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Jane M. McGregor, MA, MRCP
Department of Dermatology St Johns Institute of Dermatology St Thomas' Hospital London, England SE1 7EH

Charlotte M. Proby, MA, MRCP; John L. M. Hawk, BsC, MD, FRCP
London

Arch Dermatol. 1996;132(1):90.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Weinstock et al¹ found human papillomavirus (HPV) (type 16 or a closely related type) in 22 of 30 skin lesions in a single patient in whom multiple skin cancers developed after prolonged therapy with psoralen plus UV-A (PUVA). Although this is an interesting observation, the question remains whether HPV-16 had a functional role in the development of these tumors. Several lines of evidence suggest that HPV-16 is unlikely to play a role in the development of skin cancer in most patients, immunosuppressed or not.

The HPVs are highly host specific and show a remarkable degree of tissue specificity. Common mucosalassociated HPV types, including 16 and 18, are rarely found in keratinizing epithelia, even in chronically immunosuppressed renal transplant recipients, and, similarly, cutaneous HPV types are not found in the genital tract. Instead, recent studies implicate novel epidermodysplasia verruciformis—related cutaneous HPVs in the development of transplant-associated skin cancers^2,3 found . . . [Full Text PDF of this Article]

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