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JNCI Journal of the National Cancer Institute 2004 96(23):1790-1793; doi:10.1093/jnci/djh307
© 2004 by Oxford University Press
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© 2004 Oxford University Press

BRIEF COMMUNICATION

Impaired Processing of DNA Photoproducts and Ultraviolet Hypermutability With Loss of p16INK4a or p19ARF

Papri Sarkar-Agrawal, Irene Vergilis, Norman E. Sharpless, Ronald A. DePinho, Thomas M. Rünger

Affiliations of authors: Department of Dermatology, Boston University School of Medicine, Boston, MA (PSA, IV, TMR); Lineberger Cancer Center, University of North Carolina, Chapel Hill (NES); Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA (RADP)

Correspondence to: Thomas M. Rünger, Boston University School of Medicine, Department of Dermatology, 609 Albany St., Boston, MA 02118 (e-mail: truenger{at}bu.edu)

Reduced DNA repair has been linked to an increased risk of cutaneous malignant melanoma, but insights into the molecular mechanisms of that link are scarce. The INK4a/ARF (CDKN2a) locus, which codes for the p16INK4a and p19ARF proteins, is often mutated in sporadic and familial malignant melanoma, but it has not been directly associated with reduced DNA repair. We transfected unirradiated mouse fibroblast cells with UV-treated DNA to measure DNA repair in normal, p16INK4a mutant, p19ARF mutant, or double mutant mouse host cells. Loss of either p16INK4a or p19ARF reduced the ability of the cells to process UV-induced DNA damage, independent of cell cycle effects incurred by the loss. These results may further explain why INK4a/ARF mutations predispose to malignant melanoma, a UV-induced tumor.


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