このエントリーをはてなブックマークに追加
ID 52340
FullText URL
Author
Tatsukawa, Masashi
Takaki, Akinobu Kakenhi
Koike, Kazuko
Iwasaki, Yoshiaki ORCID Kakenhi
Kobashi, Haruhiko
Fujioka, Shin-Ichi
Sakaguchi, Kohsaku
Abstract
Background: Hepatitis B virus (HBV) is a major cause of hepatocarcinogenesis. To identify mutations relevant to hepatocellular carcinoma (HCC) development, we compared the full genome sequences of HBV from the sera of patients with and without HCC. Methods: We compared the full genome sequences of HBV isolates from 37 HCC patients (HCC group 1) and 38 patients without HCC (non-HCC group 1). We also investigated part of the core promoter region sequences from 40 HCC patients (HCC group 2) and 68 patients without HCC. Of the 68 patients who initially did not have HCC, 52 patients remained HCC-free during the follow-up period (non-HCC group 2), and 16 patients eventually developed HCC (pre-HCC group 2). Serum samples collected from patients were subjected to PCR, and the HBV DNA was directly sequenced. Results: All patients had genotype C. A comparison of the nucleotide sequences of the HBV genome between HCC group 1 and non-HCC group 1 revealed that the prevalence of G1613A and C1653T mutations in the core promoter region was significantly higher in the HCC group. These mutations tended to occur simultaneously in HCC patients. Multivariate analysis with group 2 revealed that the presence of HCC was associated with aging and the double mutation. Future emergence of HCC was associated with aging and the presence of a single G1613A mutation. Conclusions: G1613A and C1653T double mutations were frequently found in patients with HCC. A single G1613A mutation was associated with future emergence of HCC. These mutations may serve as useful markers in predicting HCC development.
Published Date
2011-10-21
Publication Title
BMC Cancer
Volume
volume11
ISSN
1471-2407
Content Type
Journal Article
Related Url
http://ousar.lib.okayama-u.ac.jp/metadata/52251
language
英語
Copyright Holders
© 2011 Tatsukawa et al; licensee BioMed Central Ltd.
File Version
publisher
Refereed
True
DOI
Web of Science KeyUT