Novel RAF-directed approaches to overcome current clinical limits and block the RAS/RAF node.
RAF
RAS
cancer resistance
inhibitors
novel therapies
paradoxical effect
Journal
Molecular oncology
ISSN: 1878-0261
Titre abrégé: Mol Oncol
Pays: United States
ID NLM: 101308230
Informations de publication
Date de publication:
16 Feb 2024
16 Feb 2024
Historique:
revised:
30
11
2023
received:
24
07
2023
accepted:
30
01
2024
medline:
16
2
2024
pubmed:
16
2
2024
entrez:
16
2
2024
Statut:
aheadofprint
Résumé
Mutations in the RAS-RAF-MEK-ERK pathway are frequent alterations in cancer and RASopathies, and while RAS oncogene activation alone affects 19% of all patients and accounts for approximately 3.4 million new cases every year, less frequent alterations in the cascade's downstream effectors are also involved in cancer etiology. RAS proteins initiate the signaling cascade by promoting the dimerization of RAF kinases, which can act as oncoproteins as well: BRAF
Identifiants
pubmed: 38362705
doi: 10.1002/1878-0261.13605
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Giovanni Armenise-Harvard Foundation
Organisme : European Research Council (ERC)
ID : 101001288
Organisme : Associazione Italiana per la Ricerca sul Cancro
ID : 25737
Informations de copyright
© 2024 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
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