Epigenetic mechanisms underlying the therapeutic effects of HDAC inhibitors in chronic myeloid leukemia.
Antineoplastic Combined Chemotherapy Protocols
/ therapeutic use
Drug Resistance, Neoplasm
/ drug effects
Epigenesis, Genetic
Fusion Proteins, bcr-abl
/ genetics
Gene Expression Profiling
Gene Expression Regulation, Leukemic
/ drug effects
Histone Deacetylase Inhibitors
/ administration & dosage
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ genetics
Protein Kinase Inhibitors
/ administration & dosage
Cancer
Histone acetylation
Personalized medicine
Targeted treatment
Journal
Biochemical pharmacology
ISSN: 1873-2968
Titre abrégé: Biochem Pharmacol
Pays: England
ID NLM: 0101032
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
01
10
2019
accepted:
05
11
2019
pubmed:
11
11
2019
medline:
18
8
2020
entrez:
11
11
2019
Statut:
ppublish
Résumé
Chronic myeloid leukemia (CML) is a hematological disorder caused by the oncogenic BCR-ABL fusion protein in more than 90% of patients. Despite the striking improvements in the management of CML patients since the introduction of tyrosine kinase inhibitors (TKis), the appearance of TKi resistance and side effects lead to treatment failure, justifying the need of novel therapeutic approaches. Histone deacetylase inhibitors (HDACis), able to modulate gene expression patterns and important cellular signaling pathways through the regulation of the acetylation status of both histone and non-histone protein targets, have been reported to display promising anti-leukemic properties alone or in combination with TKis. This review summarizes pre-clinical and clinical studies that investigated the mechanisms underlying the anticancer potential of HDACis and discusses the rationale for a combination of HDACis with TKis as a therapeutic option in CML.
Identifiants
pubmed: 31706847
pii: S0006-2952(19)30397-1
doi: 10.1016/j.bcp.2019.113698
pii:
doi:
Substances chimiques
Histone Deacetylase Inhibitors
0
Protein Kinase Inhibitors
0
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
113698Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.