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Target Oncol ; 11(2): 235-8, 2016 Apr.
Article in English | MEDLINE | ID: mdl-26264150

ABSTRACT

Vemurafenib, a specific inhibitor of mutated BRAF kinase, may activate wild-type BRAF and therefore induce squamous cell skin carcinomas in patients treated for melanoma. All vemurafenib clinical trials excluded patients with multiple primary malignant tumors; therefore, the action of this drug on concurrent BRAF wild-type malignancies remains insufficiently studied. We observed a patient, who was administered vemurafenib for BRAF mutation-containing melanoma, but experienced immediate relapse of previously controlled breast cancer disease. Interestingly, breast cancer lesions underwent regression soon after vemurafenib discontinuation. Therefore, caution must be taken while considering vemurafenib treatment for patients with multiple tumors.


Subject(s)
Antineoplastic Agents/adverse effects , Breast Neoplasms/pathology , Carcinoma, Squamous Cell/chemically induced , Indoles/adverse effects , Neoplasm Recurrence, Local/chemically induced , Sulfonamides/adverse effects , Breast Neoplasms/drug therapy , Disease Progression , Female , Humans , Indoles/therapeutic use , Melanoma/drug therapy , Melanoma/pathology , Middle Aged , Neoplasm Recurrence, Local/pathology , Neoplasm Staging , Protein Kinase Inhibitors/adverse effects , Protein Kinase Inhibitors/therapeutic use , Proto-Oncogene Proteins B-raf/antagonists & inhibitors , Proto-Oncogene Proteins B-raf/metabolism , Sulfonamides/therapeutic use , Vemurafenib
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