BRD4 degradation blocks expression of MYC and multiple forms of stem cell resistance in Ph
Animals
Blast Crisis
/ drug therapy
Cell Cycle Proteins
Cell Line, Tumor
Drug Resistance, Neoplasm
Fusion Proteins, bcr-abl
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ drug therapy
Mice
Nuclear Proteins
/ genetics
Protein Kinase Inhibitors
/ pharmacology
Proto-Oncogene Proteins c-myc
Stem Cells
Transcription Factors
/ genetics
Journal
American journal of hematology
ISSN: 1096-8652
Titre abrégé: Am J Hematol
Pays: United States
ID NLM: 7610369
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
revised:
23
06
2022
received:
08
03
2022
accepted:
02
07
2022
pubmed:
8
7
2022
medline:
17
8
2022
entrez:
7
7
2022
Statut:
ppublish
Résumé
In most patients with chronic myeloid leukemia (CML) clonal cells can be kept under control by BCR::ABL1 tyrosine kinase inhibitors (TKI). However, overt resistance or intolerance against these TKI may occur. We identified the epigenetic reader BRD4 and its downstream-effector MYC as growth regulators and therapeutic targets in CML cells. BRD4 and MYC were found to be expressed in primary CML cells, CD34
Identifiants
pubmed: 35794848
doi: 10.1002/ajh.26650
pmc: PMC9546315
doi:
Substances chimiques
BRD4 protein, human
0
Cell Cycle Proteins
0
MYC protein, human
0
Nuclear Proteins
0
Protein Kinase Inhibitors
0
Proto-Oncogene Proteins c-myc
0
Transcription Factors
0
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1215-1225Informations de copyright
© 2022 The Authors. American Journal of Hematology published by Wiley Periodicals LLC.
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