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.
Hemminki K., Xu G., Angelini S., Snellman E., Jansen C.T., Lambert B., et al. (2001). XPD exon 10 and 23 polymorphisms and DNA repair in human skin in situ. CARCINOGENESIS, 22(8), 1185-1188 [10.1093/carcin/22.8.1185].
XPD exon 10 and 23 polymorphisms and DNA repair in human skin in situ
Angelini S.;
2001
Abstract
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
