Plasma Carotenoids, Glutathione S-Transferase M1 andT1 Genetic Polymorphisms, and Risk of Hepatocellular Carcinoma: Independent and Interactive Effects
Resource
American Journal of Epidemiology 149 (7): 621-629
Journal
American Journal of Epidemiology
Pages
621-629
Date Issued
1999
Date
1999
Author(s)
Chiu Y.-H.
Chiang Y.-C.
Lee T.-H.
Santella R.M.
Chern H.-D.
Liaw Y.-F.
Chen C.-J.
Abstract
This study was conducted to assess the role of carotenoid and glutathione S-transferase (GST) M1 and T1 genetic polymorphisms in the development of hepatocellular carcinoma (HCC). A total of 84 incident cases of HCC and 375 matched controls selected from a cohort of 7,342 men (4,841 chronic hepatitis B carriers and 2,501 noncarriers) who were recruited between 1988 and 1992 in Taiwan were studied. Neither GST M1/T1 polymorphisms nor plasma levels of various carotenoids were independently associated with HCC, but they modulated smoking- and/or drinking-related HCC risk. Cumulative exposure to tobacco smoke significantly increased HCC risk in a dose- dependent manner among subjects with low plasma β-carotene levels (p for trend = 0.047) but not among those with high levels. A statistically significant effect of habitual alcohol drinking on HCC risk was observed only for those with low plasma levels of β-carotene, α-carotene, or lycopene and for GST M1 null subjects. There was evidence suggesting an interaction between the GST M1/T1 genotype and certain carotenoids in HCC associated with smoking and drinking. The strongest effect of smoking and drinking was noted among GST M1 null subjects with low plasma levels of β-carotene (smoking: adjusted odds ratio (OR) = 3.54, 95% confidence interval (CI) 1.06-11.83; drinking: OR = 8.28, 95% CI 2.40-28.61).
SDGs
Other Subjects
alcohol; alpha carotene; beta carotene; carotenoid; cigarette smoke; glutathione transferase; lycopene; article; cancer risk; chronic hepatitis; cigarette smoking; disease association; dose response; drinking behavior; environmental exposure; enzyme blood level; genetic polymorphism; hepatitis B; high risk population; human; liver cell carcinoma; major clinical study; male; risk assessment; risk factor; smoking; Taiwan; virus carrier; vitamin blood level
Type
journal article
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