Human hepatocyte carcinogenesis (Review)
- Hidenori Shiraha
- Kazuhide Yamamoto
- Masayoshi Namba
Affiliations: Department of Gastroenterology and Hepatology, Okayama University Faculty of Medicine, Okayama 700-8558, Japan, Niimi College, Nishikata 1263-2, Niimi 718-8585, Japan
- Published online on: February 19, 2013 https://doi.org/10.3892/ijo.2013.1829
Copyright: © Shiraha
et al. This is an open access article distributed under the
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Commons Attribution License [CC BY_NC 3.0].
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Hepatocellular carcinoma is the third most frequent cause of cancer-related death worldwide; and its incidence rate is increasing. Clinical and molecular medical analyses have revealed substantial information on hepatocarcinogenesis. Hepatocarcinogenesis is a stepwise process during which multiple genes are altered. Genetic changes and their biological consequences in human HCC can be divided into at least 4 groups: i) tumor suppressor genes (p53, retinoblastoma, phosphatase tensin homolog and runt-related transcription factor 3), ii) oncogenes (myc, K-ras, BRAF), iii) reactivation of developmental pathways (Wnt, hedgehog), and iv) growth factors and their receptors (transforming growth factor-α, insulin-like growth factor-2 receptor). An experimental model of human hepatocarcinogenesis such as in vitro neoplastic transformation of human hepatocytes has not been successfully achieved yet, but several immortalized human hepatocyte cell lines have been established. These immortalized human hepatocytes will become useful tools for the elucidation of hepatocarcinogenesis, especially for the initial step of multistep hepatocarcinogenesis.