Affiliations of authors: Department of Veterans Affairs Medical Center, Denver, CO (RDD); Department of Dermatology, University of Colorado at Denver & Health Sciences Center, Aurora, CO (KRJ)
Correspondence to: Robert P. Dellavalle, MD, PhD, MSPH, Veterans Affairs Medical Center, 1055 Clermont St. #165, Denver, CO 80220 (e-mail: robert.dellavalle{at}uchsc.edu).
Berwick et al. (1) describe a statistically significant positive association between melanoma survival and solar elastosis and conclude that sun exposure is positively associated with melanoma survival. Two hypotheses are offered as possible explanations for these results: 1) vitamin D synthesized by sun exposure might inhibit melanoma progression, and 2) chronic sun exposure induces melanization and increases DNA repair capacity that might result in less aggressive melanomas and better outcomes (1,2).
We suggest a third hypothesis: the results might reflect a mixed population composed of individuals who develop a less aggressive "environmental" variant of melanoma as a result of sun exposure and individuals who develop "genetic" melanoma, a more aggressive variant resulting from a genetic predisposition independent of sun exposure. Such a dichotomous population might be revealed epidemiologically by differing associations with melanoma family history, a variable not controlled for in the study's reported multivariable analysis. Moreover, family history was ascertained using a self-administered questionnaire, a method previously associated with melanoma overreporting by up to 40% (3). It has been estimated that only 5%10% of melanoma patients have a medically verifiable family history (4,5). Although a verified family history has not been shown to predict rate of survival in those with metastatic disease (5), rates of metastasis and overall melanoma survival in those with and without a family history of melanoma have not been extensively examined.
Examination of potentially different distributions of molecular markers in environmental and genetic melanomas could provide additional insight. For example, those with UV-induced melanomas might be expected to have a different vitamin D receptor status than those with melanoma resulting from genetics. A statistically significant association between variant vitamin D receptor alleles and Breslow thickness, a highly predictive prognostic indicator, has been previously demonstrated (6), but association with a family history of melanoma is not yet known.
Before the boldest clinicians start sending melanoma patients to tanning salons, family history and genetic characterization of melanoma patients in this and other survival study cohorts will be needed to correctly interpret results associating UV radiation exposure with increased melanoma survival.
REFERENCES
(1) Berwick M, Armstrong BK, Ben-Porat L, Fine J, Kricker A, Eberle C, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst 2005;97:1959.
(2) Egan KM, Sosman JA, Blot WJ. Sunlight and reduced risk of cancer: is the real story vitamin D? J Natl Cancer Inst 2005;97:1613.
(3) Aitken JF, Youl P, Green A, MacLennan R, Martin NG. Accuracy of case-reported family history of melanoma in Queensland, Australia. Melanoma Res 1996;6:3137.
(4) Hornbuckle J, Culjak G, Jarvis E, Gebski V, Coates A, Mann G, et al. Patterns of metastases in familial and non-familial melanoma. Melanoma Res 2003;13:1059.[CrossRef][ISI][Medline]
(5) de Snoo FA, Bergman W, Gruis NA. Familial melanoma: a complex disorder leading to controversy on DNA testing. Fam Cancer 2003;2:10916.[CrossRef][Medline]
(6) Hutchinson PE, Osborne JE, Lear JT, Smith AG, Bowers W, Morris PN, et al. Vitamin D receptor polymorphisms are associated with altered prognosis in patients with malignant melanoma. Clin Cancer Res 2000;6:498504.
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