Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by You, Y.-H.
Right arrow Articles by Pfeifer, G. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by You, Y.-H.
Right arrow Articles by Pfeifer, G. P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 21, No. 11, 2113-2117, November 2000
© 2000 Oxford University Press

Short Communication

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

Young-Hyun You, Piroska E. Szabó and Gerd P. Pfeifer1

Department of Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
E. Zattra, C. Coleman, S. Arad, E. Helms, D. Levine, E. Bord, A. Guillaume, M. El-Hajahmad, E. Zwart, H. van Steeg, et al.
Polypodium leucotomos Extract Decreases UV-Induced Cox-2 Expression and Inflammation, Enhances DNA Repair, and Decreases Mutagenesis in Hairless Mice
Am. J. Pathol., November 1, 2009; 175(5): 1952 - 1961.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
D. Frumkin, A. Wasserstrom, S. Itzkovitz, T. Stern, A. Harmelin, R. Eilam, G. Rechavi, and E. Shapiro
Cell Lineage Analysis of a Mouse Tumor
Cancer Res., July 15, 2008; 68(14): 5924 - 5931.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
J. Ramos, J. Villa, A. Ruiz, R. Armstrong, and J. Matta
UV Dose Determines Key Characteristics of Nonmelanoma Skin Cancer
Cancer Epidemiol. Biomarkers Prev., December 1, 2004; 13(12): 2006 - 2011.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
W. Zhang, E. Remenyik, D. Zelterman, D. E. Brash, and N. M. Wikonkal
Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations
PNAS, November 9, 2001; (2001) 241353198.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
W. Zhang, E. Remenyik, D. Zelterman, D. E. Brash, and N. M. Wikonkal
Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations
PNAS, November 20, 2001; 98(24): 13948 - 13953.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.