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Biology of transforming growth factor β in hepatocarcinogenesis
Author(s) -
Rossmanith Walter,
SchulteHermann Rolf
Publication year - 2001
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/1097-0029(20010215)52:4<430::aid-jemt1028>3.0.co;2-3
Subject(s) - transforming growth factor , biology , cancer research , hepatocellular carcinoma , genetically modified mouse , immunosuppression , hepatocyte growth factor , transgene , angiogenesis , hepatocyte , growth factor , gene , endocrinology , receptor , immunology , genetics , in vitro
TGF‐β is an important factor in the regulation of liver growth. It is an inhibitor of hepatocyte DNA synthesis and may induce active cell death, e.g., to remove excessive tissue mass. Studies using transgenic mice suggest that expression in the resting liver has to be well balanced; either under‐ or overexpression appear to cause an increased turnover of hepatocytes and to predispose to hepatocarcinogenesis. TGF‐β overexpression is frequently observed in human hepatocellular carcinomas, probably as a late event in tumor development. In men and mice, TGF‐β overexpression appears to be associated with loss of TGF‐β responsiveness often by disruption of TGF‐β signaling. However, mechanisms as mutations in TGF‐β receptor II or Smad2 and 4 genes, frequently observed in other human cancers, have only rarely been observed in hepatocellular carcinomas. Further studies may clarify the mechanisms by which hepatocellular tumors escape TGF‐β growth control, as well as analyze possible roles of TGF‐β overexpression in immunosuppression and angiogenesis. Microsc. Res. Tech. 52:430–436, 2001. © 2001 Wiley‐Liss, Inc.