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    Loss of p53 and Ink4a/Arf cooperate in a cell autonomous fashion to induce metastasis of hepatocellular carcinoma cells

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    Authors
    Chen, Ya-Wen
    Klimstra, David S.
    Mongeau, Michelle E.
    Tatem, Jessica L.
    Boyartchuk, Victor L.
    Lewis, Brian C.
    UMass Chan Affiliations
    Program in Molecular Medicine
    Program in Gene Function and Expression
    Document Type
    Journal Article
    Publication Date
    2007-08-19
    Keywords
    Animals
    Cyclin-Dependent Kinase Inhibitor p16
    Gene Deletion
    Liver Neoplasms, Experimental
    Lung Neoplasms
    Mice
    Mice, Transgenic
    Tumor Suppressor Protein p53
    Genetics and Genomics
    
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    Link to Full Text
    http://dx.doi.org/10.1158/0008-5472.CAN-07-0381
    Abstract
    Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. HCC patients frequently present with disease that has metastasized to other regions of the liver, the portal vein, lymph nodes, or lungs, leading to poor prognoses. Therefore, model systems that allow exploration of the molecular mechanisms underlying metastasis in this disease are greatly needed. We describe here a metastatic HCC model generated after the somatic introduction of the mouse polyoma virus middle T antigen to mice with liver-specific deletion of the Trp53 tumor suppressor locus and show the cell autonomous effect of p53 loss of function on HCC metastasis. We additionally find that cholangiocarcinoma also develops in these mice, and some tumors display features of both HCC and cholangiocarcinoma, suggestive of origin from liver progenitor cells. Concomitant loss of the Ink4a/Arf tumor suppressor locus accelerates tumor formation and metastasis, suggesting potential roles for the p16 and p19 tumor suppressors in this process. Significantly, tumor cell lines isolated from tumors lacking both Trp53 and Ink4a/Arf display enhanced invasion activity in vitro relative to those lacking Trp53 alone. Thus, our data illustrate a new model system amenable for the analysis of HCC metastasis.
    Source
    Cancer Res. 2007 Aug 15;67(16):7589-96. Link to article on publisher's site
    DOI
    10.1158/0008-5472.CAN-07-0381
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/43889
    PubMed ID
    17699762
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.CAN-07-0381
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