BRAF Gene and Melanoma: Back to the Future.
Margaret OttavianoEmilio Francesco GiuntaMarianna TortoraMarcello CurviettoLaura AttademoDavide BossoCinzia CardalesiMario RosanovaPietro De PlacidoErica PietroluongoVittorio RiccioBrigitta MucciSara ParolaMaria Grazia VitaleGiovannella PalmieriBruno DanieleEster Simeonenull On Behalf Of Scito YouthPublished in: International journal of molecular sciences (2021)
As widely acknowledged, 40-50% of all melanoma patients harbour an activating BRAF mutation (mostly BRAF V600E). The identification of the RAS-RAF-MEK-ERK (MAP kinase) signalling pathway and its targeting has represented a valuable milestone for the advanced and, more recently, for the completely resected stage III and IV melanoma therapy management. However, despite progress in BRAF-mutant melanoma treatment, the two different approaches approved so far for metastatic disease, immunotherapy and BRAF+MEK inhibitors, allow a 5-year survival of no more than 60%, and most patients relapse during treatment due to acquired mechanisms of resistance. Deep insight into BRAF gene biology is fundamental to describe the acquired resistance mechanisms (primary and secondary) and to understand the molecular pathways that are now being investigated in preclinical and clinical studies with the aim of improving outcomes in BRAF-mutant patients.
Keyphrases
- end stage renal disease
- wild type
- ejection fraction
- chronic kidney disease
- newly diagnosed
- prognostic factors
- metastatic colorectal cancer
- peritoneal dialysis
- squamous cell carcinoma
- signaling pathway
- type diabetes
- small cell lung cancer
- lymph node
- tyrosine kinase
- copy number
- free survival
- smoking cessation
- single molecule
- insulin resistance
- cell therapy
- combination therapy
- basal cell carcinoma
- glycemic control