLE{Pavel2023-ip,
  title    = "Comparison of the Illumina {NextSeq} 2000 and {GeneMind} Genolab
              {M} sequencing platforms for spatial transcriptomics",
  author   = "Pavel, Iamshchikov and Irina, Larionova and Tatiana, Gerashchenko
              and Denis, Piankov and Philipp, Koshkin and Sergei, Korostelev
              and Evgeny, Denisov",
  abstract = "BACKGROUND: The Illumina sequencing systems demonstrate high
              efficiency and power and remain the most popular platforms.
              Platforms with similar throughput and quality profiles but lower
              costs are under intensive development. In this study, we compared
              two platforms Illumina NextSeq 2000 and GeneMind Genolab M for
              10x Genomics Visium spatial transcriptomics. RESULTS: The
              performed comparison demonstrates that GeneMind Genolab M
              sequencing platform produces highly consistent with Illumina
              NextSeq 2000 sequencing results. Both platforms have similar
              performance in terms of sequencing quality and detection of UMI,
              spatial barcode, and probe sequence. Raw read mapping and
              following read counting produced highly comparable results that
              is confirmed by quality control metrics and strong correlation
              between expression profiles in the same tissue spots. Downstream
              analysis including dimension reduction and clustering
              demonstrated similar results, and differential gene expression
              analysis predominantly detected the same genes for both
              platforms. CONCLUSIONS: GeneMind Genolab M instrument is similar
              to Illumina sequencing efficacy and is suitable for 10x Genomics
              Visium spatial transcriptomics.",
  journal  = "BMC Genomics",
  volume   =  24,
  number   =  1,
  pages    = "102",
  month    =  mar,
  year     =  2023,
  keywords = "10x Genomics Visium; GeneMind Genolab M; Illumina NextSeq 2000;
              Sequencing; Spatial transcriptomics",
  language = "en"
}

@ARTICLE{Wu2024-oi,
  title     = "High resolution spatial profiling of kidney injury and repair
               using {RNA} hybridization-based in situ sequencing",
  author    = "Wu, Haojia and Dixon, Eryn E and Xuanyuan, Qiao and Guo, Juanru
               and Yoshimura, Yasuhiro and Debashish, Chitnis and Niesnerova,
               Anezka and Xu, Hao and Rouault, Morgane and Humphreys, Benjamin
               D",
  abstract  = "Emerging spatially resolved transcriptomics technologies allow
               for the measurement of gene expression in situ at cellular
               resolution. We apply direct RNA hybridization-based in situ
               sequencing (dRNA HybISS, Cartana part of 10xGenomics) to compare
               male and female healthy mouse kidneys and the male kidney injury
               and repair timecourse. A pre-selected panel of 200 genes is used
               to identify cell state dynamics patterns during injury and
               repair. We develop a new computational pipeline, CellScopes, for
               the rapid analysis, multi-omic integration and visualization of
               spatially resolved transcriptomic datasets. The resulting
               dataset allows us to resolve 13 kidney cell types within
               distinct kidney niches, dynamic alterations in cell state over
               the course of injury and repair and cell-cell interactions
               between leukocytes and kidney parenchyma. At late timepoints
               after injury, C3+ leukocytes are enriched near pro-inflammatory,
               failed-repair proximal tubule cells. Integration of snRNA-seq
               dataset from the same injury and repair samples also allows us
               to impute the spatial localization of genes not directly
               measured by dRNA HybISS.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  15,
  number    =  1,
  pages     = "1396",
  month     =  feb,
  year      =  2024,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Moeyersoms2023-it,
  title    = "Spatial transcriptomics identifies expression signatures specific
              to lacrimal gland adenoid cystic carcinoma cells",
  author   = "Moeyersoms, Acadia H M and Gallo, Ryan A and Zhang, Michelle G
              and Stathias, Vasileios and Maeng, Michelle M and Owens, Dawn and
              Abou Khzam, Rayan and Sayegh, Yoseph and Maza, Cynthia and
              Dubovy, Sander R and Tse, David T and Pelaez, Daniel",
  abstract = "Although primary tumors of the lacrimal gland are rare, adenoid
              cystic carcinoma (ACC) is the most common and lethal epithelial
              lacrimal gland malignancy. Traditional management of lacrimal
              gland adenoid cystic carcinoma (LGACC) involves the removal of
              the eye and surrounding socket contents, followed by
              chemoradiation. Even with this radical treatment, the 10-year
              survival rate for LGACC is 20\% given the propensity for
              recurrence and metastasis. Due to the rarity of LGACC, its
              pathobiology is not well-understood, leading to difficulties in
              diagnosis, treatment, and effective management. Here, we
              integrate bulk RNA sequencing (RNA-seq) and spatial
              transcriptomics to identify a specific LGACC gene signature that
              can inform novel targeted therapies. Of the 3499 differentially
              expressed genes identified by bulk RNA-seq, the results of our
              spatial transcriptomic analysis reveal 15 upregulated and 12
              downregulated genes that specifically arise from LGACC cells,
              whereas fibroblasts, reactive fibrotic tissue, and nervous and
              skeletal muscle account for the remaining bulk RNA-seq signature.
              In light of the analysis, we identified a transitional state cell
              or stem cell cluster. The results of the pathway analysis
              identified the upregulation of PI3K-Akt signaling, IL-17
              signaling, and multiple other cancer pathways. This study
              provides insights into the molecular and cellular landscape of
              LGACC, which can inform new, targeted therapies to improve
              patient outcomes.",
  journal  = "Cancers (Basel)",
  volume   =  15,
  number   =  12,
  month    =  jun,
  year     =  2023,
  keywords = "lacrimal gland adenoid cystic carcinoma; rare cancer; spatial
              transcriptomics; transcriptomic signature",
  language = "en"
}

@ARTICLE{Rauber2024-kd,
  title    = "{CD200+} fibroblasts form a pro-resolving mesenchymal network in
              arthritis",
  author   = "Rauber, Simon and Mohammadian, Hashem and Schmidkonz, Christian
              and Atzinger, Armin and Soare, Alina and Treutlein, Christoph and
              Kemble, Samuel and Mahony, Christopher B and Geisthoff, Manuel
              and Angeli, Mario R and Raimondo, Maria G and Xu, Cong and Yang,
              Kai-Ting and Lu, Le and Labinsky, Hannah and Saad, Mina S A and
              Gwellem, Charles A and Chang, Jiyang and Huang, Kaiyue and
              Kampylafka, Eleni and Knitza, Johannes and Bilyy, Rostyslav and
              Distler, J{\"o}rg H W and Hanlon, Megan M and Fearon, Ursula and
              Veale, Douglas J and Roemer, Frank W and B{\"a}uerle, Tobias and
              Maric, Hans M and Maschauer, Simone and Ekici, Arif B and
              Buckley, Christopher D and Croft, Adam P and Kuwert, Torsten and
              Prante, Olaf and Ca{\~n}ete, Juan D and Schett, Georg and
              Ramming, Andreas",
  abstract = "Fibroblasts are important regulators of inflammation, but whether
              fibroblasts change phenotype during resolution of inflammation is
              not clear. Here we use positron emission tomography to detect
              fibroblast activation protein (FAP) as a means to visualize
              fibroblast activation in vivo during inflammation in humans.
              While tracer accumulation is high in active arthritis, it
              decreases after tumor necrosis factor and interleukin-17A
              inhibition. Biopsy-based single-cell RNA-sequencing analyses in
              experimental arthritis show that FAP signal reduction reflects a
              phenotypic switch from pro-inflammatory MMP3+/IL6+ fibroblasts
              (high FAP internalization) to pro-resolving CD200+DKK3+
              fibroblasts (low FAP internalization). Spatial transcriptomics of
              human joints indicates that pro-resolving niches of CD200+DKK3+
              fibroblasts cluster with type 2 innate lymphoid cells, whereas
              MMP3+/IL6+ fibroblasts colocalize with inflammatory immune cells.
              CD200+DKK3+ fibroblasts stabilized the type 2 innate lymphoid
              cell phenotype and induced resolution of arthritis via
              CD200-CD200R1 signaling. Taken together, these data suggest a
              dynamic molecular regulation of the mesenchymal compartment
              during resolution of inflammation.",
  journal  = "Nat. Immunol.",
  volume   =  25,
  number   =  4,
  pages    = "682--692",
  month    =  apr,
  year     =  2024,
  language = "en"
}

