Potential conflict of interest: Nothing to report.
Cancer risk in chronic hepatitis B: Do genome-wide association studies hit the mark?†
Article first published online: 7 APR 2011
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 53, Issue 4, pages 1390–1392, April 2011
How to Cite
Casper, M., Grünhage, F., Lammert, F. (2011), Cancer risk in chronic hepatitis B: Do genome-wide association studies hit the mark?. Hepatology, 53: 1390–1392. doi: 10.1002/hep.24241
- Issue published online: 7 APR 2011
- Article first published online: 7 APR 2011
- Manuscript Received: 9 DEC 2010
- Manuscript Accepted: 2 FEB 2010
- Manuscript Revised: 1 FEB 2010
To identify susceptibility variants for hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC), we conducted a genome-wide association study by genotyping 440,794 SNPs in 355 chronic HBV carriers with HCC and 360 chronic HBV carriers without HCC, all of Chinese ancestry. We identified one intronic SNP (rs17401966) in KIF1B on chromosome 1p36.22 that was highly associated with HBV-related HCC and confirmed this association in five additional independent samples, consisting of 1,962 individuals with HCC, 1,430 control subjects and 159 family trios. Across the six studies, the association with rs17401966 was highly statistically significant (joint odds ratio = 0.61, P = 1.7 × 10−18). In addition to KIF1B, the association region tagged two other plausible causative genes, UBE4B and PGD. Our findings provide evidence that the 1p36.22 locus confers susceptibility to HBV-related HCC, and suggest that KIF1B-, UBE4B- or PGD-related pathways might be involved in the pathogenesis of this malignancy.