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mouse, mammary, cell, luminal, genes, human, cells, epithelial, signature, progenitor, pubmed, article, breast, expression, cancer, gene, google, scholar, subpopulations, mature, conserved, analysis, subsets, cas, subset, pathways, mascenriched, stem, figure, signatures, tumors, population, data, tumor, basal, subpopulation, models, profiles, species, expressed, gland, normal, file, stromal, research, tissue, populations, visvader, rna, receptor,

Topics {✒️}

conserved expression profile wnt/β-catenin signaling pathways article download pdf wnt/β-catenin pathway quantitative rt-pcr analysis marie-liesse asselin-labat ets transcription factor govern cell-fate decisions wnt-pathway inhibitors wif1 expression profile basal/mammary stem cells epithelial-mesenchymal transition reflect short-term culture luminal cell-fate commitment elevated sdf-1/cxcl12 secretion mammary gland comprises mouse mammary gland triple-negative breast cancer elgene lim human mammary gland mammary-gland morphogenesis functional mammary gland erk/mapk signaling pathways masc-enriched subset exhibited ingenuity pathway analysis bhupinder pal mammary stem cell masc-enriched/bipotent progenitor single stem cell article lim quantitative rt-pcr cell stem cell luminal-restricted population isolated triple-negative receptor phenotype basal cd49fhicd29hicd24+sca1- subset average log fold-change related subjects common cell-surface markers full size image open software development author correspondence gene profiling analysis mammary cell subpopulations cell-fate decisions stem cell marker gene expression profiling asselin-labat ml p53-null mouse model mammary tumor profiles epithelial-mesenchymal transitions

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         headline:Transcriptome analyses of mouse and human mammary cell subpopulations reveal multiple conserved genes and pathways
         description:Molecular characterization of the normal epithelial cell types that reside in the mammary gland is an important step toward understanding pathways that regulate self-renewal, lineage commitment, and differentiation along the hierarchy. Here we determined the gene expression signatures of four distinct subpopulations isolated from the mouse mammary gland. The epithelial cell signatures were used to interrogate mouse models of mammary tumorigenesis and to compare with their normal human counterpart subsets to identify conserved genes and networks. RNA was prepared from freshly sorted mouse mammary cell subpopulations (mammary stem cell (MaSC)-enriched, committed luminal progenitor, mature luminal and stromal cell) and used for gene expression profiling analysis on the Illumina platform. Gene signatures were derived and compared with those previously reported for the analogous normal human mammary cell subpopulations. The mouse and human epithelial subset signatures were then subjected to Ingenuity Pathway Analysis (IPA) to identify conserved pathways. The four mouse mammary cell subpopulations exhibited distinct gene signatures. Comparison of these signatures with the molecular profiles of different mouse models of mammary tumorigenesis revealed that tumors arising in MMTV-Wnt-1 and p53 -/- mice were enriched for MaSC-subset genes, whereas the gene profiles of MMTV-Neu and MMTV-PyMT tumors were most concordant with the luminal progenitor cell signature. Comparison of the mouse mammary epithelial cell signatures with their human counterparts revealed substantial conservation of genes, whereas IPA highlighted a number of conserved pathways in the three epithelial subsets. The conservation of genes and pathways across species further validates the use of the mouse as a model to study mammary gland development and highlights pathways that are likely to govern cell-fate decisions and differentiation. It is noteworthy that many of the conserved genes in the MaSC population have been considered as epithelial-mesenchymal transition (EMT) signature genes. Therefore, the expression of these genes in tumor cells may reflect basal epithelial cell characteristics and not necessarily cells that have undergone an EMT. Comparative analyses of normal mouse epithelial subsets with murine tumor models have implicated distinct cell types in contributing to tumorigenesis in the different models.
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            Ingenuity Pathway Analysis
            Luminal Cell
            Mouse Mammary Gland
            Mammary Stem Cell
            Cancer Research
            Oncology
            Surgical Oncology
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      headline:Transcriptome analyses of mouse and human mammary cell subpopulations reveal multiple conserved genes and pathways
      description:Molecular characterization of the normal epithelial cell types that reside in the mammary gland is an important step toward understanding pathways that regulate self-renewal, lineage commitment, and differentiation along the hierarchy. Here we determined the gene expression signatures of four distinct subpopulations isolated from the mouse mammary gland. The epithelial cell signatures were used to interrogate mouse models of mammary tumorigenesis and to compare with their normal human counterpart subsets to identify conserved genes and networks. RNA was prepared from freshly sorted mouse mammary cell subpopulations (mammary stem cell (MaSC)-enriched, committed luminal progenitor, mature luminal and stromal cell) and used for gene expression profiling analysis on the Illumina platform. Gene signatures were derived and compared with those previously reported for the analogous normal human mammary cell subpopulations. The mouse and human epithelial subset signatures were then subjected to Ingenuity Pathway Analysis (IPA) to identify conserved pathways. The four mouse mammary cell subpopulations exhibited distinct gene signatures. Comparison of these signatures with the molecular profiles of different mouse models of mammary tumorigenesis revealed that tumors arising in MMTV-Wnt-1 and p53 -/- mice were enriched for MaSC-subset genes, whereas the gene profiles of MMTV-Neu and MMTV-PyMT tumors were most concordant with the luminal progenitor cell signature. Comparison of the mouse mammary epithelial cell signatures with their human counterparts revealed substantial conservation of genes, whereas IPA highlighted a number of conserved pathways in the three epithelial subsets. The conservation of genes and pathways across species further validates the use of the mouse as a model to study mammary gland development and highlights pathways that are likely to govern cell-fate decisions and differentiation. It is noteworthy that many of the conserved genes in the MaSC population have been considered as epithelial-mesenchymal transition (EMT) signature genes. Therefore, the expression of these genes in tumor cells may reflect basal epithelial cell characteristics and not necessarily cells that have undergone an EMT. Comparative analyses of normal mouse epithelial subsets with murine tumor models have implicated distinct cell types in contributing to tumorigenesis in the different models.
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         Mammary Gland
         Ingenuity Pathway Analysis
         Luminal Cell
         Mouse Mammary Gland
         Mammary Stem Cell
         Cancer Research
         Oncology
         Surgical Oncology
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      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:Department of Medical Oncology, The Royal Melbourne Hospital, Parkville, Australia
      name:Department of Medicine, The University of Melbourne, The Royal Melbourne Hospital, Parkville, Australia
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:Department of Medical Biology, The University of Melbourne, Parkville, Australia
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:Department of Medical Biology, The University of Melbourne, Parkville, Australia

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