Semin Liver Dis 1997; 17(4): 351-355
DOI: 10.1055/s-2007-1007212
ORIGINAL ARTICLE

© 1997 by Thieme Medical Publishers, Inc.

Liver Tumors and Host Defense

Edward Tabor
  • Division of Transfusion Transmitted Diseases, Food and Drug Administration, Bethesda, Maryland
Further Information

Publication History

Publication Date:
17 March 2008 (online)

ABSTRACT

Complex molecular and cellular mechanisms exist to protect cells against tumor formation and to protect the entire organism against further development and spread of established tumors. The p53 tumor suppressor gene controls the cell cycle through at least two mechanisms, namely, mitotic arrest and apoptosis. Human hepato-cellular carcinomas (HCCs) are often found to have mutant p53, or sometimes may have dysfunctional p53 as a result of its being bound by viral or cellular proteins. Another mechanism of host response is the production of transforming growth factor β1, which acts on receptors in normal hepatocytes to cause inhibition of DNA synthesis; abnormalities of transforming growth factor β1 have been documented in HCCs, but their biologic significance is unclear. Other host defense mechanisms include cellular responses to the tumor and the proliferation of substances with anticoagulant properties.

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