TY - JOUR
T1 - BRAF gene and melanoma
T2 - Back to the future
AU - SCITO YOUTH
AU - Ottaviano, Margaret
AU - Giunta, Emilio Francesco
AU - Tortora, Marianna
AU - Curvietto, Marcello
AU - Attademo, Laura
AU - Bosso, Davide
AU - Cardalesi, Cinzia
AU - Rosanova, Mario
AU - De Placido, Pietro
AU - Pietroluongo, Erica
AU - Riccio, Vittorio
AU - Mucci, Brigitta
AU - Parola, Sara
AU - Vitale, Maria Grazia
AU - Palmieri, Giovannella
AU - Daniele, Bruno
AU - Simeone, Ester
N1 - Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/4
Y1 - 2021/4
N2 - 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.
AB - 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.
KW - BRAF mutation
KW - Immunotherapy
KW - Melanoma
KW - Targeted therapy
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U2 - 10.3390/ijms22073474
DO - 10.3390/ijms22073474
M3 - Review article
C2 - 33801689
AN - SCOPUS:85103056144
SN - 1661-6596
VL - 22
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 7
M1 - 3474
ER -