EZH2 in Myeloid Malignancies.
ASXL1
CML
EZH2
MDS
MPN
PRC2
mutations
myeloid malignancies
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
08 07 2020
08 07 2020
Historique:
received:
12
06
2020
revised:
01
07
2020
accepted:
02
07
2020
entrez:
12
7
2020
pubmed:
12
7
2020
medline:
13
4
2021
Statut:
epublish
Résumé
Our understanding of the significance of epigenetic dysregulation in the pathogenesis of myeloid malignancies has greatly advanced in the past decade. Enhancer of Zeste Homolog 2 (EZH2) is the catalytic core component of the Polycomb Repressive Complex 2 (PRC2), which is responsible for gene silencing through trimethylation of H3K27. EZH2 dysregulation is highly tumorigenic and has been observed in various cancers, with EZH2 acting as an oncogene or a tumor-suppressor depending on cellular context. While loss-of-function mutations of EZH2 frequently affect patients with myelodysplastic/myeloproliferative neoplasms, myelodysplastic syndrome and myelofibrosis, cases of chronic myeloid leukemia (CML) seem to be largely characterized by EZH2 overexpression. A variety of other factors frequently aberrant in myeloid leukemia can affect PRC2 function and disease pathogenesis, including Additional Sex Combs Like 1 (
Identifiants
pubmed: 32650416
pii: cells9071639
doi: 10.3390/cells9071639
pmc: PMC7407223
pii:
doi:
Substances chimiques
ASXL1 protein, human
0
Repressor Proteins
0
EZH2 protein, human
EC 2.1.1.43
Enhancer of Zeste Homolog 2 Protein
EC 2.1.1.43
Polycomb Repressive Complex 2
EC 2.1.1.43
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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