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Inhibition of mutated, activated BRAF in metastatic melanoma.
TLDR
Treatment of metastatic melanoma with PLX4032 in patients with tumors that carry the V600E BRAF mutation resulted in complete or partial tumor regression in the majority of patients.
Improved survival with vemurafenib in melanoma with BRAF V600E mutation.
TLDR
Vemurafenib produced improved rates of overall and progression-free survival in patients with previously untreated melanoma with the BRAF V600E mutation in a phase 3 randomized clinical trial.
Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial
TLDR
Dabrafenib significantly improved progression-free survival compared with dacarbazine, and skin-related toxic effects, fever, fatigue, arthralgia, and headache were uncommon in both groups.
Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET
TLDR
The data show that exosome production, transfer and education of bone marrow cells supports tumor growth and metastasis, has prognostic value and offers promise for new therapeutic directions in the metastatic process.
Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma
TLDR
The structure-guided discovery of PLX4032 (RG7204), a potent inhibitor of oncogenic B-RAF kinase activity, and a remarkably high 81% response rate in metastatic melanoma patients treated at an oral dose of 960 mg twice daily are described, demonstrating that BRAF-mutant melanomas are highly dependent on B- RAF kinases activity.
Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion.
TLDR
It is found that stroma-mediated resistance is common, particularly to targeted agents, and the systematic dissection of interactions between tumours and their micro-environment can uncover important mechanisms underlying drug resistance.
RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)
TLDR
The model that inhibition of ERK signalling by RAF inhibitors is dependent on levels of RAS–GTP too low to support RAF dimerization is supported and a novel mechanism of acquired resistance in patients is identified: expression of splicing isoforms of BRAF(V600E) that dimerize in a RAS-independent manner.
Dabrafenib in patients with Val600Glu or Val600Lys BRAF-mutant melanoma metastatic to the brain (BREAK-MB): a multicentre, open-label, phase 2 trial.
TLDR
Dabrafenib has activity and an acceptable safety profile in patients with Val600Glu BRAF-mutant melanoma and brain metastases irrespective of whether they are untreated or have been previously treated but have progressed.
RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF inhibitors.
BACKGROUND Cutaneous squamous-cell carcinomas and keratoacanthomas are common findings in patients treated with BRAF inhibitors. METHODS We performed a molecular analysis to identify oncogenic
Phase III multicenter randomized trial of the Dartmouth regimen versus dacarbazine in patients with metastatic melanoma.
TLDR
There was no difference in survival time and only a small, statistically nonsignificant increase in tumor response for stage IV melanoma patients treated with the Dartmouth regimen compared with dacarbazine.
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