BH3 Mimetics in AML Therapy: Death and Beyond?
BCL2 proteins
acute myeloid leukemia
natural and synthetic BH3 mimetics
targeted combinatorial strategies
Journal
Trends in pharmacological sciences
ISSN: 1873-3735
Titre abrégé: Trends Pharmacol Sci
Pays: England
ID NLM: 7906158
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
09
04
2020
revised:
01
09
2020
accepted:
10
09
2020
pubmed:
10
10
2020
medline:
8
6
2021
entrez:
9
10
2020
Statut:
ppublish
Résumé
B cell lymphoma 2 (BCL2) homology domain 3 (BH3) mimetics are targeted therapeutic agents that allow response prediction and patient stratification. BH3 mimetics are prototypical activators of the mitochondrial death program in cancer. They emerged as important modulators of cellular mechanisms contributing to poor therapeutic responses, including cancer cell stemness, cancer-specific metabolic routes, paracrine signaling to the tumor microenvironment, and immune modulation. We present an overview of the antagonism between BH3 mimetics and antiapoptotic BCL2 proteins. We focus on acute myeloid leukemia (AML), a cancer with reduced therapeutic options that have recently been improved by BH3 mimetics.
Identifiants
pubmed: 33032835
pii: S0165-6147(20)30210-8
doi: 10.1016/j.tips.2020.09.004
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Proto-Oncogene Proteins c-bcl-2
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
793-814Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.