BH3 Mimetics in AML Therapy: Death and Beyond?


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
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

793-814

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Claudia Cerella (C)

Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, L-2540 Luxembourg, Luxembourg.

Mario Dicato (M)

Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, L-2540 Luxembourg, Luxembourg.

Marc Diederich (M)

Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul 151-742, South Korea. Electronic address: marcdiederich@snu.ac.kr.

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Classifications MeSH