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[Cancer Research 60, 5612-5616, October 15, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

A Variant within the DNA Repair Gene XRCC3 Is Associated with the Development of Melanoma Skin Cancer1

Samantha L. Winsey, Neil A. Haldar, Howard P. Marsh, Mike Bunce, Sara E. Marshall, Adrian L. Harris2, Fenella Wojnarowska and Ken I. Welsh

Department of Dermatology [S. L. W., F. W.], Transplant Immunology [S. L. W., N. A. H., H. P. M., M. B., S. E. M., K. I. W.], and the Medical Oncology Unit Imperial Cancer Research Fund [H. P. M., A. L. H.], University of Oxford, Churchill Hospital, Oxford 0X3 7LJ, United Kingdom

Exposure to UV radiation is a major risk factor for the development of malignant melanoma. DNA damage caused by UV radiation is thought to play a major role in carcinogenesis induction. Multiprotein pathways involved in repairing UV-DNA damage are the base excision, the nucleotide excision, and the homologous double-stranded DNA repair pathways. This study used a sequence-specific primer PCR (PCR-SSP) genotyping method to investigate the association between polymorphisms in DNA repair genes from these pathways with the development of malignant melanoma. The patient cohort was comprised of 125 individuals with malignant melanoma with lesions or staging suggesting a high risk of relapse or metastatic disease. The control population consisted of 211 individuals. We found the presence of a T allele in exon 7 (position 18067) of the XRCC3 gene was significantly associated with melanoma development (P = 0.004; odds ratio, 2.36; relative risk, 1.74). This gene codes for a protein involved in the homologous pathway of double-stranded DNA repair, thought to repair chromosomal fragmentation, translocations, and deletions. These results may provide further insights into the pathogenesis and the mechanism of UV-radiation induced carcinogenesis as well as having a role in prevention.




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