@ARTICLE{Sans2023-ny,
  title    = "Spatial transcriptomics of intraductal papillary mucinous
              neoplasms of the pancreas identifies {NKX6-2} as a driver of
              gastric differentiation and indolent biological potential",
  author   = "Sans, Marta and Makino, Yuki and Min, Jimin and Rajapakshe, Kimal
              I and Yip-Schneider, Michele and Schmidt, C Max and Hurd, Mark W
              and Burks, Jared K and Gomez, Javier A and Thege, Fredrik I and
              Fahrmann, Johannes F and Wolff, Robert A and Kim, Michael P and
              Guerrero, Paola A and Maitra, Anirban",
  abstract = "Intraductal papillary mucinous neoplasms (IPMN) of the pancreas
              are bona fide precursor lesions of pancreatic ductal
              adenocarcinoma (PDAC). The most common subtype of IPMNs harbors a
              gastric foveolar-type epithelium, and these low-grade mucinous
              neoplasms are harbingers of IPMNs with high-grade dysplasia and
              cancer. The molecular underpinning of gastric differentiation in
              IPMNs is unknown, although identifying drivers of this indolent
              phenotype might enable opportunities for intercepting progression
              to high-grade IPMN and cancer. We conducted spatial
              transcriptomics on a cohort of IPMNs, followed by orthogonal and
              cross-species validation studies, which established the
              transcription factor NKX6-2 as a key determinant of gastric cell
              identity in low-grade IPMNs. Loss of NKX6-2 expression is a
              consistent feature of IPMN progression, while reexpression of
              Nkx6-2 in murine IPMN lines recapitulates the aforementioned
              gastric transcriptional program and glandular morphology. Our
              study identifies NKX6-2 as a previously unknown transcription
              factor driving indolent gastric differentiation in IPMN
              pathogenesis. SIGNIFICANCE: Identification of the molecular
              features driving IPMN development and differentiation is critical
              to prevent cancer progression and enhance risk stratification. We
              used spatial profiling to characterize the epithelium and
              microenvironment of IPMN, which revealed a previously unknown
              link between NKX6-2 and gastric differentiation, the latter
              associated with indolent biological potential. See related
              commentary by Ben-Shmuel and Scherz-Shouval, p. 1768. This
              article is highlighted in the In This Issue feature, p. 1749.",
  journal  = "Cancer Discov.",
  volume   =  13,
  number   =  8,
  pages    = "1844--1861",
  month    =  aug,
  year     =  2023,
  language = "en"
}

@ARTICLE{Gharaie2023-mn,
  title    = "Single cell and spatial transcriptomics analysis of kidney double
              negative {T} lymphocytes in normal and ischemic mouse kidneys",
  author   = "Gharaie, Sepideh and Lee, Kyungho and Noller, Kathleen and Lo,
              Emily K and Miller, Brendan and Jung, Hyun Jun and Newman-Rivera,
              Andrea M and Kurzhagen, Johanna T and Singla, Nirmish and
              Welling, Paul A and Fan, Jean and Cahan, Patrick and Noel,
              Sanjeev and Rabb, Hamid",
  abstract = "T cells are important in the pathogenesis of acute kidney injury
              (AKI), and TCR+CD4-CD8- (double negative-DN) are T cells that
              have regulatory properties. However, there is limited information
              on DN T cells compared to traditional CD4+ and CD8+ cells. To
              elucidate the molecular signature and spatial dynamics of DN T
              cells during AKI, we performed single-cell RNA sequencing
              (scRNA-seq) on sorted murine DN, CD4+, and CD8+ cells combined
              with spatial transcriptomic profiling of normal and post AKI
              mouse kidneys. scRNA-seq revealed distinct transcriptional
              profiles for DN, CD4+, and CD8+ T cells of mouse kidneys with
              enrichment of Kcnq5, Klrb1c, Fcer1g, and Klre1 expression in DN T
              cells compared to CD4+ and CD8+ T cells in normal kidney tissue.
              We validated the expression of these four genes in mouse kidney
              DN, CD4+ and CD8+ T cells using RT-PCR and Kcnq5, Klrb1, and
              Fcer1g genes with the NIH human kidney precision medicine project
              (KPMP). Spatial transcriptomics in normal and ischemic mouse
              kidney tissue showed a localized cluster of T cells in the outer
              medulla expressing DN T cell genes including Fcer1g. These
              results provide a template for future studies in DN T as well as
              CD4+ and CD8+ cells in normal and diseased kidneys.",
  journal  = "Sci. Rep.",
  volume   =  13,
  number   =  1,
  pages    = "20888",
  month    =  nov,
  year     =  2023,
  language = "en"
}

@ARTICLE{Mei2023-fx,
  title     = "Siglec-9 acts as an immune-checkpoint molecule on macrophages in
               glioblastoma, restricting T-cell priming and immunotherapy
               response",
  author    = "Mei, Yan and Wang, Xiumei and Zhang, Ji and Liu, Dan and He,
               Junjie and Huang, Chunliu and Liao, Jing and Wang, Yingzhao and
               Feng, Yongyi and Li, Hongyu and Liu, Xiuying and Chen, Lingdan
               and Yi, Wei and Chen, Xi and Bai, Hong-Min and Wang, Xinyu and
               Li, Yiyi and Wang, Lixiang and Liang, Zhigang and Ren, Xianwen
               and Qiu, Li and Hui, Yuan and Zhang, Qingling and Leng, Qibin
               and Chen, Jun and Jia, Guangshuai",
  abstract  = "Neoadjuvant immune-checkpoint blockade therapy only benefits a
               limited fraction of patients with glioblastoma multiforme (GBM).
               Thus, targeting other immunomodulators on myeloid cells is an
               attractive therapeutic option. Here, we performed single-cell
               RNA sequencing and spatial transcriptomics of patients with GBM
               treated with neoadjuvant anti-PD-1 therapy. We identified unique
               monocyte-derived tumor-associated macrophage subpopulations with
               functional plasticity that highly expressed the
               immunosuppressive SIGLEC9 gene and preferentially accumulated in
               the nonresponders to anti-PD-1 treatment. Deletion of Siglece
               (murine homolog) resulted in dramatically restrained tumor
               development and prolonged survival in mouse models.
               Mechanistically, targeting Siglece directly activated both CD4+
               T cells and CD8+ T cells through antigen presentation, secreted
               chemokines and co-stimulatory factor interactions. Furthermore,
               Siglece deletion synergized with anti-PD-1/PD-L1 treatment to
               improve antitumor efficacy. Our data demonstrated that Siglec-9
               is an immune-checkpoint molecule on macrophages that can be
               targeted to enhance anti-PD-1/PD-L1 therapeutic efficacy for GBM
               treatment.",
  journal   = "Nat. Cancer",
  publisher = "Springer Science and Business Media LLC",
  volume    =  4,
  number    =  9,
  pages     = "1273--1291",
  month     =  sep,
  year      =  2023,
  copyright = "https://www.springernature.com/gp/researchers/text-and-data-mining",
  language  = "en"
}

