4.6 Article

A novel single nucleotide polymorphism in XRCC4 gene is associated with oral cancer susceptibility in Taiwanese patients

期刊

ORAL ONCOLOGY
卷 44, 期 9, 页码 898-902

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.oraloncology.2007.11.007

关键词

XRCC4; polymorphism; oral cancer; carcinogenesis

资金

  1. China Medical University and Hospital [DMR-97-061]
  2. Terry Fox Cancer Research Foundation
  3. National Science Council [NSC 95-2320-B-039-014-MY3]

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The DNA double strand break repair gene XRCC4, an important caretaker of genome stability, is suggested to play a role in the development of human carcinogenesis. However, no evidence has been provided showing that XRCC4 was associated with oral oncology. In this hospital-based case-control study, the association of XRCC4 G-1394T (rs6869366), intron 3 (rs28360071), intron 7 (rs28360317), and intron 7 (rs1805377) polymorphisms with oral cancer risk in a Taiwanese population was first investigated. In total, 318 patients with oral cancer and 318 age- and gender-matched healthy controls were genotyped. We found a significant different distribution in the frequency of the XRCC4 intron 3 genotype, but not the XRCC4 G-1394T or intron 7 genotypes, between the oral. cancer and control. groups. Those who had heterozygous del/ins at XRCC4 intron 3 showed a 1.57-fold (95% confidence interval = 1.12-2.21) increased risk of oral. cancer compared to those with ins/ins. As for XRCC4 G-1394T or intron 7 polymorphisms, there was no difference in the distribution between the oral cancer and control groups. There were significant gene-environment interactions between XRCC4 intron 3 genotype with smoking and with betel. quid chewing, but not with alcoholism. In smoker and betel, quid chewer groups, the XRCC4 intron 3 del variants exhibited 2.57- and 3.03-fold higher risks than the ins genotype, respectively. Our results firstly suggest that the XRCC4 intron 3 del genotype may be associated with oral oncology and may be a novel useful marker for primary prevention and anticancer intervention. (C) 2007 Elsevier Ltd. All rights reserved.

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