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Zhang YJ. Interactions of chemical carcinogens and genetic variation in hepatocellular carcinoma. World J Hepatol. 2010;2(3):94-102doi: 10.4254/wjh.v2.i3.94.
Zhang, Y. J. (2010). Interactions of chemical carcinogens and genetic variation in hepatocellular carcinoma. World journal of hepatology, 2(3), 94-102. https://doi.org/10.4254/wjh.v2.i3.94
Zhang, Yu-Jing. "Interactions of chemical carcinogens and genetic variation in hepatocellular carcinoma." World journal of hepatology vol. 2,3 (2010): 94-102. doi: https://doi.org/10.4254/wjh.v2.i3.94
Zhang YJ. Interactions of chemical carcinogens and genetic variation in hepatocellular carcinoma. World J Hepatol. 2010 Mar 27;2(3):94-102. doi: 10.4254/wjh.v2.i3.94. PMID: 21160980; PMCID: PMC2999273.
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World J Hepatol. 2010 Mar 27;2(3):94-102. doi: 10.4254/wjh.v2.i3.94.

Interactions of chemical carcinogens and genetic variation in hepatocellular carcinoma.

World journal of hepatology

Yu-Jing Zhang

Affiliations

  1. Yu-Jing Zhang, Department of Environmental Health Sciences, Mailman School of Public Health and Cancer Center of Columbia University, New York, NY 10032, United States.

PMID: 21160980 PMCID: PMC2999273 DOI: 10.4254/wjh.v2.i3.94

Abstract

In the etiology of hepatocellular carcinoma (HCC), in addition to hepatitis B virus and hepatitis C virus infections, chemical carcinogens also play important roles. For example, aflatoxin B(1) (AFB(1)) epoxide reacts with guanine in DNA and can lead to genetic changes. In HCC, the tumor suppressor gene p53 codon 249 mutation is associated with AFB(1) exposure and mutations in the K-ras oncogene are related to vinyl chloride exposure. Numerous genetic alterations accumulate during the process of hepatocarcinogenesis. Chemical carcinogen DNA-adduct formation is the basis for these genetic changes and also a molecular marker which reflects exposure level and biological effects. Metabolism of chemical carcinogens, including their activation and detoxification, also plays a key role in chemical hepatocarcinogenesis. Cytochrome p450 enzymes, N-acetyltransferases and glutathione S-transferases are involved in activating and detoxifying chemical carcinogens. These enzymes are polymorphic and genetic variation influences biological response to chemical carcinogens. This genetic variation has been postulated to influence the variability in risk for HCC observed both within and across populations. Ongoing studies seek to fully understand the mechanisms by which genetic variation in response to chemical carcinogens impacts on HCC risk.

Keywords: 4-aminobiphenyl; Aflatoxin B1; Chemical carcinogens; Cytochrome p450 enzymes; Genetic variation; Glutathione S-transferase; Hepatitis B virus; Hepatitis C virus; Hepatocellular carcinoma; Polycyclic aromatic hydrocarbons

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