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Review
. 2002 Jul;51(1):132-9.
doi: 10.1136/gut.51.1.132.

Cocarcinogenic effects of alcohol in hepatocarcinogenesis

Affiliations
Review

Cocarcinogenic effects of alcohol in hepatocarcinogenesis

F Stickel et al. Gut. 2002 Jul.

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.

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Figures

Figure 1
Figure 1
Alcohol as a promoter of hepatocarcinogenesis. Both activation and inactivation of procarcinogens can occur. Alcohol per se is a tumour promoter but may contribute to initiation via procarcinogen activation. ADH, alcohol dehydrogenase; ALDH, aldehyde dehydrogenase; CYP 2E1, cytochrome P450 2E1; HCC, hepatocellular carcinoma.
Figure 2
Figure 2
Interaction of alcohol with methyl transfer. Alcohol impairs one carbon metabolism via interfering with (1) folate uptake and generation of tetrahydrofolate (THF); (2) degradation of pyridoxal-5`-phosphate (PLP) at several sites; and (3) inhibition of methyl transfer to DNA via inhibition of methyltransferase, resulting in hypomethylation and consequently enhanced transcription of certain oncogenes.

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