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Hepatitis B, Aflatoxin B₁, and p53 Codon 249 Mutation in Hepatocellular Carcinomas from Guangxi, People’s Republic of China, and a Meta-analysis of Existing Studies¹

Laboratory of Molecular Carcinogenesis [M. C. S., J. A. T.], Epidemiology Branch [S. J. L., J. A. T.], and Biostatistics Branch [D. M. U.], National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California 90033 [M. C. Y.]; and Cancer Institute of Guangxi, Nanning, Guangxi 530021, People’s Republic of China [Z-Q. Z.]

The incidence of hepatocellular carcinomas (HCC) varies widely worldwide, with some of the highest incidence rates found in China. Chronic infection with the hepatitis B virus (HBV) and exposure to aflatoxins in foodstuffs are the main risk factors. A G to T transversion at codon 249 of the p53 gene (249^ser) is commonly found in HCCs from patients in regions with dietary aflatoxin exposure. Because HBV infection is often endemic in high aflatoxin exposure areas, it is still unclear whether HBV acts as a confounder or as a synergistic partner in the development of the 249^ser p53 mutation. Our report has two aims. First, we contribute data on HCCs from southern Guangxi, a high aflatoxin exposure area. Using DNA sequencing, we found that 36% (18 of 50) of tumors had a 249^ser mutation. Also, 50% (30 of 60) were positive for p53 protein accumulation and 78% (28 of 36) were positive for HBV surface antigen, as detected by immunohistochemistry. Second, we present a meta-analysis, using our results along with those from 48 published studies, that examines the interrelationships among aflatoxin exposure, HBV infection, and p53 mutations in HCCs. We used a method that takes into account both within-study and study-to-study variability and found that the mean proportion of HCCs with the 249^ser mutation was positively correlated with aflatoxin exposure (P = 0.0001). We found little evidence for an HBV-aflatoxin interaction modulating the presence of the p53 249^ser mutation or any type of p53 mutation.

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