Abstract
Vemurafenib is a low molecular weight, orally available, inhibitor of oncogenic V600 BRAF serine–threonine kinase. It is effective in the treatment of v-raf murine sarcoma viral oncogene homolog B1 (BRAF) V600-located melanomas.1 The drug specifically targets tumor cells that harbor activating mutations in BRAF gene, most commonly the substitution of glutamic acid for valine at codon 600 (V600E). Selective BRAF inhibition therapy is associated with malignant and benign growths. Among these are keratoacanthomas, cutaneous squamous cell carcinomas, warty dyskeratomas, verrucous keratoses, acantholytic dyskeratoses, and widespread eruptions. Recent studies showed that squamous cell carcinoma (SCC) and keratoacanthomas developed in 20%–57% of patients who are on vemurafenib therapy.2,3 Cutaneous malignancies occur more frequently than other kinase inhibitor molecules after vemurafenib therapy
Published Version
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