News Release

Hepatitis B viral load, genotype affect liver cancer risk, study finds

Peer-Reviewed Publication

Journal of the National Cancer Institute

Infection with a specific subtype of hepatitis B virus (HBV) and a high viral load are associated both independently and additively with an increased risk of a type of liver cancer, according to a new study in the February 16 issue of the Journal of the National Cancer Institute.

Chronic infection with HBV has been established as a cause of hepatocellular carcinoma (HCC), a type of liver cancer. More than 350 million people worldwide have a chronic infection with one of the seven known genotypes, or subtypes, of HBV. Although there are some known risk factors for HCC development, it is unclear what role HBV subtype or viral load--the amount of the virus in the blood--might have on cancer development.

To determine whether HBV genotype and viral load are associated with HCC risk, Ming-Whei Yu, Ph.D., of National Taiwan University in Taipei, and colleagues conducted a nested case–control study among male Taiwanese HBV carriers who had not been diagnosed with HCC. HBV DNA levels--a measure of viral load--and genotypes were determined for 154 case patients (men who were diagnosed with HCC during 14 years of follow-up) and 316 control subjects.

Greater viral load was associated with an increased risk of HCC; men in the quintile with the highest viral load had more than seven times the risk of HCC compared with men in the lowest quintile. Genotype C was associated with a five-fold increased risk of HCC compared with all other genotypes. Genotype C was also associated with increased viral load. In addition, the effects of genotype C and increased viral load were additive; men carrying genotype C who had a high viral load had nearly 26.5 times the risk of developing HCC as men with other genotypes who were in the lowest two quintiles of viral load.

"[W]e found that higher plasma HBV DNA levels and infection with genotype C HBV were independently (and additively) associated with an increased risk of HCC among Taiwanese men," the authors write. "The longitudinal stability of these factors and their positive associations with HCC across 10-year age groups ranging from age 30 years to older than age 60 years suggest that they may be important markers for defining high-risk patients for antiviral treatment among HBV carriers."

In an editorial, James J. Goedert, M.D., of the National Cancer Institute, describes the significance of this new research in the path toward eliminating HBV infection and HBV-associated HCC, particularly in Asia where genotype C HBV is more common. "The slow, but sure, approach to reducing liver cancer mortality over the next 50 years is primary prevention of HCC by universal HBV vaccination, particularly of infants in the remote hillside, grassland, forest, and riverbank communities of Africa, Asia, and South America, where HCC mortality is 20-fold higher than it is in the United States," he writes.

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Contacts:

  • Article: Ming-Whei Yu, National Taiwan University, mingwhei@ha.mc.ntu.edu.tw
  • Editorial: National Cancer Institute Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov

    Citations:

  • Article: Yu M-W, Yeh S-H, Chen P-J, Liaw Y-F, Lin C-L, Liu C-J, et al. Hepatitis B Virus Genotype and DNA Level and Hepatocellular Carcinoma: A Prospective Study in Men. J Natl Cancer Inst 2005;97:265–72.
  • Editorial: Goedert JJ. Preventing Infection-Associated Cancer: From Bench to Hillside. J Natl Cancer Inst 2005;97:245–6.

    Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oupjournals.org/.


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