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    Spontaneous expression of embryonic factors and p53 point mutations in aged mesenchymal stem cells: a model of age-related tumorigenesis in mice

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    Authors
    Li, Hanchen
    Fan, Xueli
    Kovi, Ramesh C.
    Jo, YunJu
    Moquin, Brian
    Konz, Richard
    Stoicov, Calin
    Kurt-Jones, Evelyn A.
    Grossman, Steven R.
    Lyle, Stephen
    Rogers, Arlin B.
    Montrose, Marshall
    Houghton, JeanMarie
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    Student Authors
    Ramesh C. Kovi; Calin Stoicov
    UMass Chan Affiliations
    Department of Medicine, Division of Hematology/Oncology
    Department of Medicine, Division of Gastroenterology
    Department of Cancer Biology
    Document Type
    Journal Article
    Publication Date
    2007-11-17
    Keywords
    Adipocytes; Animals; Bone Marrow Transplantation; Cell Line, Transformed; Cell Transformation, Neoplastic; Endothelial Cells; Fibrosarcoma; *Gene Expression Regulation, Neoplastic; *Genes, p53; Male; Mesenchymal Stem Cells; Mice; Mice, Inbred C57BL; *Point Mutation; Time Factors
    Cancer Biology
    Life Sciences
    Medicine and Health Sciences
    
    Metadata
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    Link to Full Text
    http://dx.doi.org/10.1158/0008-5472.CAN-07-2665
    Abstract
    Aging is the single most common risk factor for cancer. Peripheral and marrow-derived stem cells are long lived and are candidate cells for the cancer-initiating cell. Repeated rounds of replication are likely required for accumulation of the necessary genetic mutations. Based on the facts that mesenchymal stem cells (MSC) transform with higher frequency than other cell types, and tumors in aged C57BL/6 mice are frequently fibrosarcomas, we used a genetically tagged bone marrow (BM) transplant model to show that aged mice develop MSC-derived fibrosarcomas. We further show that, with aging, MSCs spontaneously transform in culture and, when placed into our mouse model, recapitulated the naturally occurring fibrosarcomas of the aged mice with gene expression changes and p53 mutation similar to the in vivo model. Spontaneously transformed MSCs contribute directly to the tumor, tumor vasculature, and tumor adipose tissue, recruit additional host BM-derived cells (BMDC) to the area, and fuse with the host BMDC. Unfused transformed MSCs act as the cancer stem cell and are able to form tumors in successive mice, whereas fusion restores a nonmalignant phenotype. These data suggest that MSCs may play a key role in age-related tumors, and fusion with host cells restores a nonmalignant phenotype, thereby providing a mechanism for regulating tumor cell activity.
    Source
    Cancer Res. 2007 Nov 15;67(22):10889-98. Link to article on publisher's site
    DOI
    10.1158/0008-5472.CAN-07-2665
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33723
    PubMed ID
    18006834
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.CAN-07-2665
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    Morningside Graduate School of Biomedical Sciences Scholarly Publications

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