In melanoma, the adaptative cell response to BRAF inhibitors includes altered patterns of
cytokine production contributing to tumor progression and drug resistance. Among the …

Melanoma harboring BRAF mutations frequently develop resistance to BRAF inhibitors,
limiting the impact of treatment. Here, we establish a mechanism of resistance and …

Melanoma treatment with the BRAF V600E inhibitor vemurafenib provides therapeutic
benefits but the common emergence of drug resistance remains a challenge. We generated …

Abstract The BRAF V600E mutation confers constitutive kinase activity and accounts for>
90% of BRAF mutations in melanoma. This genetic alteration is a current therapeutic target; …

Acquired clinical resistance to vemurafenib, a selective BRAFV600E inhibitor, arises
frequently after short-term chemotherapy. Because inhibitions of targets in the RAF–MEK …

Malignant melanoma is challenging to treat, and metastatic cases need chemotherapy
strategies. Targeted inhibition of commonly mutant BRAF V600E by inhibitors is efficient but …

Purpose To assess pharmacodynamic effects and intrinsic and acquired resistance
mechanisms of the BRAF inhibitor vemurafenib in BRAF V600-mutant melanoma, leading to …

V600E being the most common mutation in BRAF, leads to constitutive activation of the
MAPK signaling pathway. The majority of V600E BRAF positive melanoma patients treated …

Background Development of resistance to inhibitors of BRAF (BRAFi) and MEK (MEKi)
remains a great challenge for targeted therapy in patients with BRAF-mutant melanoma …

Background Malignant melanoma is an aggressive tumor type that often develops drug
resistance to targeted therapeutics. The production of colony stimulating factor 1 (CSF-1) in …