@ARTICLE{Nakata2023-sb,
  title     = "Genetic vulnerability to Crohn's disease reveals a spatially
               resolved epithelial restitution program",
  author    = "Nakata, Toru and Li, Chenhao and Mayassi, Toufic and Lin, Helen
               and Ghosh, Koushik and Segerstolpe, {\AA}sa and Diamond, Emma L
               and Herbst, Paula and Biancalani, Tommaso and Gaddam, Shreya and
               Parkar, Saurabh and Lu, Ziqing and Jaiswal, Alok and Li, Bihua
               and Creasey, Elizabeth A and Lefkovith, Ariel and Daly, Mark J
               and Graham, Daniel B and Xavier, Ramnik J",
  abstract  = "Effective tissue repair requires coordinated intercellular
               communication to sense damage, remodel the tissue, and restore
               function. Here, we dissected the healing response in the
               intestinal mucosa by mapping intercellular communication at
               single-cell resolution and integrating with spatial
               transcriptomics. We demonstrated that a risk variant for Crohn's
               disease, hepatocyte growth factor activator (HGFAC) Arg509His
               (R509H), disrupted a damage-sensing pathway connecting the
               coagulation cascade to growth factors that drive the
               differentiation of wound-associated epithelial (WAE) cells and
               production of a localized retinoic acid (RA) gradient to promote
               fibroblast-mediated tissue remodeling. Specifically, we showed
               that HGFAC R509H was activated by thrombin protease activity but
               exhibited impaired proteolytic activation of the growth factor
               macrophage-stimulating protein (MSP). In Hgfac R509H mice,
               reduced MSP activation in response to wounding of the colon
               resulted in impaired WAE cell induction and delayed healing.
               Through integration of single-cell transcriptomics and spatial
               transcriptomics, we demonstrated that WAE cells generated RA in
               a spatially restricted region of the wound site and that mucosal
               fibroblasts responded to this signal by producing extracellular
               matrix and growth factors. We further dissected this WAE
               cell-fibroblast signaling circuit in vitro using a genetically
               tractable organoid coculture model. Collectively, these studies
               exploited a genetic perturbation associated with human disease
               to disrupt a fundamental biological process and then
               reconstructed a spatially resolved mechanistic model of tissue
               healing.",
  journal   = "Sci. Transl. Med.",
  publisher = "American Association for the Advancement of Science (AAAS)",
  volume    =  15,
  number    =  719,
  pages     = "eadg5252",
  month     =  oct,
  year      =  2023,
  language  = "en"
}

@ARTICLE{Pham2023-ey,
  title    = "Robust mapping of spatiotemporal trajectories and cell-cell
              interactions in healthy and diseased tissues",
  author   = "Pham, Duy and Tan, Xiao and Balderson, Brad and Xu, Jun and
              Grice, Laura F and Yoon, Sohye and Willis, Emily F and Tran, Minh
              and Lam, Pui Yeng and Raghubar, Arti and Kalita-de Croft,
              Priyakshi and Lakhani, Sunil and Vukovic, Jana and Ruitenberg,
              Marc J and Nguyen, Quan H",
  abstract = "Spatial transcriptomics (ST) technologies generate multiple data
              types from biological samples, namely gene expression, physical
              distance between data points, and/or tissue morphology. Here we
              developed three computational-statistical algorithms that
              integrate all three data types to advance understanding of
              cellular processes. First, we present a spatial graph-based
              method, pseudo-time-space (PSTS), to model and uncover
              relationships between transcriptional states of cells across
              tissues undergoing dynamic change (e.g. neurodevelopment, brain
              injury and/or microglia activation, and cancer progression). We
              further developed a spatially-constrained two-level permutation
              (SCTP) test to study cell-cell interaction, finding highly
              interactive tissue regions across thousands of ligand-receptor
              pairs with markedly reduced false discovery rates. Finally, we
              present a spatial graph-based imputation method with neural
              network (stSME), to correct for technical noise/dropout and
              increase ST data coverage. Together, the algorithms that we
              developed, implemented in the comprehensive and fast stLearn
              software, allow for robust interrogation of biological processes
              within healthy and diseased tissues.",
  journal  = "Nat. Commun.",
  volume   =  14,
  number   =  1,
  pages    = "7739",
  month    =  nov,
  year     =  2023,
  language = "en"
}

@ARTICLE{Andrews2024-eh,
  title    = "Single-cell, single-nucleus, and spatial transcriptomics
              characterization of the immunological landscape in the healthy
              and {PSC} human liver",
  author   = "Andrews, Tallulah S and Nakib, Diana and Perciani, Catia T and
              Ma, Xue Zhong and Liu, Lewis and Winter, Erin and Camat, Damra
              and Chung, Sai W and Lumanto, Patricia and Manuel, Justin and
              Mangroo, Shantel and Hansen, Bettina and Arpinder, Bal and
              Thoeni, Cornelia and Sayed, Blayne and Feld, Jordan and Gehring,
              Adam and Gulamhusein, Aliya and Hirschfield, Gideon M and
              Ricciuto, Amanda and Bader, Gary D and McGilvray, Ian D and
              MacParland, Sonya",
  abstract = "BACKGROUND \& AIMS: Primary sclerosing cholangitis (PSC) is an
              immune-mediated cholestatic liver disease for which there is an
              unmet need to understand the cellular composition of the affected
              liver and how it underlies disease pathogenesis. We aimed to
              generate a comprehensive atlas of the PSC liver using multi-omic
              modalities and protein-based functional validation. METHODS: We
              employed single-cell and single-nucleus RNA sequencing (47,156
              cells and 23,000 nuclei) and spatial transcriptomics (one sample
              by 10x Visium and five samples with Nanostring GeoMx DSP) to
              profile the cellular ecosystem in 10 PSC livers. Transcriptomic
              profiles were compared to 24 neurologically deceased donor livers
              (107,542 cells) and spatial transcriptomics controls, as well as
              18,240 cells and 20,202 nuclei from three PBC livers. Flow
              cytometry was performed to validate PSC-specific differences in
              immune cell phenotype and function. RESULTS: PSC explants with
              parenchymal cirrhosis and prominent periductal fibrosis contained
              a population of cholangiocyte-like hepatocytes that were
              surrounded by diverse immune cell populations. PSC-associated
              biliary, mesenchymal, and endothelial populations expressed
              chemokine and cytokine transcripts involved in immune cell
              recruitment. Additionally, expanded CD4+ T cells and recruited
              myeloid populations in the PSC liver expressed the corresponding
              receptors to these chemokines and cytokines, suggesting potential
              recruitment. Tissue-resident macrophages, by contrast, were
              reduced in number and exhibited a dysfunctional and downregulated
              inflammatory response to lipopolysaccharide and
              interferon-$\gamma$ stimulation. CONCLUSIONS: We present a
              comprehensive atlas of the PSC liver and demonstrate an
              exhaustion-like phenotype of myeloid cells and markers of chronic
              cytokine expression in late-stage PSC lesions. This atlas expands
              our understanding of the cellular complexity of PSC and has
              potential to guide the development of novel treatments. IMPACT
              AND IMPLICATIONS: Primary sclerosing cholangitis (PSC) is a rare
              liver disease characterized by chronic inflammation and
              irreparable damage to the bile ducts, which eventually results in
              liver failure. Due to a limited understanding of the underlying
              pathogenesis of disease, treatment options are limited. To
              address this, we sequenced healthy and diseased livers to compare
              the activity, interactions, and localization of immune and
              non-immune cells. This revealed that hepatocytes lining PSC scar
              regions co-express cholangiocyte markers, whereas immune cells
              infiltrate the scar lesions. Of these cells, macrophages, which
              typically contribute to tissue repair, were enriched in
              immunoregulatory genes and demonstrated a lack of responsiveness
              to stimulation. These cells may be involved in maintaining
              hepatic inflammation and could be a target for novel therapies.",
  journal  = "J. Hepatol.",
  month    =  jan,
  year     =  2024,
  keywords = "Liver; Myeloid Dysfunction; Primary Sclerosing Cholangitis;
              Single Cell RNA sequencing; Spatial Transcriptomics",
  language = "en"
}

