Study Examines Proteins' Relation to DNA Repair and Malignant Melanoma

Main Category: Melanoma / Skin Cancer
Article Date: 01 Dec 2004 - 3:00 PDT


A reduced capacity to repair UV-induced DNA damage has been associated with an increased risk of cutaneous malignant melanoma, but the molecular mechanism of the association is not known. The INK4a/ARF locus, which contains two known tumor suppressors, is often mutated in melanomas and in the cells of patients with familial malignant melanoma, but it is not known if the locus is involved in DNA repair.

In a new study, Thomas M. R�nger, M.D., of the Boston University School of Medicine, and colleagues measured and compared DNA repair in cells from normal mice and cells from mice with one or both of the tumor suppressors mutated. The mutant cells had a lower capacity for DNA repair compared with the normal cells. The authors conclude that mutation of the INK4a/ARF locus may predispose people to melanoma because of a reduced ability to repair sun-induced DNA damage in addition to the loss of tumor suppressor function.

Contact: Thomas M. R�nger, Boston University School of Medicine, 617-638-5551, truenger@bu.edu

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oupjournals.org.

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Journal of the National Cancer Institute

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