Mitogen-activated protein kinase blockade in melanoma: intermittent versus continuous therapy, from preclinical to clinical data.
Animals
Clinical Trials, Phase I as Topic
Clinical Trials, Phase II as Topic
Drug Administration Schedule
Drug Screening Assays, Antitumor
Humans
Melanoma
/ drug therapy
Mitogen-Activated Protein Kinase Kinases
/ antagonists & inhibitors
Mitogen-Activated Protein Kinases
/ antagonists & inhibitors
Protein Kinase Inhibitors
/ administration & dosage
Proto-Oncogene Proteins B-raf
/ antagonists & inhibitors
Randomized Controlled Trials as Topic
Journal
Current opinion in oncology
ISSN: 1531-703X
Titre abrégé: Curr Opin Oncol
Pays: United States
ID NLM: 9007265
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
pubmed:
15
12
2020
medline:
6
8
2021
entrez:
14
12
2020
Statut:
ppublish
Résumé
Although targeted therapy provides a high response rate and rapid disease control in advanced melanoma, most patients experience disease progression due to acquired resistance mechanisms leading to reactivation of mitogen-activated protein kinase pathway. The purpose of this article is to review the recently published data on the impact of an intermittent versus continuous dosing schedule of BRAF and MEK inhibition in advanced melanoma to determine the best approach in clinical practice. Some preclinical studies have highlighted the concept that drug-resistant cells may also display drug dependency, such that intermittent dosing of targeted therapy may prevent the emergence of lethal drug resistance. Moreover, clinical observations have suggested that repeated treatment after a break or an intervening therapy may provide clinical benefit. However, recent preclinical and clinical studies have also failed to demonstrate an advantage of intermittent dosing and showed a similar efficacy of the intermittent versus continuous regimens of BRAF and MEK inhibitors in mice models and phase 2 clinical trial. Owing to these discordant results, continuous dosing of BRAF and MEK inhibitors remains the optimal therapeutic approach until additional clinical data demonstrate the superiority of another combination or dosing regimen.
Identifiants
pubmed: 33315631
pii: 00001622-202103000-00006
doi: 10.1097/CCO.0000000000000706
doi:
Substances chimiques
Protein Kinase Inhibitors
0
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Mitogen-Activated Protein Kinase Kinases
EC 2.7.12.2
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
127-132Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
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