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- Title
Identification of sequence polymorphism in the D-Loop region of mitochondrial DNA as a risk factor for hepatocellular carcinoma with distinct etiology.
- Authors
Ruixing Zhang; Fengbin Zhang; Cuiju Wang; Shunxiang Wang; Yih-Horng Shiao; Zhanjun Guo
- Abstract
Background: Hepatocellular carcinoma (HCC) is frequently preceded by hepatitis virus infection or alcohol abuse. Genetic backgrounds may increase susceptibility to HCC from these exposures. Methods: Mitochondrial DNA (mtDNA) of peripheral blood, tumor, and/or adjacent non-tumor tissue from 49 hepatitis B virus-related and 11 alcohol-related HCC patients, and from 38 controls without HCC were examined for single nucleotide polymorphisms (SNPs) and mutations in the D-Loop region. Results: Single nucleotide polymorphisms (SNPs) in the D-loop region of mt DNA were examined in HCC patients. Individual SNPs, namely the 16266C/T, 16293A/G, 16299A/G, 16303G/A, 242C/T, 368A/G, and 462C/T minor alleles, were associated with increased risk for alcohol- HCC, and the 523A/del was associated with increased risks of both HCC types. The mitochondrial haplotypes under the M haplogroup with a defining 489C polymorphism were detected in 27 (55.1%) of HBV-HCCand 8 (72.7%) of alcohol- HCC patients, and in 15 (39.5%) of controls. Frequencies of the 489T/152T, 489T/523A, and 489T/525C haplotypes were significantly reduced in HBV-HCC patients compared with controls. In contrast, the haplotypes of 489C with 152T, 249A, 309C, 523Del, or 525Del associated significantly with increase of alcohol-HCC risk. Mutations in the D-Loop region were detected in 5 adjacent non-tumor tissues and increased in cancer stage (21 of 49 HBV-HCC and 4 of 11 alcohol- HCC, p < 0.002). Conclusions: In sum, mitochondrial haplotypes may differentially predispose patients to HBV-HCC and alcohol- HCC. Mutations of the mitochondrial D-Loop sequence may relate to HCC development.
- Subjects
LIVER cancer; CANCER patients; VIRUS diseases; LIVER metastasis; HEPATITIS B; TUMORS; DNA; GENES
- Publication
Journal of Experimental & Clinical Cancer Research (17569966), 2010, Vol 29, p130
- ISSN
1756-9966
- Publication type
Article
- DOI
10.1186/1756-9966-29-130