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Carcinogenesis, Vol. 22, No. 8, 1185-1188, August 2001
© 2001 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

XPD exon 10 and 23 polymorphisms and DNA repair in human skin in situ

Kari Hemminki3,, Guogang Xu, Sabrina Angelini, Erna Snellman1,, Christer T. Jansen2,, Bo Lambert and Sai-Mei Hou

Department of Biosciences at Novum, Karolinska Institute, 14157 Huddinge, Sweden,
1 Department of Dermatology, Päijät-Häme Central Hospital, 15850 Lahti, Finland and
2 Department of Dermatology, University of Turku, 20520 Turku, Finland

Forty-four Finnish volunteers who were previously studied with regard to the repair rate of UV-specific cyclobutane pyrimidine dimers in the skin were genotyped for XPD polymorphisms at codons 312 (exon 10 G->A, Asp->Asn) and 751 (exon 23 A->C, Lys->Gln). The repair rate was measured at 24 h for two different cyclobutane dimers. The data did not show consistent XPD genotype-specific differences in DNA repair rates among all subjects. The combined exon 10 AA and exon 23 CC genotype was associated with an ~50% depression of repair rate but this was of borderline statistical significance. However, the exon 23 C allele was associated with depressed repair among subjects aged 50 years or older and the result was consistent with both dimers.


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