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Acquired resistance and clonal evolution in melanoma during BRAF inhibitor therapy.
Exposure to a histone deacetylase inhibitor has detrimental effects on human lymphocyte viability and function.
The oncogenic BRAF kinase inhibitor PLX4032/RG7204 does not affect the viability or function of human lymphocytes across a wide range of concentrations.
Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation.
Melanoma whole-exome sequencing identifies (V600E)B-RAF amplification-mediated acquired B-RAF inhibitor resistance.
BRAF inhibitor vemurafenib improves the antitumor activity of adoptive cell immunotherapy.
Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors.
RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF inhibitors.
Host immunity contributes to the anti-melanoma activity of BRAF inhibitors.
Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032.
Inhibition of colony stimulating factor-1 receptor improves antitumor efficacy of BRAF inhibition.