Carcinogenesis, Vol. 22, No. 8, 1289-1294,
August 2001
© 2001 Oxford University Press
CARCINOGENESIS |
Genetic polymorphisms of glutathione S-transferases M1 and T1 associated with susceptibility to aflatoxin-related hepatocarcinogenesis among chronic hepatitis B carriers: a nested case–control study in Taiwan
1 School of Public Health, National Defense Medical Center, Taipei, Taiwan,
2 Institute of Aboriginal Health, Tzu Chi University, Hualien County, Taiwan,
3 Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Taiwan,
4 Liver Unit, Kaohsiung Medical Center, Chang Gung Memorial Hospital, Kaohsiung County, Taiwan, Republic of China and
5 Division of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA
This study was conducted to investigate the modifying effect of glutathione S-transferase (GST) M1 and T1 polymorphisms on aflatoxin-induced hepatocarcinogenesis among chronic hepatitis B virus surface antigen (HBsAg) carriers. A total of 79 HBsAg-positive cases of hepatocellular carcinoma (HCC) diagnosed between 1991 and 1997 were identified and individually matched to one or two HBsAg-positive controls on age, gender, residence and date of recruitment from the same cancer screening cohort in Taiwan. Blood samples were tested for hepatitis B and C viral markers by enzyme immunoassay and for aflatoxin B1 (AFB1)–albumin adducts by competitive enzyme-linked immunosorbent assay. GSTM1 and GSTT1 genotypes were determined by PCR. There was a statistically significant relationship between detectable levels of AFB1–albumin adducts in serum and risk of HCC among chronic HBsAg carriers, with an adjusted odds ratio (OR) of 2.0 [95% confidence interval (CI) 1.1–3.7]. In addition, the effect of aflatoxin exposure on HCC risk was more pronounced among chronic HBsAg carriers with the GSTT1 null genotype (OR 3.7, 95% CI 1.5–9.3) than those who were non-null (OR 0.9, 95% CI 0.3–2.4). The interaction between serum AFB1–albumin adduct level and GSTT1 genotype was statistically significant (P = 0.03). For GSTM1 the effect of aflatoxin exposure on HCC risk in those with the null genotype was also greater (adjusted OR 2.8, 95% CI 1.0–7.8) than in those with the gene present (adjusted OR 1.8, 95% CI 0.8–4.5), but the difference was not significant (P = 0.91). Notably, when the interaction between aflatoxin exposure and GSTT1 genotype was considered, aflatoxin exposure by itself was not a significant determinant of HCC risk among chronic HBsAg carriers. These results demonstrate the importance of gene–environment interactions in the multifactorial development of HCC.
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