Abstract

There is much evidence suggesting a close association between hepatitis B virus (HBV) infection and the development of primary hepatocellular carcinoma (PHC), although the mechanism by which HBV participates in the development of PHC remains to be elucidated. The importance of this relationship to public health can be appreciated by the fact that PHC is the most common cancer in the world (at least 250,000 new cases annually), that there are approximately 200 million HBV carriers worldwide, and that persistent infection with HBV may be required for the development of PHC [1–3]. The latter point is supported by much epidemiological data, including a study showing that the relative risk of HBV carriers developing PHC as compared to noncarriers is more than 200, which is one of the highest relative risks known for a human cancer [4]. In some populations, the lifetime risk of chronic carriers developing PHC is as high as 50% in males, and almost half of all deaths in carriers 40 years or older have been attributed to PHC [4,5]. A better understanding of this relationship at cellular and molecular levels, then, will have a significant impact upon public health.

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