Article Text
Review
Cocarcinogenic effects of alcohol in hepatocarcinogenesis
Abstract
Alcohol is a major aetiological factor in hepatocarcinogenesis but our understanding of its importance as a modulating factor is just beginning to emerge. In the present review, a number of possible cofactors and mechanisms are discussed by which alcohol may enhance the development of hepatoma. These include dietary or environmental carcinogens ingested along with alcoholic beverages, alcoholic cirrhosis as a precancerous condition, and the effects of alcohol metabolism.
- alcohol
- hepatocellular carcinoma
- hepatitis B
- hepatitis C
- acetaldehyde
- cytochrome P450
- methylation
- cocarcinogen
- AA, acetaldehyde
- ADH, alcohol dehydrogenase
- AFB1
- aflatoxin B1
- ALD, alcoholic liver disease
- ALDH, aldehyde dehydrogenase
- DMN, dimethyl-nitrosamine
- CYP 2E1, cytochrome P450 2E1
- HBV, hepatitis B virus
- HCC, hepatocellular carcinoma
- HCV, hepatitis C virus
- MB, Mallory body
- NK, natural killer
- RA, retinoic acid
- ROS, reactive oxygen species
- SAH, S-adenosylhomocysteine
- SAM, S-adenosylmethionine
- TNF-α, tumour necrosis factor α
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- alcohol
- hepatocellular carcinoma
- hepatitis B
- hepatitis C
- acetaldehyde
- cytochrome P450
- methylation
- cocarcinogen
- AA, acetaldehyde
- ADH, alcohol dehydrogenase
- AFB1
- aflatoxin B1
- ALD, alcoholic liver disease
- ALDH, aldehyde dehydrogenase
- DMN, dimethyl-nitrosamine
- CYP 2E1, cytochrome P450 2E1
- HBV, hepatitis B virus
- HCC, hepatocellular carcinoma
- HCV, hepatitis C virus
- MB, Mallory body
- NK, natural killer
- RA, retinoic acid
- ROS, reactive oxygen species
- SAH, S-adenosylhomocysteine
- SAM, S-adenosylmethionine
- TNF-α, tumour necrosis factor α