Histopathologic diagnosis of dysplastic nevi: Concordance among pathologists convened by the world health organization melanoma programme

Clemente, Claudio; Cochran, Alistair J.; Elder, David E.; Levene, Arnold; MacKie, Rona M.; Mihm, Martín C.; Rilke, F; Cascinelli, Natale; Fitzpatrick, Thomas B.; Sober, Arthur J.

doi:10.1016/0046-8177(91)90078-4

Cited by 144 publications

(93 citation statements)

References 14 publications

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“…All nevi met the criteria proposed for atypical melanocytic nevi, 34,35 and comprised 43 junctional and 80 compound melanocytic nevi, graded atypical melanocytic nevi-mild in 31 (25%), atypical melanocytic nevi-moderate in 61 (50%), and atypical melanocytic nevi-severe in 31 (25%), classified according to the criteria shown in Table 5. A topographic gradient was observed from junctional to dermal compartments for all markers in all melanocytic lesions, the values being higher in malignant than in benign lesions.…”

Section: Resultsmentioning

confidence: 99%

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

et al. 2011

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Atypical (dysplastic) melanocytic nevi are clinically heterogeneous malignant melanoma precursors, for which no topographic analysis of cell kinetic, cell cycle regulators and microsatellite profile is available. We selected low-grade atypical melanocytic nevi (92), high-grade atypical melanocytic nevi (41), melanocytic nevi (18 junctional, 25 compound) and malignant melanomas (16 radial growth phase and 27 vertical growth phase). TP53, CDKN2A, CDKN1A, and CDKN1B microsatellite patterns were topographically studied after microdissection; Ki-67, TP53, CDKN2A, CDKN1A, and CDKN1B expressions and DNA fragmentation by in situ end labeling for apoptosis were topographically scored. Results were statistically analyzed. A decreasing junctional-dermal marker expression gradient was observed, directly correlating with atypical melanocytic nevus grading. High-grade atypical melanocytic nevi revealed coexistent TP53-CDKN2A-CDKN1B microsatellite abnormalities, and significantly higher junctional Ki67-TP53 expression (inversely correlated with CDKN1A-CDKN1B expression and in situ end labeling). Malignant melanomas showed coexistent microsatellite abnormalities (CDKN2A-CDKN1B), no topographic gradient, and significantly decreased expression. Melanocytic nevi and low-grade atypical melanocytic nevi revealed sporadic junctional CDKN2A microsatellite abnormalities and no significant topographic kinetic differences. High-grade atypical melanocytic nevi accumulate junctional TP53-CDKN1A-CDKN1B microsatellite abnormalities, being progression TP53-independent and better assessed in the dermis. Melanocytic nevi and low-grade atypical melanocytic nevi show low incidence of microsatellite abnormalities, and kinetic features that make progression unlikely.

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Section: Resultsmentioning

confidence: 99%

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

et al. 2011

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“…Among a panel of international melanoma pathologists, criteria for the diagnosis of dysplastic nevi were agreed upon. The mean concordance overall for a review of 114 mixed (radial growth phase melanoma, dysplastic nevi, banal nevi) specimens was 92% (Clemente et al, 1991). Even among general dermatopathologists, there was high concordance with melanoma specialists in the reading of dysplastic nevi (Weinstock et al, 1997).…”

Section: Number and Type Of Nevimentioning

confidence: 95%

Melanoma etiology: where are we?

Tucker¹,

Goldstein²

2003

Oncogene

241

147

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Melanoma incidence rates are rising rapidly, particularly in older men. Older men are also more likely to have thick melanomas, which confer high mortality and morbidity. The reasons for the rate of increase are not known; increasing sun and UV exposure, however, is the major hypothesized explanation. In the past several years, two major susceptibility genes for melanoma, CDKN2A and CDK4, have been identified, but the two genes together account for a minority of familial melanoma. Other highrisk susceptibility genes are being sought actively. Genetic epidemiologic studies suggest that penetrance of each of the two identified genes is altered by other factors, either genetic or environmental. Epidemiologic studies have also identified other major host factors important in the development of melanoma. In European, North American, and Australian populations, the presence of clinically identified dysplastic nevi confers greatly increased risk of melanoma. A new measure of sun exposure, based on individual residential history, confers substantially increased risk of melanoma. Recent surveys of sun behavior in the US reveal extensive sunburning and use of tanning beds in adolescents and adults. Sun protective behaviors are not as prevalent as in Australia, where population rates of melanoma are stabilizing.

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“…[1][2][3][4][5][6][7] Clinically, they are characterized by four major properties ( Figure 1): Their size tends to be greater than that of common nevi but less than that of melanomas; in the most common definition, dysplastic nevi are 5 mm in diameter or greater. Also by definition, dysplastic nevi contain a junctional component, which clinically is macular or flat, sometimes with a 'pebbly' surface.…”

Section: Dysplastic Nevimentioning

confidence: 99%

“…Histologically, dysplastic nevi are characterized by two major categories of criteria: architectural and cytologic 1,3,[3][4][5][6]33 ( Figures 2 and 3). Architecturally, just as is true by definition clinically, dysplastic nevi are larger than common acquired nevi and the diagnosis should be made cautiously in lesions smaller than about 4 mm in diameter on the slide.…”

Section: Dysplastic Nevimentioning

confidence: 99%

Precursors to melanoma and their mimics: nevi of special sites

2006

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Melanocytic nevi, which are benign tumors of melanocytes, may have occasional cosmetic significance but, for the most part, they are important only in relation to melanoma. Nevi are the most important simulants of melanoma, both clinically and histologically, and can usually be reliably distinguished from melanomas using published criteria. Some lesions are characterized by greater degrees of atypia and may be more difficult to diagnose. Dysplastic nevi are among the most important simulants of melanoma. Nevi may also be important as potential precursors of melanoma; however, most nevi are stable and will not progress to malignancy. Nevi are vastly more common than melanomas and the rate of progression of individual lesions is very low. Therefore, nevi are not as a rule managed by wholesale excision to prevent melanoma. Nevi are also important as risk markers, identifying individuals at greater risk of developing melanoma in the future. Dysplastic nevi and, to a lesser extent, common acquired and congenital nevi are among the most important melanoma risk markers. Nevi of special sites have been identified as nevi that may show atypical features suggestive of a dysplastic nevus or of a melanoma. However, they are not risk markers and they are not malignancies. Nevi of genital skin, acral skin, and flexural skin are among the most important 'nevi of special sites'. It is important, in considering the differential diagnosis of a lesion in a special site, to avoid overcalling such a lesion as a melanoma or a dysplastic nevus because this could lead to excessive treatment. Conversely, it is important to avoid undercalling a lesion that is a dysplastic nevus or a melanoma as a nevus of special sites, because in this circumstance a patient could lose the opportunity either for surveillance to recognize a developing melanoma at an early, curable stage, or for definitive treatment of an established malignancy. In this monograph, dysplastic nevi and nevi of special sites are compared and contrasted in relation to melanoma.

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Histopathologic diagnosis of dysplastic nevi: Concordance among pathologists convened by the world health organization melanoma programme

Cited by 144 publications

References 14 publications

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

Melanoma etiology: where are we?

Precursors to melanoma and their mimics: nevi of special sites

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