keratoacanthoma/fatigue

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Safety of vemurafenib in patients with BRAF V600 mutated metastatic melanoma: the Spanish experience.

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OBJECTIVE Vemurafenib tolerability was assessed in a large, open-label, multicentre study in patients with BRAF V600 mutated advanced melanoma. We investigated safety, tolerability and efficacy of vemurafenib in Spanish patients participating in that study. METHODS Patients with previously treated

A case of vemurafenib-induced keratosis pilaris-like eruption.

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Vemurafenib, a selective BRAF kinase inhibitor, is a new anti-cancer drug recently proven to improve survival in patients with metastatic melanoma harboring the BRAF V600E mutation. BRAF is one of three RAF kinases (ARAF, BRAF, CRAF) involved in the MAP kinase pathway. Mutations in BRAF are reported

Cutaneous squamous cell carcinoma and inflammation of actinic keratoses associated with sorafenib.

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BACKGROUND Sorafenib-induced dermatologic toxicity is common and consists primarily of dry skin, maculopapular rash, hand-foot skin reaction, and alopecia. Cutaneous squamous cell carcinoma (SCC) and inflammation of actinic keratosis (AK) were reported in 2 patients treated with sorafenib (Lacouture

Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib.

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BACKGROUND Approximately 50% of melanomas harbor activating (V600) mutations in the serine-threonine protein kinase B-RAF (BRAF). The oral BRAF inhibitor vemurafenib (PLX4032) frequently produced tumor regressions in patients with BRAF V600-mutant metastatic melanoma in a phase 1 trial and improved

Vemurafenib for the treatment of melanoma.

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BACKGROUND Metastatic melanoma is an aggressive disease resistant to chemotherapy. Recent clinical trials have reported improved survival for two novel agents; ipilimumab, a humanized, IgG1 monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and vemurafenib , a BRAF

The role of BRAF V600 mutation in melanoma.

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BRAF is a serine/threonine protein kinase activating the MAP kinase/ERK-signaling pathway. About 50 % of melanomas harbors activating BRAF mutations (over 90 % V600E). BRAFV600E has been implicated in different mechanisms underlying melanomagenesis, most of which due to the deregulated activation of

Phase II Pilot Study of Vemurafenib in Patients With Metastatic BRAF-Mutated Colorectal Cancer.

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OBJECTIVE BRAF V600E mutation is seen in 5% to 8% of patients with metastatic colorectal cancer (CRC) and is associated with poor prognosis. Vemurafenib, an oral BRAF V600 inhibitor, has pronounced activity in patients with metastatic melanoma, but its activity in patients with BRAF V600E-positive

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