Mitochondrial D-loop mutations and deletion profiles of cancerous and noncancerous liver tissue in hepatitis B virus-infected liver

Wheelhouse, Nicholas M; Lai, P B S; Wigmore, S J; Ross, J A; Harrison, D J

Abstract

The largest single underlying cause of hepatocellular carcinoma (HCC) worldwide is hepatitis B virus (HBV) infection. Hepatitis B virus increases cellular oxidative stress and the development of HCC occurs after a long latency period. The study was carried out to determine whether mitochondrial DNA abnormalities were associated with HCC in individuals with HBV. The frequency of mutation and deletion of specific areas of the mitochondrial genome in tumour and matched normal tissue of patients with HBV infection was investigated in the current study. The percentage of control subjects harbouring D-loop mutations was 11%, which was significantly lower than that observed in both the noncancerous (49%, P=0.033) and tumour tissue (59%, P=0.014) of patients with HCC. In contrast, the number of cases in which the common 4977 bp deletion of the mitochondrial genome was detected was significantly greater in control liver and noncancerous liver tissue of subjects with HCC (100 and 95%, respectively) than in cancerous liver tissue (28%, P

Citation

Wheelhouse, N. M., Lai, P. B. S., Wigmore, S. J., Ross, J. A., & Harrison, D. J. (2005). Mitochondrial D-loop mutations and deletion profiles of cancerous and noncancerous liver tissue in hepatitis B virus-infected liver. British Journal of Cancer, 92(7), 1268-1272. https://doi.org/10.1038/sj.bjc.6602496

• Journal Article Type: Article
• Acceptance Date: Feb 8, 2005
• Online Publication Date: Mar 22, 2005
• Publication Date: 2005-04
• Deposit Date: Jul 21, 2016
• Journal: British Journal of Cancer
• Print ISSN: 0007-0920
• Electronic ISSN: 1532-1827
• Publisher: Cancer Research UK
• Peer Reviewed: Peer Reviewed
• Volume: 92
• Issue: 7
• Pages: 1268-1272
• DOI: https://doi.org/10.1038/sj.bjc.6602496
• Keywords: Mitochondrial DNA, inflammation, viral hepatitis, tumorigenesis,
• Public URL: http://researchrepository.napier.ac.uk/Output/304757
• Related Public URLs: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361973/pdf/92-6602496a.pdf