A 39-year-old white male was treated with vemurafenib, cobimetinib, and atezolizumab for a stage IV (T0, N3, M1) BRAF-V600E mutated malignant melanoma in the context of a clinical trial.
The use of selective BRAF inhibitors (BRAFi) has produced remarkable outcomes for patients with advanced cutaneous melanoma harboring a <i>BRAF<sup>V600E</sup></i> mutation.
Upregulation of MC1R expression was determined in BRAF<sup>V600E</sup> cells (A2058) and BRAF wild-type melanoma cells (MEWO) by quantitative real-time polymerase chain reaction, flow cytometry, and receptor-ligand binding assays.
Our analysis of data has demonstrated that combined BRAF and MEK inhibitor-based treatment is associated with an increased risk of all-grade rash and a decreased risk of all-grade and high-grade HK, SP, alopecia, cSCC, HFS, and PR compared with single BRAF inhibitor alone in melanoma patients.
Novel studies investigating the biologic characteristics of acral MM reported variable results: the overall mutational rates ranged respectively between 8.5% and 23% for KIT, between 3.6% and 33.3% for BRAF and between 3% and 47% for NRAS in ALMs.
BRAF mutation status might contribute an effect on both disease-free and overall survival in stage III cutaneous melanomas treated with intermediate dose interferon-alpha.
There is no standard oncological treatment available for metastatic UM patients, and BRAF/MEK and immune checkpoint inhibitors show disappointing results when compared to cutaneous melanoma (CM).
Cost-effectiveness of dabrafenib and trametinib in combination as adjuvant treatment of BRAFV600E/K mutation-positive melanoma from a US healthcare payer perspective.
We present the case of a 58-year-old man with a completely regressed metastatic melanoma who developed a second melanoma with concomitant involution of papillomatous nevi under BRAF inhibitors treatment.
The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Cutaneous melanoma have been significantly revised over the past few years in response to emerging data on immune checkpoint inhibitor therapies and BRAF-targeted therapy.
Discrete transcriptional states were defined in cell lines and melanoma patient specimens that predicted initial sensitivity to BRAF inhibition and the potential for effective re-challenge following resistance.
Expert opinion: While other BRAF/MEK inhibitor combinations have achieved a median overall survival (OS) of 22 months, patients with advanced BRAF mutation-positive melanoma treated with encorafenib plus binimetinib achieved a median OS of 33.6 months in the phase III COLUMBUS trial.
Here, we show that Bap1 deletion in melanocytes cooperates with the constitutively active, oncogenic form of BRAF (BRAF<sup>V600E</sup> ) and UV to cause melanoma in mice, albeit at very low frequency.
Inhibition of the mitogen-activated protein kinase (MAPK) pathway as well as programmed death 1 receptor (PD-1) blockade was shown to prolong overall survival (OS) in patients with advanced B-Raf proto-oncogene (BRAF)-mutant melanoma.
The oncogenic BRAF inhibitor vemurafenib improves outcomes for patients with advanced BRAF<sup>V600</sup> mutation-positive melanoma compared with cytotoxic chemotherapy.