Liver tumors and host defense.
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 hepatocellular 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 beta 1, which acts on receptors in normal hepatocytes to cause inhibition of DNA synthesis; abnormalities of transforming growth factor beta 1 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.
Tabor
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Division of Transfusion Transmitted Diseases, Food and Drug Administration, Bethesda, Maryland 20852-1448, USA.
D000917:Antibody Formation / Q000502:physiology; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000276:immunology*; D002471:Cell Transformation, Neoplastic / Q000276:immunology*; D016147:Genes, Tumor Suppressor / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D008113:Liver Neoplasms / Q000235:genetics / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000276:immunology
D016212:Transforming Growth Factor beta