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Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
It is shown that melanomas escape B-RAF(V600E) targeting not through secondary B-RF(V 600E) mutations but via receptor tyrosine kinase (RTK)-mediated activation of alternative survival pathway(s) or activated RAS-mediated reactivation of the MAPK pathway, suggesting additional therapeutic strategies. Expand
PD-1 blockade induces responses by inhibiting adaptive immune resistance
It is shown that pre-existing CD8+ T cells distinctly located at the invasive tumour margin are associated with expression of the PD-1/PD-L1 immune inhibitory axis and may predict response to therapy. Expand
Inhibition of mutated, activated BRAF in metastatic melanoma.
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. Expand
Improved survival with vemurafenib in melanoma with BRAF V600E mutation.
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. Expand
Pembrolizumab versus Ipilimumab in Advanced Melanoma.
The anti-PD-1 antibody pembrolizumab prolonged progression-free survival and overall survival and had less high-grade toxicity than did ipilimumab in patients with advanced melanoma. Expand
Safety and tumor responses with lambrolizumab (anti-PD-1) in melanoma.
In patients with advanced melanoma, including those who had had disease progression while they had been receiving ipilimumab, treatment with lambrolizumab resulted in a high rate of sustained tumor regression, with mainly grade 1 or 2 toxic effects. Expand
Genomic and Transcriptomic Features of Response to Anti-PD-1 Therapy in Metastatic Melanoma
It is found that overall high mutational loads associate with improved survival, and tumors from responding patients are enriched for mutations in the DNA repair gene BRCA2, suggesting that attenuating the biological processes that underlie IPRES may improve anti-PD-1 response in melanoma and other cancer types. Expand
Genetic basis for clinical response to CTLA-4 blockade in melanoma.
These findings define a genetic basis for benefit from CTLA-4 blockade in melanoma and provide a rationale for examining exomes of patients for whom anti-CTLA- 4 agents are being considered. Expand
Improved overall survival in melanoma with combined dabrafenib and trametinib.
Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall survival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations, without increased overall toxicity. Expand
Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib.
  • J. Sosman, Kevin B Kim, +22 authors A. Ribas
  • Medicine
  • The New England journal of medicine
  • 23 February 2012
Vemurafenib induces clinical responses in more than half of patients with previously treated BRAF V600-mutant metastatic melanoma, and the median overall survival in this study with a long follow-up was approximately 16 months. Expand