@ARTICLE{Di_Marco2023-jg,
  title    = "Spatial transcriptomics map of the embryonic mouse brain - a tool
              to explore neurogenesis",
  author   = "Di Marco, Barbara and V{\'a}zquez-Mar{\'\i}n, Javier and Monyer,
              Hannah and Centanin, L{\'a}zaro and Alfonso, Julieta",
  abstract = "The developing brain has a well-organized anatomical structure
              comprising different types of neural and non-neural cells. Stem
              cells, progenitors and newborn neurons tightly interact with
              their neighbouring cells and tissue microenvironment, and this
              intricate interplay ultimately shapes the output of neurogenesis.
              Given the relevance of spatial cues during brain development, we
              acknowledge the necessity for a spatial transcriptomics map
              accessible to the neurodevelopmental community. To fulfil this
              need, we generated spatially resolved RNA sequencing (RNAseq)
              data from embryonic day 13.5 mouse brain sections immunostained
              for mitotic active neural and vascular cells. Unsupervised
              clustering defined specific cell type populations of diverse
              lineages and differentiation states. Differential expression
              analysis revealed unique transcriptional signatures across
              specific brain areas, uncovering novel features inherent to
              particular anatomical domains. Finally, we integrated existing
              single-cell RNAseq datasets into our spatial transcriptomics map,
              adding tissue context to single-cell RNAseq data. In summary, we
              provide a valuable tool that enables the exploration and
              discovery of unforeseen molecular players involved in
              neurogenesis, particularly in the crosstalk between different
              cell types.",
  journal  = "Biol. Open",
  volume   =  12,
  number   =  10,
  month    =  oct,
  year     =  2023,
  keywords = "Gene expression atlas; Mouse telencephalon; Neurodevelopment;
              Single-cell and spatial transcriptomics data integration",
  language = "en"
}

@ARTICLE{Kawai2023-en,
  title     = "Clonal proliferation within smooth muscle cells in unstable
               human atherosclerotic lesions",
  author    = "Kawai, Kenji and Sakamoto, Atsushi and Mokry, Michal and Ghosh,
               Saikat Kumar B and Kawakami, Rika and Xu, Weili and Guo, Liang
               and Fuller, Daniela T and Tanaka, Takamasa and Shah, Palak and
               Cornelissen, Anne and Sato, Yu and Mori, Masayuki and Konishi,
               Takao and Vozenilek, Aimee E and Dhingra, Roma and Virmani, Renu
               and Pasterkamp, Gerard and Finn, Aloke V",
  abstract  = "BACKGROUND: Studies in humans and mice using the expression of
               an X-linked gene or lineage tracing, respectively, have
               suggested that clones of smooth muscle cells (SMCs) exist in
               human atherosclerotic lesions but are limited by either spatial
               resolution or translatability of the model. METHODS: Phenotypic
               clonality can be detected by X-chromosome inactivation patterns.
               We investigated whether clones of SMCs exist in unstable human
               atheroma using RNA in situ hybridization (BaseScope) to identify
               a naturally occurring 24-nucleotide deletion in the 3'UTR of the
               X-linked BGN (biglycan) gene, a proteoglycan highly expressed by
               SMCs. BGN-specific BaseScope probes were designed to target the
               wild-type or deletion mRNA. Three different coronary artery
               plaque types (erosion, rupture, and adaptive intimal thickening)
               were selected from heterozygous females for the deletion BGN.
               Hybridization of target RNA-specific probes was used to
               visualize the spatial distribution of mutants. A clonality index
               was calculated from the percentage of each probe in each region
               of interest. Spatial transcriptomics were used to identify
               differentially expressed transcripts within clonal and nonclonal
               regions. RESULTS: Less than one-half of regions of interest in
               the intimal plaque were considered clonal with the mean percent
               regions of interest with clonality higher in the intimal plaque
               than in the media. This was consistent for all plaque types. The
               relationship of the dominant clone in the intimal plaque and
               media showed significant concordance. In comparison with the
               nonclonal lesions, the regions with SMC clonality had lower
               expression of genes encoding cell growth suppressors such as
               CD74, SERF-2 (small EDRK-rich factor 2), CTSB (cathepsin B), and
               HLA-DPA1 (major histocompatibility complex, class II, DP alpha
               1), among others. CONCLUSIONS: Our novel approach to examine
               clonality suggests atherosclerosis is primarily a disease of
               polyclonally and to a lesser extent clonally expanded SMCs and
               may have implications for the development of antiatherosclerotic
               therapies.",
  journal   = "Arterioscler. Thromb. Vasc. Biol.",
  publisher = "Ovid Technologies (Wolters Kluwer Health)",
  volume    =  43,
  number    =  12,
  pages     = "2333--2347",
  month     =  dec,
  year      =  2023,
  keywords  = "atherosclerosis; biglycan; coronary artery disease; gene
               expression; pathology",
  language  = "en"
}

