Clinical ReviewUltraviolet A and melanoma: A review☆,☆☆,★
Section snippets
Basic science evidence
Cancer may be viewed as a disease that progresses through multiple stages that involve initiation, promotion, progression, and metastasis. Each stage is accompanied by further changes in DNA. UVB is known to cause mutations in oncogenes and tumor suppressor genes that eventually initiate the cascade of events resulting in skin cancers.14, 15, 16 To substantiate that UVA has the potential to induce melanoma, it is necessary to demonstrate that UVA is capable of producing biologic damage. It has
Epidemiologic evidence
Epidemiologic observations often reveal associations that provide valuable clues and new channels for further investigations, but these observations are not a substitute for understanding the pathogeneses of diseases. The validity of epidemiologic studies can be undermined by recall bias and confounding factors.
Clinical evidence
There are few controlled clinical studies investigating the independent effects that UVA radiation exerts on human skin. However, there are several clinical situations in which UVA is used to treat cutaneous diseases (eg, psoriasis, atopic dermatitis, cutaneous T-cell lymphomas, granuloma annulare, scleroderma)89 from which indirect conclusions can be drawn. Unlike therapeutic UVB radiation, therapeutic UVA plus psoralens is associated with the development of large, irregular, unevenly
Discussion
In this review, we have examined evidence from various disciplines that surround the controversy concerning UVA as a causative factor in the development of human melanoma. Although no studies have shown this conclusively, we believe that the evidence currently available to us does not allow this relationship to be ruled out.
The clinical implications of a role for UVA in causing human melanoma are important. People who frequently use sunbeds and sunlamps have exposed themselves to large
Acknowledgements
We thank Darrell S. Rigel, MD, for his valuable suggestions. Brookhaven National Laboratory is operated by Brookhaven Science Associates for the US Department of Energy. We thank Jackie M. Tripp, MD, for his assistance in the preparation of this manuscript.
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Supported by The Ronald O. Perelman Department of Dermatology, New York University School of Medicine; Joseph H. Hazen Foundation; Mary and Emanuel Rosenthal Foundation; Kaplan Comprehensive Cancer Center (Cancer Center Support Core Grant 5P30-CA-16087); the Blair O. Rogers Medical Research Fund; Rahr Family Foundation; and Stavros S. Niarchos Foundation fund of the Skin Cancer Foundation.
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Reprint requests: Alfred W. Kopf, MD, The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 550 First Ave, H164, New York, NY 10016. E-mail: [email protected].
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J Am Acad Dermatol 2001;44:837-46