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  • Endothelial Progenitor Cells Control the Angiogenic Switch in Mouse Lung Metastasis

    Author(s)
    Gao, Dingcheng
    J. Nolan, Daniel
    S. Mellick, Albert
    Bambino, Kathryn
    McDonnell, Kevin
    Mittal, Vivek
    Griffith University Author(s)
    Mellick, Albert S.
    Year published
    2008
    Metadata
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    Abstract
    Angiogenesis-mediated progression of micrometastasis to lethal macrometastasis is the major cause of death in cancer patients. Here, using mouse models of pulmonary metastasis, we identify bone marrow (BM)-derived endothelial progenitor cells (EPCs) as critical regulators of this angiogenic switch. We show that tumors induce expression of the transcription factor Id1 in the EPCs and that suppression of Id1 after metastatic colonization blocked EPC mobilization, caused angiogenesis inhibition, impaired pulmonary macrometastases, and increased survival of tumor-bearing animals. These findings establish the role of EPCs in ...
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    Angiogenesis-mediated progression of micrometastasis to lethal macrometastasis is the major cause of death in cancer patients. Here, using mouse models of pulmonary metastasis, we identify bone marrow (BM)-derived endothelial progenitor cells (EPCs) as critical regulators of this angiogenic switch. We show that tumors induce expression of the transcription factor Id1 in the EPCs and that suppression of Id1 after metastatic colonization blocked EPC mobilization, caused angiogenesis inhibition, impaired pulmonary macrometastases, and increased survival of tumor-bearing animals. These findings establish the role of EPCs in metastatic progression in preclinical models and suggest that selective targeting of EPCs may merit investigation as a therapy for cancer patients with lung metastases.
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    Journal Title
    Science
    Volume
    319
    Publisher URI
    http://www.sciencemag.org/journals/
    DOI
    https://doi.org/10.1126/science.1150224
    Copyright Statement
    Self-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
    Publication URI
    http://hdl.handle.net/10072/26676
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