@ARTICLE{Zhong2023-zy,
  title     = "Multi-species atlas resolves an axolotl limb development and
               regeneration paradox",
  author    = "Zhong, Jixing and Aires, Rita and Tsissios, Georgios and Skoufa,
               Evangelia and Brandt, Kerstin and Sandoval-Guzm{\'a}n, Tatiana
               and Aztekin, Can",
  abstract  = "Humans and other tetrapods are considered to require
               apical-ectodermal-ridge (AER) cells for limb development, and
               AER-like cells are suggested to be re-formed to initiate limb
               regeneration. Paradoxically, the presence of AER in the axolotl,
               a primary model organism for regeneration, remains
               controversial. Here, by leveraging a single-cell
               transcriptomics-based multi-species atlas, composed of axolotl,
               human, mouse, chicken, and frog cells, we first establish that
               axolotls contain cells with AER characteristics. Further
               analyses and spatial transcriptomics reveal that axolotl limbs
               do not fully re-form AER cells during regeneration. Moreover,
               the axolotl mesoderm displays part of the AER machinery,
               revealing a program for limb (re)growth. These results clarify
               the debate about the axolotl AER and the extent to which the
               limb developmental program is recapitulated during regeneration.",
  journal   = "Nat. Commun.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  14,
  number    =  1,
  pages     = "6346",
  month     =  oct,
  year      =  2023,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}

@ARTICLE{Lequain2023-md,
  title    = "Spatial transcriptomics reveals signatures of histopathological
              changes in muscular sarcoidosis",
  author   = "Lequain, Hippolyte and D{\'e}gletagne, Cyril and Streichenberger,
              Nathalie and Valantin, Julie and Simonet, Thomas and Schaeffer,
              Laurent and S{\`e}ve, Pascal and Leblanc, Pascal",
  abstract = "Sarcoidosis is a multisystemic disease characterized by
              non-caseating granuloma infiltrating various organs. The form
              with symptomatic muscular involvement is called muscular
              sarcoidosis. The impact of immune cells composing the granuloma
              on the skeletal muscle is misunderstood. Here, we investigated
              the granuloma-skeletal muscle interactions through spatial
              transcriptomics on two patients affected by muscular sarcoidosis.
              Five major transcriptomic clusters corresponding to
              perigranuloma, granuloma, and three successive muscle tissue
              areas (proximal, intermediate, and distal) around the granuloma
              were identified. Analyses revealed upregulated pathways in the
              granuloma corresponding to the activation of T-lymphocytes and
              monocytes/macrophages cytokines, the upregulation of
              extracellular matrix signatures, and the induction of the
              TGF-$\beta$ signaling in the perigranuloma. A comparison between
              the proximal and distal muscles to the granuloma revealed an
              inverse correlation between the distance to the granuloma and the
              upregulation of cellular response to
              interferon-$\gamma$/$\alpha$, TNF-$\alpha$, IL-1,4,6, fibroblast
              proliferation, epithelial to mesenchymal cell transition, and the
              downregulation of muscle gene expression. These data shed light
              on the intercommunications between granulomas and the muscle
              tissue and provide pathophysiological mechanisms by showing that
              granuloma immune cells have a direct impact on proximal muscle
              tissue by promoting its progressive replacement by fibrosis via
              the expression of pro-inflammatory and profibrosing signatures.
              These data could possibly explain the evolution towards a state
              of disability for some patients.",
  journal  = "Cells",
  volume   =  12,
  number   =  23,
  month    =  nov,
  year     =  2023,
  keywords = "Visium; fibrosis; granuloma; muscular sarcoidosis; skeletal
              muscle; spatial transcriptomic",
  language = "en"
}

@ARTICLE{Yu2024-eh,
  title     = "Spatial transcriptomics reveals a low extent of
               transcriptionally active hepatitis {B} virus integration in
               patients with {HBsAg} loss",
  author    = "Yu, Xiaoqi and Gong, Qiming and Yu, Demin and Chen, Yongyan and
               Jing, Ying and Zoulim, Fabien and Zhang, Xinxin",
  abstract  = "OBJECTIVE: Hepatitis B virus (HBV) can integrate into the
               chromosomes of infected hepatocytes, contributing to the
               production of hepatitis B surface antigen (HBsAg) and to
               hepatocarcinogenesis. In this study, we aimed to explore whether
               transcriptionally active HBV integration events spread
               throughout the liver tissue in different phases of chronic HBV
               infection, especially in patients with HBsAg loss. DESIGN: We
               constructed high-resolution spatial transcriptomes of liver
               biopsies containing 13 059 tissue spots from 18 patients with
               chronic HBV infection to analyse the occurrence and relative
               distribution of transcriptionally active viral integration
               events. Immunohistochemistry was performed to evaluate the
               expression of HBsAg and HBV core antigen. Intrahepatic
               covalently closed circular DNA (cccDNA) levels were quantified
               by real-time qPCR. RESULTS: Spatial transcriptome sequencing
               identified the presence of 13 154 virus-host chimeric reads in
               7.86\% (1026 of 13 059) of liver tissue spots in all patients,
               including three patients with HBsAg loss. These HBV integration
               sites were randomly distributed on chromosomes and can localise
               in host genes involved in hepatocarcinogenesis, such as ALB, CLU
               and APOB. Patients who were receiving or had received antiviral
               treatment had a significantly lower percentage of viral
               integration-containing spots and significantly fewer chimeric
               reads than treatment-na{\"\i}ve patients. Intrahepatic cccDNA
               levels correlated well with viral integration events.
               CONCLUSION: Transcriptionally active HBV integration occurred in
               chronically HBV-infected patients at different phases, including
               in patients with HBsAg loss. Antiviral treatment was associated
               with a decreased number and extent of transcriptionally active
               viral integrations, implying that early treatment intervention
               may further reduce the number of viral integration events.",
  journal   = "Gut",
  publisher = "BMJ",
  volume    =  73,
  number    =  5,
  pages     = "797--809",
  month     =  apr,
  year      =  2024,
  keywords  = "chronic viral hepatitis; hepatitis B; liver biopsy",
  language  = "en"
}

@ARTICLE{Ng2024-ut,
  title    = "Deterministic reprogramming of neutrophils within tumors",
  author   = "Ng, Melissa S F and Kwok, Immanuel and Tan, Leonard and Shi,
              Changming and Cerezo-Wallis, Daniela and Tan, Yingrou and Leong,
              Keith and Calvo, Gabriel F and Yang, Katharine and Zhang, Yuning
              and Jin, Jingsi and Liong, Ka Hang and Wu, Dandan and He, Rui and
              Liu, Dehua and Teh, Ye Chean and Bleriot, Camille and Caronni,
              Nicoletta and Liu, Zhaoyuan and Duan, Kaibo and Narang, Vipin and
              Ballesteros, Iv{\'a}n and Moalli, Federica and Li, Mengwei and
              Chen, Jinmiao and Liu, Yao and Liu, Lianxin and Qi, Jingjing and
              Liu, Yingbin and Jiang, Lingxi and Shen, Baiyong and Cheng, Hui
              and Cheng, Tao and Angeli, Veronique and Sharma, Ankur and Loh,
              Yuin-Han and Tey, Hong Liang and Chong, Shu Zhen and Iannacone,
              Matteo and Ostuni, Renato and Hidalgo, Andr{\'e}s and Ginhoux,
              Florent and Ng, Lai Guan",
  abstract = "Neutrophils are increasingly recognized as key players in the
              tumor immune response and are associated with poor clinical
              outcomes. Despite recent advances characterizing the diversity of
              neutrophil states in cancer, common trajectories and mechanisms
              governing the ontogeny and relationship between these neutrophil
              states remain undefined. Here, we demonstrate that immature and
              mature neutrophils that enter tumors undergo irreversible
              epigenetic, transcriptional, and proteomic modifications to
              converge into a distinct, terminally differentiated dcTRAIL-R1+
              state. Reprogrammed dcTRAIL-R1+ neutrophils predominantly
              localize to a glycolytic and hypoxic niche at the tumor core and
              exert pro-angiogenic function that favors tumor growth. We found
              similar trajectories in neutrophils across multiple tumor types
              and in humans, suggesting that targeting this program may provide
              a means of enhancing certain cancer immunotherapies.",
  journal  = "Science",
  volume   =  383,
  number   =  6679,
  pages    = "eadf6493",
  month    =  jan,
  year     =  2024,
  language = "en"
}

