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Signalling and chemosensitivity assays in melanoma: is mutated status a prerequisite for targeted therapy?
Author(s) -
Passeron Thierry,
Lacour JeanPhilippe,
Allegra Maryline,
Ségalen Coralie,
Deville Anne,
Thyss Antoine,
Giacchero Damien,
Ortonne JeanPaul,
Bertolotto Corine,
Ballotti Robert,
Bahadoran Philippe
Publication year - 2011
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2011.01385.x
Subject(s) - neuroblastoma ras viral oncogene homolog , sorafenib , melanoma , mapk/erk pathway , cancer research , dacarbazine , targeted therapy , genotyping , kinome , medicine , mutation , kinase , biology , oncology , gene , cancer , genetics , genotype , kras , hepatocellular carcinoma
Selection for targeted therapies in melanoma is currently based on the search for mutations in selected genes. We aimed at evaluating the interest of signalling and chemosensitivity studies in addition to genotyping for assessing the best suitable treatment in an individual patient. We extracted genomic DNA and melanoma cells from tumor tissue of a skin metastasis of a 17‐year‐old woman with stage IV melanoma progressing despite three successive lines of treatment. Despite the absence of mutation in BRAF, NRAS cKIT, the MAPK pathway was activated and a significant response to sorafenib, a mitogen‐activated protein kinase (MAPK)/RAF inhibitor, was found in signalling and chemosensitivity assays. A treatment combining sorafenib and dacarbazine produced a partial response for 9 months, with marked necrosis in some lesions. Chemosensitivity assays and signalling pathway studies could be of great value in addition to genotyping for assessing the most appropriate treatment in melanoma.