Targeting the multifaceted BRAF in cancer: New directions.
Oncotarget
; 15: 486-492, 2024 Jul 16.
Article
en En
| MEDLINE
| ID: mdl-39018217
ABSTRACT
Activating mutations in the mitogen-activated protein kinase (MAPK) pathway represent driver alterations governing tumorigenesis, metastasis, and therapy resistance. MAPK activation predominantly occurs through genomic alterations in RAS and BRAF. BRAF is an effector kinase that functions downstream of RAS and propagates this oncogenic activity through MEK and ERK. Across cancers, BRAF alterations include gain-of-function mutations, copy-number alterations, and structural rearrangements. In cancer patients, BRAF-targeting precision therapeutics are effective against Class I BRAF alterations (p.V600 hotspot mutations) in tumors such as melanomas, thyroid cancers, and colorectal cancers. However, numerous non-Class I BRAF inhibitors are also in development and have been explored in some cancers. Here we discuss the diverse forms of BRAF alterations found in human cancers and the strategies to inhibit them in patients harboring cancers of distinct origins.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Proteínas Proto-Oncogénicas B-raf
/
Inhibidores de Proteínas Quinasas
/
Terapia Molecular Dirigida
/
Neoplasias
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Oncotarget
Año:
2024
Tipo del documento:
Article
País de afiliación:
Estados Unidos