@ARTICLE{Cherief2023-hx,
  title    = "{TrkA-mediated} sensory innervation of injured mouse tendon
              supports tendon sheath progenitor cell expansion and tendon
              repair",
  author   = "Cherief, Masnsen and Xu, Jiajia and Li, Zhao and Tower, Robert J
              and Ramesh, Sowmya and Qin, Qizhi and Gomez-Salazar, Mario and
              Yea, Ji-Hye and Lee, Seungyong and Negri, Stefano and Xu, Mingxin
              and Price, Theodore and Kendal, Adrian R and Fan, Chen-Ming and
              Clemens, Thomas L and Levi, Benjamin and James, Aaron W",
  abstract = "Peripheral neurons terminate at the surface of tendons partly to
              relay nociceptive pain signals; however, the role of peripheral
              nerves in tendon injury and repair remains unclear. Here, we show
              that after Achilles tendon injury in mice, there is new nerve
              growth near tendon cells that express nerve growth factor (NGF).
              Conditional deletion of the Ngf gene in either myeloid or
              mesenchymal mouse cells limited both innervation and tendon
              repair. Similarly, inhibition of the NGF receptor tropomyosin
              receptor kinase A (TrkA) abrogated tendon healing in mouse tendon
              injury. Sural nerve transection blocked the postinjury increase
              in tendon sensory innervation and the expansion of tendon sheath
              progenitor cells (TSPCs) expressing tubulin polymerization
              promoting protein family member 3. Single cell and spatial
              transcriptomics revealed that disruption of sensory innervation
              resulted in dysregulated inflammatory signaling and transforming
              growth factor-$\beta$ (TGF$\beta$) signaling in injured mouse
              tendon. Culture of mouse TSPCs with conditioned medium from
              dorsal root ganglia neuron further supported a role for neuronal
              mediators and TGF$\beta$ signaling in TSPC proliferation.
              Transcriptomic and histologic analyses of injured human tendon
              biopsy samples supported a role for innervation and TGF$\beta$
              signaling in human tendon regeneration. Last, treating mice after
              tendon injury systemically with a small-molecule partial agonist
              of TrkA increased neurovascular response, TGF$\beta$ signaling,
              TSPC expansion, and tendon tissue repair. Although further
              studies should investigate the potential effects of denervation
              on mechanical loading of tendon, our results suggest that
              peripheral innervation is critical for the regenerative response
              after acute tendon injury.",
  journal  = "Sci. Transl. Med.",
  volume   =  15,
  number   =  727,
  pages    = "eade4619",
  month    =  dec,
  year     =  2023,
  language = "en"
}

@ARTICLE{Rahimikollu2024-fs,
  title    = "{SLIDE}: Significant Latent Factor Interaction Discovery and
              Exploration across biological domains",
  author   = "Rahimikollu, Javad and Xiao, Hanxi and Rosengart, Annaelaine and
              Rosen, Aaron B I and Tabib, Tracy and Zdinak, Paul M and He, Kun
              and Bing, Xin and Bunea, Florentina and Wegkamp, Marten and
              Poholek, Amanda C and Joglekar, Alok V and Lafyatis, Robert A and
              Das, Jishnu",
  abstract = "Modern multiomic technologies can generate deep multiscale
              profiles. However, differences in data modalities,
              multicollinearity of the data, and large numbers of irrelevant
              features make analyses and integration of high-dimensional omic
              datasets challenging. Here we present Significant Latent Factor
              Interaction Discovery and Exploration (SLIDE), a first-in-class
              interpretable machine learning technique for identifying
              significant interacting latent factors underlying outcomes of
              interest from high-dimensional omic datasets. SLIDE makes no
              assumptions regarding data-generating mechanisms, comes with
              theoretical guarantees regarding identifiability of the latent
              factors/corresponding inference, and has rigorous false discovery
              rate control. Using SLIDE on single-cell and spatial omic
              datasets, we uncovered significant interacting latent factors
              underlying a range of molecular, cellular and organismal
              phenotypes. SLIDE outperforms/performs at least as well as a wide
              range of state-of-the-art approaches, including other latent
              factor approaches. More importantly, it provides biological
              inference beyond prediction that other methods do not afford.
              Thus, SLIDE is a versatile engine for biological discovery from
              modern multiomic datasets.",
  journal  = "Nat. Methods",
  month    =  feb,
  year     =  2024,
  language = "en"
}

@ARTICLE{Lowe2024-nf,
  title    = "Tertiary lymphoid structures sustain cutaneous {B} cell activity
              in hidradenitis suppurativa",
  author   = "Lowe, Margaret M and Cohen, Jarish N and Moss, Madison I and
              Clancy, Sean and Adler, James P and Yates, Ashley E and Naik,
              Haley B and Yadav, Rashi and Pauli, Mariela and Taylor, Ian and
              McKay, Austin and Harris, Hobart and Kim, Esther and Hansen,
              Scott L and Rosenblum, Michael D and Moreau, Joshua M",
  abstract = "Hidradenitis suppurativa (HS) is a chronic skin condition
              affecting approximately 1\% of the US population. HS skin lesions
              are highly inflammatory and characterized by a large immune
              infiltrate. While B cells and plasma cells comprise a major
              component of this immune milieu, the biology and the contribution
              of these cells in HS pathogenesis are unclear. We aimed to
              investigate the dynamics and microenvironmental interactions of B
              cells within cutaneous HS lesions. Combining histological
              analysis, single-cell RNA sequencing, and spatial transcriptomics
              profiling of HS lesions, we defined the tissue microenvironment
              relative to B cell activity within this disease. Our findings
              identified tertiary lymphoid structures (TLSs) within HS lesions
              and described organized interactions among T cells, B cells,
              antigen-presenting cells, and skin stroma. We found evidence that
              B cells within HS TLSs actively underwent maturation, including
              participation in germinal center reactions and class switch
              recombination. Moreover, skin stroma and accumulating T cells
              were primed to support the formation of TLSs and facilitate B
              cell recruitment during HS. Our data definitively demonstrated
              the presence of TLSs in lesional HS skin and point to ongoing
              cutaneous B cell maturation through class switch recombination
              and affinity maturation during disease progression in this
              inflamed nonlymphoid tissue.",
  journal  = "JCI Insight",
  volume   =  9,
  number   =  3,
  month    =  feb,
  year     =  2024,
  keywords = "Adaptive immunity; Dermatology; Immunology; Skin",
  language = "en"
}

