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.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents / adverse effects*
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Breast Neoplasms / drug therapy
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Breast Neoplasms / pathology*
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Carcinoma, Squamous Cell / chemically induced*
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Disease Progression
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Female
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Humans
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Indoles / adverse effects*
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Indoles / therapeutic use
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Melanoma / drug therapy
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Melanoma / pathology
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Middle Aged
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Neoplasm Recurrence, Local / chemically induced*
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Neoplasm Recurrence, Local / pathology
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Neoplasm Staging
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Protein Kinase Inhibitors / adverse effects
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Protein Kinase Inhibitors / therapeutic use
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Proto-Oncogene Proteins B-raf / antagonists & inhibitors
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Proto-Oncogene Proteins B-raf / metabolism
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Sulfonamides / adverse effects*
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Sulfonamides / therapeutic use
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Vemurafenib
Substances
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Antineoplastic Agents
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Indoles
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Protein Kinase Inhibitors
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Sulfonamides
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Vemurafenib
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BRAF protein, human
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Proto-Oncogene Proteins B-raf