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PubMed2002

DNA repair, dysplastic nevi, and sunlight sensitivity in the development of cutaneous malignant melanoma.

BACKGROUND: Exposure to UV radiation is associated with cutaneous malignant melanoma (CMM). In mammalian cells, UV radiation induces DNA damage that can be repaired by the nucleotide excision repair system. We designed this case-control study to determine whether DNA repair capacity (DRC) is associated with the risk of CMM and to identify risk factors that may interact biologically with DRC in the development of melanoma. METHODS: Global DRC was measured in lymphocytes with the host-cell reactivation assay. Data were analyzed by use of multiple regression models. All statistical tests were two-sided. RESULTS: DRC could be determined for 132 case patients with incident melanoma and for 145 age- and sex-matched control subjects. No statistically significant association between melanoma risk and DRC by itself was found (odds ratio [OR] = 1.0; 95% confidence interval [CI] = 0.6 to 1.7, adjusted for age, sex, lymphocyte viability, and sample storage time). DRC, however, strongly influenced CMM risk in individuals with a low tanning ability or dysplastic nevi. Individuals with a low tanning ability and a low DRC had a higher risk for CMM (OR = 8.6; 95% CI = 2.7 to 27.5) than individuals with a higher tanning ability and a high DRC. Likewise, individuals with dysplastic nevi and a low DRC had a higher relative risk (OR = 6.7; 95% CI = 2.4 to 18.6) than those lacking dysplastic nevi and having a high DRC. Subjects with dysplastic nevi and a high DRC had an intermediate risk. A likelihood-ratio test gave statistically significant interactions between DRC and tanning response (P =.001) and between DRC and dysplastic nevus status (P =.04), which were independently associated with CMM risk. CONCLUSIONS: DRC may modify the risk for melanoma in the presence of other strong risk factors, such as a low tanning ability and the presence of dysplastic nevi. The occurrence of melanoma in subjects without these risk factors appears to be independent of DRC.

Adult↗
PubMed1994

Melanoma in situ on facial skin damaged by sunlight.

Solar lentigines ("liver spots") commonly occur on sun-damaged skin in the elderly population. Although they are benign, it is difficult in practice to distinguish solar letigines and junctional nevi from melanoma in situ. We report a patient who developed melanoma on the same site as a previously diagnosed solar lentigo. We also review the histopathological criteria for differentiating these benign lesions from potentially malignant ones.

Aged↗
PubMed1984

Morphologic alterations of epidermal melanocytes and melanosomes in PUVA lentigines: a comparative ultrastructural investigation of lentigines induced by PUVA and sunlight.

Ultrastructural studies were conducted in order to determine morphologic and functional differences in melanocytes and melanosomes in PUVA lentigines and solar lentigines, and light-protected buttock skin. Compared to melanocytes in solar lentigines from 7 subjects and light-protected buttock skin from 5 subjects (none of these subjects had received UV radiation therapy), melanocytes in PUVA lentigines from 6 subjects generally had longer and more numerous dendrites, and showed more active melanogenesis. Basal keratinocytes in PUVA lentigines had a significantly increased frequency of large, single melanosomes, and revealed significantly larger individual melanosomes within compound melanosomes. Other findings in some PUVA lentigines included the close apposition of Langerhans cells to melanocytes, and atypical nuclear, cytoplasmic and melanosomal alterations, including melanosomal pleomorphism and melanin macroglobules. The presence of relatively large and predominantly single melanosomes in basal keratinocytes of PUVA lentigines suggests more active melanogenesis and/or an irreversible somatic alteration. It will be important to determine the clinical course and ultrastructural findings of PUVA lentigines that persist long after PUVA is discontinued.

Adult↗
PubMed1989

Human melanocytic neoplasms and their etiologic relationship with sunlight.

Two hypotheses have been presented. The first states that melanomas commonly evolve from normal melanocytes by a tumor progression pathway from a banal nevus to a nevus with dysplasia, to a micro-invasive, and then to a fully evolved, tumorigenic, primary melanoma which has competence for metastasis. It is important to note that not all melanomas follow this complete pathway. As Foulds noted long ago, tumors may bypass any of the stages of tumor progression. Thus, many melanomas do not, apparently, arise in nevi, and melanomas may evolve "fully formed" as pure tumorigenic nodules. However, from the biological point of view, study of the benign potential precursors (nevi and, especially, dysplastic nevi as well as microinvasive melanomas) may well reveal mechanisms of progression that are applicable to all melanomas, and perhaps to other solid tumors as well. From a clinical viewpoint, follow-up and education of patients at increased risk for melanoma, and early diagnosis of melanomas in their curable, microinvasive stages may result in a reduction of mortality from the disease, even without influencing its overall incidence. The melanomas that occur on plantar and palmar (acral) skin appear to progress through a microinvasive stage similar to that of other cutaneous melanomas. However, the significance of precursor and marker lesions (if any exist) in acral melanoma remains to be elucidated by clinicopathologic and epidemiologic studies. The possibility of etiologic agents other than UV light, such as chemical carcinogens and/or viruses, should be investigated in these cases. The second hypothesis presented here, that UV light is etiologic for the common cutaneous melanoma of white populations, has support from clinical, epidemiologic, and biologic observations. From a biologic viewpoint, ultraviolet light has all of the properties that might enable it to act as a complete carcinogen, and to enhance tumor progression in melanocytic "potential-precursor" lesions. Clinically, it seems appropriate to encourage patients (and members of the general population, as well) to adopt sensible attitudes to sun exposure. By such means, it is possible that some melanomas might be prevented, or that the rate and incidence of progression to more-advanced stages might be inhibited.

Adolescent↗