% The entry below contains non-ASCII chars that could not be converted
% to a LaTeX equivalent.
@ARTICLE{Cortese2023-sc,
  title     = "High-resolution analysis of mononuclear phagocytes reveals
               {GPNMB} as a prognostic marker in human colorectal liver
               metastasis",
  author    = "Cortese, Nina and Carriero, Roberta and Barbagallo, Marialuisa
               and Putignano, Anna Rita and Costa, Guido and Giavazzi, Fabio
               and Grizzi, Fabio and Pasqualini, Fabio and Peano, Clelia and
               Basso, Gianluca and Marchini, Sergio and Colombo, Federico
               Simone and Soldani, Cristiana and Franceschini, Barbara and Di
               Tommaso, Luca and Terracciano, Luigi and Donadon, Matteo and
               Torzilli, Guido and Kunderfranco, Paolo and Mantovani, Alberto
               and Marchesi, Federica",
  abstract  = "Patients with colorectal liver metastasis (CLM) present with
               heterogenous clinical outcomes and improved classification is
               needed to ameliorate the therapeutic output. Macrophages (Mϕ)
               hold promise as prognostic classifiers and therapeutic targets.
               Here, stemming from a single-cell analysis of mononuclear
               phagocytes infiltrating human CLM, we identified two Mϕ markers
               associated with distinct populations with opposite clinical
               relevance. The invasive margin of CLM was enriched in
               pro-inflammatory monocyte-derived Mϕ (MoMϕ) expressing the
               monocytic marker SERPINB2, and a more differentiated population,
               tumor-associated Mϕ (TAM), expressing glycoprotein nonmetastatic
               melanoma protein B (GPNMB). SERPINB2+ MoMϕ had an early
               inflammatory profile, whereas GPNMB+ TAMs were enriched in
               pathways of matrix degradation, angiogenesis, and lipid
               metabolism and were found closer to the tumor margin, as
               confirmed by spatial transcriptomics on CLM specimens. In a
               cohort of patients, a high infiltration of SERPINB2+ cells
               independently associated with longer disease-free survival (DFS;
               P = 0.033), whereas a high density of GPNMB+ cells correlated
               with shorter DFS (P = 0.012) and overall survival (P = 0.002).
               Cell-cell interaction analysis defined opposing roles for MoMϕ
               and TAMs, suggesting that SERPINB2+ and GPNMB+ cells are
               discrete populations of Mϕ and may be exploited for further
               translation to an immune-based stratification tool. This study
               provides evidence of how multi-omics approaches can identify
               nonredundant, clinically relevant markers for further
               translation to immune-based patient stratification tools and
               therapeutic targets. GPNMB has been shown to set Mϕ in an
               immunosuppressive mode. Our high dimensional analyses provide
               further evidence that GPNMB is a negative prognostic indicator
               and a potential player in the protumor function of Mϕ
               populations.",
  journal   = "Cancer Immunol. Res.",
  publisher = "American Association for Cancer Research (AACR)",
  volume    =  11,
  number    =  4,
  pages     = "405--420",
  month     =  apr,
  year      =  2023,
  language  = "en"
}

@ARTICLE{Huuki-Myers2023-ix,
  title    = "Integrated single cell and unsupervised spatial transcriptomic
              analysis defines molecular anatomy of the human dorsolateral
              prefrontal cortex",
  author   = "Huuki-Myers, Louise and Spangler, Abby and Eagles, Nick and
              Montgomery, Kelsey D and Kwon, Sang Ho and Guo, Boyi and
              Grant-Peters, Melissa and Divecha, Heena R and Tippani, Madhavi
              and Sriworarat, Chaichontat and Nguyen, Annie B and Ravichandran,
              Prashanthi and Tran, Matthew N and Seyedian, Arta and
              {PsychENCODE consortium} and Hyde, Thomas M and Kleinman, Joel E
              and Battle, Alexis and Page, Stephanie C and Ryten, Mina and
              Hicks, Stephanie C and Martinowich, Keri and Collado-Torres,
              Leonardo and Maynard, Kristen R",
  abstract = "Generation of a molecular neuroanatomical map of the human
              prefrontal cortex reveals novel spatial domains and cell-cell
              interactions relevant for psychiatric disease. The molecular
              organization of the human neocortex has been historically studied
              in the context of its histological layers. However, emerging
              spatial transcriptomic technologies have enabled unbiased
              identification of transcriptionally-defined spatial domains that
              move beyond classic cytoarchitecture. Here we used the Visium
              spatial gene expression platform to generate a data-driven
              molecular neuroanatomical atlas across the anterior-posterior
              axis of the human dorsolateral prefrontal cortex (DLPFC).
              Integration with paired single nucleus RNA-sequencing data
              revealed distinct cell type compositions and cell-cell
              interactions across spatial domains. Using PsychENCODE and
              publicly available data, we map the enrichment of cell types and
              genes associated with neuropsychiatric disorders to discrete
              spatial domains. Finally, we provide resources for the scientific
              community to explore these integrated spatial and single cell
              datasets at research.libd.org/spatialDLPFC/.",
  journal  = "bioRxivorg",
  month    =  feb,
  year     =  2023,
  language = "en"
}

@ARTICLE{Maynard2021-wa,
  title     = "Transcriptome-scale spatial gene expression in the human
               dorsolateral prefrontal cortex",
  author    = "Maynard, Kristen R and Collado-Torres, Leonardo and Weber, Lukas
               M and Uytingco, Cedric and Barry, Brianna K and Williams,
               Stephen R and Catallini, 2nd, Joseph L and Tran, Matthew N and
               Besich, Zachary and Tippani, Madhavi and Chew, Jennifer and Yin,
               Yifeng and Kleinman, Joel E and Hyde, Thomas M and Rao, Nikhil
               and Hicks, Stephanie C and Martinowich, Keri and Jaffe, Andrew E",
  abstract  = "We used the 10x Genomics Visium platform to define the spatial
               topography of gene expression in the six-layered human
               dorsolateral prefrontal cortex. We identified extensive
               layer-enriched expression signatures and refined associations to
               previous laminar markers. We overlaid our laminar expression
               signatures on large-scale single nucleus RNA-sequencing data,
               enhancing spatial annotation of expression-driven clusters. By
               integrating neuropsychiatric disorder gene sets, we showed
               differential layer-enriched expression of genes associated with
               schizophrenia and autism spectrum disorder, highlighting the
               clinical relevance of spatially defined expression. We then
               developed a data-driven framework to define unsupervised
               clusters in spatial transcriptomics data, which can be applied
               to other tissues or brain regions in which morphological
               architecture is not as well defined as cortical laminae. Last,
               we created a web application for the scientific community to
               explore these raw and summarized data to augment ongoing
               neuroscience and spatial transcriptomics research (
               http://research.libd.org/spatialLIBD ).",
  journal   = "Nat. Neurosci.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  24,
  number    =  3,
  pages     = "425--436",
  month     =  mar,
  year      =  2021,
  language  = "en"
}

