We are analyzing https://link.springer.com/article/10.1007/s10911-005-2537-2.

Title:
Stem/Progenitor Cells in Mouse Mammary Gland Development and Breast Cancer | Journal of Mammary Gland Biology and Neoplasia
Description:
Breast cancer is a genetically and clinically heterogeneous disease. It is unclear whether different target cells contribute to this heterogeneity and which cell types are most susceptible to oncogenesis. Stem cells are speculated to be the cellular origin of at least a subset of human breast cancers. To begin to address these issues, we have isolated and characterized cell populations enriched in normal mammary stem/progenitors and have studied the expression of putative stem/progenitor markers in tumors derived from genetically engineered mice. Specifically, transgenic activation of Wnt signaling in the mammary gland induces tumors comprised of epithelial and myoepithelial cells harboring the same genetic defect implying that the tumor arose from transformation of a bipotent progenitor cell. On the other hand, transgenic activation of Neu signaling induces tumors comprising cells of more limited lineage capacity. Thus, the heterogeneity of different breast cancers may reflect the activation of different oncogenic pathways, different cellular targets in which these genetic changes occur, or both.
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Keywords {🔍}

google, scholar, pubmed, cas, cells, mammary, article, cancer, cell, stem, breast, gland, mouse, human, epithelial, development, rosen, sci, natl, expression, wnt, smith, proc, acad, usa, biol, tumors, population, jeffrey, cellular, cancers, signaling, tumor, clarke, nature, privacy, cookies, content, journal, biology, neoplasia, stemprogenitor, activation, res, differentiation, rev, dev, side, gene, oncogene,

Topics {✒️}

normal mammary stem/progenitors erbb2-induced mammary tumorigenesis putative stem/progenitor markers month download article/chapter progenitor/stem cells derived label-retaining epithelial cells murine tumor models mmtv-neu transgenic mice side population cells pharmacological gsk-3-specific inhibitor stem/progenitor cells cancer stem cells mammary gland biology epithelial stem cell mammary progenitor cells mouse mammary gland distinct “side population” stem cell niche granulocyte-macrophage progenitors side-population sca-1 human mammary gland wound edge keratinocytes mouse mammary adenocarcinomas stem cell differentiation full article pdf stem cell origin bipotent progenitor cell breast cancer published breast cancer incidence human tumor cells clinically heterogeneous disease transgenes encoding components mcdermott sp distinct cellular progenitors germ-line expression privacy choices/manage cookies target cells contribute myoepithelial cells harboring breast tumor subtypes stem cells human breast cancers human breast tumours int-2-initiated tumors differential gene expression human breast carcinoma related subjects wnt effectors correlates borresen-dale al gene expression patterns limited lineage capacity

Questions {❓}

Will cancer stem cells provide new therapeutic targets?

Schema {🗺️}

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         description:Breast cancer is a genetically and clinically heterogeneous disease. It is unclear whether different target cells contribute to this heterogeneity and which cell types are most susceptible to oncogenesis. Stem cells are speculated to be the cellular origin of at least a subset of human breast cancers. To begin to address these issues, we have isolated and characterized cell populations enriched in normal mammary stem/progenitors and have studied the expression of putative stem/progenitor markers in tumors derived from genetically engineered mice. Specifically, transgenic activation of Wnt signaling in the mammary gland induces tumors comprised of epithelial and myoepithelial cells harboring the same genetic defect implying that the tumor arose from transformation of a bipotent progenitor cell. On the other hand, transgenic activation of Neu signaling induces tumors comprising cells of more limited lineage capacity. Thus, the heterogeneity of different breast cancers may reflect the activation of different oncogenic pathways, different cellular targets in which these genetic changes occur, or both.
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