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Relationship of DNA Repair to Carcinogenesis in Xeroderma Pigmentosum

Dermatology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20014

Radioautograms of intact ultraviolet (UV)-irradiated epidermis from a patient with xeroderma pigmentosum showed no detectable abnormality in UV-induced thymidine-³H incorporation. This result is consistent with findings in this patient's UV-irradiated skin fibroblasts and lymphocytes and contrasts with findings in cells from typical xeroderma pigmentosum patients, all of which exhibit an impaired ability to repair UV-damaged DNA. The development of numerous tumors in the presence of apparently normal DNA repair suggests that some mechanism other than enhancement of UV carcinogenesis by defective DNA repair may be responsible for skin tumor formation in this patient and perhaps in all patients with xeroderma pigmentosum.

¹ Present address: Department of Medicine, The Children's Hospital Medical Center, 300 Longwood Ave., Boston, Mass. 02115.

Received 9/ 5/72. Accepted 1/18/73.

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