Thin Primary Cutaneous Malignant Melanoma: A Prognostic Tree for 10-Year Metastasis Is More Accurate Than American Joint Committee on Cancer Staging

Gimotty, Phyllis A.; Guerry, DuPont; Ming, Michael E.; Elenitsas, Rosalie; Xu, Xiaowei; Czerniecki, Brian J.; Spitz, Francis R.; Schuchter, Lynn M.; Elder, David E.

doi:10.1200/jco.2004.12.015

Cited by 182 publications

(180 citation statements)

References 32 publications

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“…High-grade atypical melanocytic nevi revealed the features of established neoplasms (advantageous kinetics, expressed telomerase, and accumulated microsatellite abnormalities, Figure 4), 1 but different from both radial-and vertical-growthphase malignant melanoma. 41,42 The microsatellite patterns do not fit a continuous evolution model from high-grade dysplasia to vertical-growth-phase melanoma: The profiles of malignant melanomas in radial and vertical growth phases (phenotype, kinetics, and CCR microsatellite profile) were different, in that radial-growth-phase malignant melanomas showed microsatellite patterns not fitting the transition between high-grade atypical melanocytic nevi and vertical-growth-phase malignant melanomas. This profile unlikely represents a continuous evolution within a common pathway (linear model of progression); this will explain the difficulty in designing common screening or therapeutic targets for these two different malignancies.…”

Section: Discussionmentioning

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: Discussionmentioning

confidence: 99%

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

et al. 2011

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“…62 The Philadelphia group has shown a 10-year metastatic rate in men with vertical growth phase melanoma of 31% when a mitotic rate of greater than 0 was identified, vs a 4% mortality rate when the mitotic rate was 0. 63 Barnhill et al 58 studied the impact of mitotic rate upon survival for 650 consecutive primary cutaneous melanoma patients in a logistic regression model. Using 0 vs 1-6 vs 46 mitoses per square millimeter as their discriminative categories, they found that both moderate (1-6/ mm 2 ) and high (46/mm 2 ) mitotic activity were independent prognostic variables.…”

Section: Mitotic Ratementioning

confidence: 99%

Prognosticators of melanoma, the melanoma report, and the sentinel lymph node

2006

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Since the 1960s, the clinical characteristics of melanoma, its histopathology and its biological basis have been the subject of intense study at pigmented lesion clinics in North America, Europe, and Australia. More recently, the immense database of the Melanoma Committee of the American Joint Committee on Cancer (AJCC) has been exploited through complex mathematical models to measure the impact of various histologic features of primary melanomas and of sentinel lymph node deposits and to correlate these parameters with patient survival. The wealth of modern information available to pathologists and clinicians has become of vital interest to the prognostication of the individual patient with melanoma. The purpose of this review is to bring to the attention of anatomic pathologists the essential characteristics of the pathology report for primary cutaneous melanoma in the modern era.

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“…The protocol was approved by Institutional Review Board at University of Pennsylvania. One hundred and forty patients were selected from a total of 489 patients who had at least 10 years of follow-up and had paraffin blocks available for IHC staining [9]. Subjects were selected using stratified random sampling where strata were defined by the occurrence of a ten-year metastasis and tumor thickness (three groups were defined using AJCC T1-T3 criteria as: < 1mm, 1-2 mm and > 2 mm).…”

Section: Methods Study Patients and Study Designmentioning

confidence: 99%

Lymphatic invasion revealed by multispectral imaging is common in primary melanomas and associates with prognosis

Gimotty

Guerry

et al. 2008

Human Pathology

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Lymphatic invasion by tumor cells has been noted infrequently in primary melanomas. Our primary hypotheses were that using immunohistochemical markers of lymphatic vessels and of tumor cells would improve detection of lymphatic invasion and that lymphatic invasion would correlate with regional nodal metastatic disease. This study included 106 patients who were diagnosed between 1972 and 1991 and who had ≥ 10 years of follow up. We performed dual immunohistochemical stains for podoplanin (for lymphatic vessels) and S-100 (for melanoma cells). Lymphatic invasion was identified by light microscopy and confirmed by multispectral imaging analysis. Lymphatic invasion was detected by morphology alone in 5 cases (4.7%) in contrast to immunohistochemical staining augmented by multispectral imaging analysis where 35 cases (33%) were identified (p <0.0001). Lymphatic invasion was significantly associated with time to regional nodal metastatic disease, as well as first metastasis and melanoma-specific death. "Local metastasis", defined by immunohistochemistry-detected lymphatic invasion, satellites or neural invasion, identified 64% of those who had regional nodal metastatic disease within 5 years of diagnosis. Lymphatic invasion is an under-observed phenomenon in primary melanomas that can be better detected by immunohistochemical staining. The presence of lymphatic invasion may be a clinically useful predictor of regionally metastatic disease.

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Thin Primary Cutaneous Malignant Melanoma: A Prognostic Tree for 10-Year Metastasis Is More Accurate Than American Joint Committee on Cancer Staging

Cited by 182 publications

References 32 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

Prognosticators of melanoma, the melanoma report, and the sentinel lymph node

Lymphatic invasion revealed by multispectral imaging is common in primary melanomas and associates with prognosis

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