Genes involved in hepatocellular carcinoma: deregulation in cell cycling and apoptosis
A Tannapfel, C Wittekind - Virchows Archiv, 2002 - Springer
A Tannapfel, C Wittekind
Virchows Archiv, 2002•SpringerHepatocellular carcinoma (HCC) accounts for 8–90% of liver cancers and is one of the most
frequent carcinomas throughout the world. The disease is more prevalent in parts of Africa
and Asia than in North and South America and Europe, with a strong etiological association
with viral hepatitis, hemochromatosis, known liver (hepatic) carcinogens, and toxins
(mycotoxins). Clinical and molecular medical analyses have yielded a considerable amount
of information about liver carcinogenesis. Many genes undergo somatic aberrations, with a …
frequent carcinomas throughout the world. The disease is more prevalent in parts of Africa
and Asia than in North and South America and Europe, with a strong etiological association
with viral hepatitis, hemochromatosis, known liver (hepatic) carcinogens, and toxins
(mycotoxins). Clinical and molecular medical analyses have yielded a considerable amount
of information about liver carcinogenesis. Many genes undergo somatic aberrations, with a …
Abstract
Hepatocellular carcinoma (HCC) accounts for 8–90% of liver cancers and is one of the most frequent carcinomas throughout the world. The disease is more prevalent in parts of Africa and Asia than in North and South America and Europe, with a strong etiological association with viral hepatitis, hemochromatosis, known liver (hepatic) carcinogens, and toxins (mycotoxins). Clinical and molecular medical analyses have yielded a considerable amount of information about liver carcinogenesis. Many genes undergo somatic aberrations, with a tendency to cluster at genes involved in cell cycle regulation, in the p53 and Wnt/catenin pathways of signal transduction and cellular adhesion, and in the TGF-β/IGF axis. Since HCC may arise both in liver cirrhosis and in noncirrhotic liver, one may speculate that different hepatocarcinogenetic pathways exist. Recent results of high-output gene analysis using cDNA microarrays support the idea of different genetic alterations in HCC with or without cirrhosis.
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