OBJECTIVE: To study the association between susceptibility to aflatoxin B1 (AFB1)-related hepatocellular carcinoma(HCC) and the null genotypes of detoxication gene gstM1 and gstT1. METHODS: Peripheral blood white blood cells DNA samples were obtained from all the subjects including 140 HCC cases and 536 controls from AFB1 high risk area Guangxi. gstM1 and gstT1 polymorphisms were detected by polymerase chain reaction technique. RESULTS: (1) gstM1- and gstT1-present were associated with decreasing risk of HCC. gstM1- and gstT1-null were associated with the increasing risk of HCC [adjusted OR (95 % CI) = 2.07 (1.20-3.57) and 1.44 (0.85-2.45), respectively]; (2) The appearance of both gstM1- and gstT1-null genotypes were more susceptible to HCC than either one of them(adjusted OR and 95% CI are 2.43 and (1.19-4.97); (3) From low/median to high level of AFB1 exposure, both gstM1- and gstTl-null genotypes were associated with significantly conspicuous increasing risk of HCC [adjusted OR(95% CI) = 12.76(5.38-30.24) and 7.82(3.61-16.90) respectively]. CONCLUSION: It was suggested that: genetic polymorphisms of gstM1 and gstT1 were susceptible to HCC; individuals who were gstM1- or gstT1-null would have an increasing risk of developing HCC while individuals with both nulls were more susceptible. There was evidence of interaction between gstM1- and gstT1-null and the level of AFB1 exposure which was associated with the increasing risk of HCC.
OBJECTIVE: To study the association between susceptibility to aflatoxin B1 (AFB1)-related hepatocellular carcinoma(HCC) and the null genotypes of detoxication gene gstM1 and gstT1. METHODS: Peripheral blood white blood cells DNA samples were obtained from all the subjects including 140 HCC cases and 536 controls from AFB1 high risk area Guangxi. gstM1 and gstT1 polymorphisms were detected by polymerase chain reaction technique. RESULTS: (1) gstM1- and gstT1-present were associated with decreasing risk of HCC. gstM1- and gstT1-null were associated with the increasing risk of HCC [adjusted OR (95 % CI) = 2.07 (1.20-3.57) and 1.44 (0.85-2.45), respectively]; (2) The appearance of both gstM1- and gstT1-null genotypes were more susceptible to HCC than either one of them(adjusted OR and 95% CI are 2.43 and (1.19-4.97); (3) From low/median to high level of AFB1 exposure, both gstM1- and gstTl-null genotypes were associated with significantly conspicuous increasing risk of HCC [adjusted OR(95% CI) = 12.76(5.38-30.24) and 7.82(3.61-16.90) respectively]. CONCLUSION: It was suggested that: genetic polymorphisms of gstM1 and gstT1 were susceptible to HCC; individuals who were gstM1- or gstT1-null would have an increasing risk of developing HCC while individuals with both nulls were more susceptible. There was evidence of interaction between gstM1- and gstT1-null and the level of AFB1 exposure which was associated with the increasing risk of HCC.