Hepatocellular carcinoma is one of the leading causes of
cancer death worldwide. The etiology of
liver cancer is multifactorial, and
infection with hepatitis B virus (HBV), whose pathogenesis is exacerbated by the acquisition of mutations that accelerate
carcinogenesis, or hepatitis C virus (HCV) and dietary exposure to
aflatoxin B(1) all contribute to elevating one's risk for this disease. In this study, we sought to determine the contributions of these agents by measuring the occurrence of an HBV 1762(T)/1764(A) double mutation, an
aflatoxin-specific 249(G-->T) mutation of the p53 gene, and HCV in plasma of 34 HCC cases and 68 age- and gender-matched controls, and in 25 liver
tumors from northern Thailand. In total, 14 cases, 5 controls, and 19
tumors had detectable levels of HBV
DNA. All 14 cases, 2 controls (2.9%), and 17
tumors (89.5%) were positive for the HBV double mutation. Nine cases (26.5%), 10 controls (14.7%), and 6
tumors (24%) were positive for the p53 mutation. Five cases (14.7%), no controls, and 4
tumors (16%) had both mutations. The median age of HCC diagnosis in these 5 cases was 34 years versus 51 years for other cases. Five cases (14.7%) and 1 control (1.5%) were HCV
enzyme immunoassay positive. Thus, specific HBV, HCV, and
aflatoxin biomarkers reveal the complexity of risks contributing to HCC in northern Thailand and suggest further application of these
biomarkers as intermediate end points in prevention, intervention trials, and etiologic investigations.