PP54. INCREASED C-MYC COPY NUMBERS ON THE BACKGROUND OF CDKN2A LOSS IS ASSOCIATED WITH IMPROVED SURVIVAL IN NODULAR MELANOMA
D. KOYNOVA1, E. Jordanova2, N. Kukutsch3, P. van der Velden3, D. Toncheva1 and N. Gruis3 1. Department of Medical Genetics, Medical University, Sofia, Bulgaria; 2. Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands; 3. Department of Dermatology, Leiden University Medical Center, Leiden, the Netherlands e-mail: dragatoncheva@yahoo.com
*Corresponding Author:
page: 72

Abstract

Nodular melanoma is the most aggressive variant of malignant melanoma which represents about 20-30% of all melanoma cases. In order to obtain better insight into the genetic background of this specific type of melanoma, we aimed to analyze the frequency of CDKN2A deletion and C-MYC increased copy number changes. The impact of these aberrations on the metastatic potential and patient's survival was considered. Fluorescent in situ hybridization with C-MYC and CDKN2A specific fluorescent-labelled probes were applied on isolated nuclei from 49 paraffin-embedded primary nodular melanomas. The study showed CDKN2A deletion in 73.47% of the analyzed cases of which 22.45% additionally displayed C-MYC increased copy numbers. CDKN2A deletions were observed in melanomas with Breslow thickness ≤1.0 and ≥1.1 mm whereas C-MYC gain in combination with CDKN2A deletion appeared only in tumors ≥1.1 mm. The combined C-MYC and CDKN2A aberrations were found predominantly in the non-metastasizing group of primary NM. The survival analysis furthermore demonstrated that patients with combined CDKN2A and C-MYC aberrations have a significantly better prognosis than carriers of CDKN2A deletion only (p = 0. 0218). We conclude that C-MYC increased copy number changes on the background of CDKN2A deletions seem to be related to a low metastatic potential and better patients' outcome in primary nodular melanomas.




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