@ARTICLE{Wu2021-zq,
  title     = "A single-cell and spatially resolved atlas of human breast
               cancers",
  author    = "Wu, Sunny Z and Al-Eryani, Ghamdan and Roden, Daniel Lee and
               Junankar, Simon and Harvey, Kate and Andersson, Alma and
               Thennavan, Aatish and Wang, Chenfei and Torpy, James R and
               Bartonicek, Nenad and Wang, Taopeng and Larsson, Ludvig and
               Kaczorowski, Dominik and Weisenfeld, Neil I and Uytingco, Cedric
               R and Chew, Jennifer G and Bent, Zachary W and Chan, Chia-Ling
               and Gnanasambandapillai, Vikkitharan and Dutertre,
               Charles-Antoine and Gluch, Laurence and Hui, Mun N and Beith,
               Jane and Parker, Andrew and Robbins, Elizabeth and Segara,
               Davendra and Cooper, Caroline and Mak, Cindy and Chan, Belinda
               and Warrier, Sanjay and Ginhoux, Florent and Millar, Ewan and
               Powell, Joseph E and Williams, Stephen R and Liu, X Shirley and
               O'Toole, Sandra and Lim, Elgene and Lundeberg, Joakim and Perou,
               Charles M and Swarbrick, Alexander",
  abstract  = "Breast cancers are complex cellular ecosystems where heterotypic
               interactions play central roles in disease progression and
               response to therapy. However, our knowledge of their cellular
               composition and organization is limited. Here we present a
               single-cell and spatially resolved transcriptomics analysis of
               human breast cancers. We developed a single-cell method of
               intrinsic subtype classification (SCSubtype) to reveal recurrent
               neoplastic cell heterogeneity. Immunophenotyping using cellular
               indexing of transcriptomes and epitopes by sequencing (CITE-seq)
               provides high-resolution immune profiles, including new
               PD-L1/PD-L2+ macrophage populations associated with clinical
               outcome. Mesenchymal cells displayed diverse functions and
               cell-surface protein expression through differentiation within
               three major lineages. Stromal-immune niches were spatially
               organized in tumors, offering insights into antitumor immune
               regulation. Using single-cell signatures, we deconvoluted large
               breast cancer cohorts to stratify them into nine clusters,
               termed 'ecotypes', with unique cellular compositions and
               clinical outcomes. This study provides a comprehensive
               transcriptional atlas of the cellular architecture of breast
               cancer.",
  journal   = "Nat. Genet.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  53,
  number    =  9,
  pages     = "1334--1347",
  month     =  sep,
  year      =  2021,
  language  = "en"
}

@ARTICLE{Kuppe2022-zy,
  title     = "Spatial multi-omic map of human myocardial infarction",
  author    = "Kuppe, Christoph and Ramirez Flores, Ricardo O and Li, Zhijian
               and Hayat, Sikander and Levinson, Rebecca T and Liao, Xian and
               Hannani, Monica T and Tanevski, Jovan and W{\"u}nnemann, Florian
               and Nagai, James S and Halder, Maurice and Schumacher, David and
               Menzel, Sylvia and Sch{\"a}fer, Gideon and Hoeft, Konrad and
               Cheng, Mingbo and Ziegler, Susanne and Zhang, Xiaoting and
               Peisker, Fabian and Kaesler, Nadine and Saritas, Turgay and Xu,
               Yaoxian and Kassner, Astrid and Gummert, Jan and Morshuis,
               Michiel and Amrute, Junedh and Veltrop, Rogier J A and Boor,
               Peter and Klingel, Karin and Van Laake, Linda W and Vink, Aryan
               and Hoogenboezem, Remco M and Bindels, Eric M J and Schurgers,
               Leon and Sattler, Susanne and Schapiro, Denis and Schneider,
               Rebekka K and Lavine, Kory and Milting, Hendrik and Costa, Ivan
               G and Saez-Rodriguez, Julio and Kramann, Rafael",
  abstract  = "Myocardial infarction is a leading cause of death worldwide1.
               Although advances have been made in acute treatment, an
               incomplete understanding of remodelling processes has limited
               the effectiveness of therapies to reduce late-stage mortality2.
               Here we generate an integrative high-resolution map of human
               cardiac remodelling after myocardial infarction using
               single-cell gene expression, chromatin accessibility and spatial
               transcriptomic profiling of multiple physiological zones at
               distinct time points in myocardium from patients with myocardial
               infarction and controls. Multi-modal data integration enabled us
               to evaluate cardiac cell-type compositions at increased
               resolution, yielding insights into changes of the cardiac
               transcriptome and epigenome through the identification of
               distinct tissue structures of injury, repair and remodelling. We
               identified and validated disease-specific cardiac cell states of
               major cell types and analysed them in their spatial context,
               evaluating their dependency on other cell types. Our data
               elucidate the molecular principles of human myocardial tissue
               organization, recapitulating a gradual cardiomyocyte and myeloid
               continuum following ischaemic injury. In sum, our study provides
               an integrative molecular map of human myocardial infarction,
               represents an essential reference for the field and paves the
               way for advanced mechanistic and therapeutic studies of cardiac
               disease.",
  journal   = "Nature",
  publisher = "Springer Science and Business Media LLC",
  volume    =  608,
  number    =  7924,
  pages     = "766--777",
  month     =  aug,
  year      =  2022,
  language  = "en"
}

@ARTICLE{Erickson2022-ia,
  title     = "Spatially resolved clonal copy number alterations in benign and
               malignant tissue",
  author    = "Erickson, Andrew and He, Mengxiao and Berglund, Emelie and
               Marklund, Maja and Mirzazadeh, Reza and Schultz, Niklas and
               Kvastad, Linda and Andersson, Alma and Bergenstr{\aa}hle, Ludvig
               and Bergenstr{\aa}hle, Joseph and Larsson, Ludvig and Alonso
               Galicia, Leire and Shamikh, Alia and Basmaci, Elisa and
               D{\'\i}az De St{\aa}hl, Teresita and Rajakumar, Timothy and
               Doultsinos, Dimitrios and Thrane, Kim and Ji, Andrew L and
               Khavari, Paul A and Tarish, Firaz and Tanoglidi, Anna and
               Maaskola, Jonas and Colling, Richard and Mirtti, Tuomas and
               Hamdy, Freddie C and Woodcock, Dan J and Helleday, Thomas and
               Mills, Ian G and Lamb, Alastair D and Lundeberg, Joakim",
  abstract  = "Defining the transition from benign to malignant tissue is
               fundamental to improving early diagnosis of cancer1. Here we use
               a systematic approach to study spatial genome integrity in situ
               and describe previously unidentified clonal relationships. We
               used spatially resolved transcriptomics2 to infer spatial copy
               number variations in >120,000 regions across multiple organs, in
               benign and malignant tissues. We demonstrate that genome-wide
               copy number variation reveals distinct clonal patterns within
               tumours and in nearby benign tissue using an organ-wide approach
               focused on the prostate. Our results suggest a model for how
               genomic instability arises in histologically benign tissue that
               may represent early events in cancer evolution. We highlight the
               power of capturing the molecular and spatial continuums in a
               tissue context and challenge the rationale for treatment
               paradigms, including focal therapy.",
  journal   = "Nature",
  publisher = "Springer Science and Business Media LLC",
  volume    =  608,
  number    =  7922,
  pages     = "360--367",
  month     =  aug,
  year      =  2022,
  copyright = "https://creativecommons.org/licenses/by/4.0",
  language  = "en"
}