Oncogenic BRAF mutations and p16 expression in melanocytic nevi and melanoma in the Polish population.

Introduction: Twenty-five - fifty percent of skin melanomas arise from nevi. Melanocyte proliferation is activated by , then is arrested, but single nevi transform to melanomas. p16 controls arrest, and p16 loss may promote transformation.

Aim: To analyze , p16 expression and melanocyte proliferation in dermal, compound and dysplastic nevi, cells of primary and metastatic melanoma in the Polish population.

Material And Methods: One hundred and thirty-two nevi (dermal, compound, dysplastic) and 41 melanomas (, primary, metastatic) were studied. BRAF was assessed by cobas 4800 BRAF Mutation Test, High Resolution Melting Assay validated with: pyrosequencing and immunohistochemistry. p16 and Ki67 expression was analyzed by IHC.

Results: Eighty-two percent of nevi and 57% of melanomas display expression. Most dermal and compound nevi had > 50% of p16(+) cells. dysplastic nevi had a low number of p16(+) cells. Nevi without (WT), had 90% of cells p16(+). In 60% of and primary melanomas, there was a low number of cells of p16(+). Fifty percent of WT metastatic melanoma and 33% of showed a high level of p16. The number of Ki67(+) cells in dysplastic nevi was very low. In 25% of melanomas in and 55% of WT, > 10% cells were Ki67(+). All primary melanomas and 66% of WT had > 10% Ki67(+) cells. Twenty percent of and WT metastases had > 10% of Ki67(+), however, 62% of and 32% of WT samples had > 50% of Ki67(+) cells.

Conclusions: and p16 are more frequent in nevi than in melanoma . A significantly higher p16 expression was observed in mutated nevi than in WT, while in melanoma it was just the opposite. The proliferation rate of melanoma cells negatively correlated with p16 expression.