Hepatitis C Virus And Cancer: A Summary Review Of Epidemiologic And Meta-Analytical Studies And Portfolio Analyses Of Funded Grants

Tram LAM, National Institute of Health, United States
DATHE M. 1 , QADIR X. 1 , LANE C. 1 , LAI G. 1 , CARRICK D. 1 , SCHULLY S. 1 , ELLISON G. 1

1 Epidemiology and Genomics Research Program, Division Cancer Control and Population Sciences, National Cancer Institute, National Institute of Health, Rockville, Maryland, United States of America

Background: The global burden of infection with Hepatitis C virus (HCV) is substantial (~130-150 million people experiencing chronic HCV infection). HCV infection is one of the leading causes of liver cancer (2nd cause of cancer-related deaths worldwide), and emerging evidence suggests an etiologic role in the development of other cancer sites.  To obtain a global view of the research landscape and the state of the science on the epidemiology of HCV and cancer risk, we assessed the robustness of the evidence using meta-analyses (2006-2014), summarized emerging evidence (2010-2015), and analyzed current funding from the U.S. National Cancer Institute (NCI). 

Methods: We identified relevant publications (original articles and meta-analyses) and funded grants using PubMed and the National Institutes of Health’s Information for Management, Planning, Analysis, and Coordination database, respectively.  For meta-analyses, we assessed qualitatively the strength of evidence based on a priori criteria and calculated the population attributable fraction (PAF) of individual cancer caused by HCV.

Results: The meta-analytic evidence for HCV infection is ‘strong’ for hepatocellular cancer (HCC), ‘moderate’ for pancreatic cancer, and ‘low’ for cholangiocarcinoma; the associated PAF’s are 20-23%, 1%, and 5-6%, respectively.  For HCC, there is evidence of additive effect modification with hepatitis B virus (HBV), and genotype 1b appears to be the HCV mutation reportedly associated with risk. Evidence suggests an interplay between HCV infection and co-morbid conditions (e.g., diabetes/obesity), associations with non-liver cancers (e.g., non-Hodgkin lymphoma and renal), and racial/ethnic differences. The current NCI’s funding portfolio for the epidemiology of HCV-associated cancers is sparse with no HCV-focused grants.

Conclusions: There is robust evidence linking HCV infection with HCC, with the strongest risks associated with HCV genotype 1b and co-infection with HBV.  Summary of literature review, coupled with a dearth of funding on HCV-focused grants, suggests that the etiology of HCV in cancer warrants further investigation.