Journal Article

Cyclobutane pyrimidine dimers form preferentially at the major <i>p53</i> mutational hotspot in UVB-induced mouse skin tumors

Young-Hyun You, Piroska E. Szabó and Gerd P. Pfeifer

in Carcinogenesis

Volume 21, issue 11, pages 2113-2117
Published in print November 2000 | ISSN: 0143-3334
Published online November 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.11.2113
Cyclobutane pyrimidine dimers form preferentially at the major p53 mutational hotspot in UVB-induced mouse skin tumors

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The most prevalent DNA lesion induced by UV irradiation is the cyclobutane pyrimidine dimer (CPD) which forms at positions of neighboring pyrimidines. In mouse skin tumors induced by irradiation with UVB (280–320 nm) lamps or solar UV simulators, a major mutational hotspot occurs at codon 270 (Arg→Cys) involving a sequence change from 5′-TCGT to 5′-TTGT. We have shown previously that CPD formation by UVB or sunlight is enhanced up to 10-fold at 5′-CCG and 5′-TCG sequences due to the presence of 5-methylcytosine bases. Sequence analysis showed that the CpG at codon 270 is methylated in mouse epidermis at a level of ~85%. Irradiation of mouse skin or mouse cells in culture produced the strongest CPD signal within exon 8 at the 5′-TCG sequence which is part of codon 270. Time course experiments showed that CPDs at this particular sequence persist longer than at several neighboring positions. The data suggest that formation of CPDs is responsible for induction of the major p53 mutational hotspot in UV-induced mouse skin tumors.

Keywords: CPD, cyclobutane pyrimidine dimer; LMPCR, ligationmediated polymerase chain reaction.

Journal Article.  3251 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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