Micro-RNA-125a mediates the effects of hypomethylating agents in chronic myelomonocytic leukemia.
Animals
Antimetabolites, Antineoplastic
/ therapeutic use
Azacitidine
/ therapeutic use
DNA Methylation
/ drug effects
Decitabine
/ therapeutic use
Disease Models, Animal
Gene Expression Regulation
/ drug effects
Genome-Wide Association Study
Humans
Leukemia, Myelomonocytic, Chronic
/ drug therapy
Mice
RNA, Messenger
Azacitidine
Chronic myelomonocytic leukemia
Hypomethylating agent
Tumor suppressor
miRNA
Journal
Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977
Informations de publication
Date de publication:
06 01 2021
06 01 2021
Historique:
received:
03
06
2020
accepted:
17
11
2020
entrez:
7
1
2021
pubmed:
8
1
2021
medline:
15
12
2021
Statut:
epublish
Résumé
Chronic myelomonocytic leukemia (CMML) is an aggressive hematopoietic malignancy that arises from hematopoietic stem and progenitor cells (HSPCs). Patients with CMML are frequently treated with epigenetic therapeutic approaches, in particular the hypomethylating agents (HMAs), azacitidine (Aza) and decitabine (Dec). Although HMAs are believed to mediate their efficacy via re-expression of hypermethylated tumor suppressors, knowledge about relevant HMA targets is scarce. As silencing of tumor-suppressive micro-RNAs (miRs) by promoter hypermethylation is a crucial step in malignant transformation, we asked for a role of miRs in HMA efficacy in CMML. Initially, we performed genome-wide miR-expression profiling in a Kras Taken together, we report decreased expression of miR-125a in CMML and delineate its relevance as mediator of HMA efficacy within this neoplasia.
Sections du résumé
BACKGROUND
Chronic myelomonocytic leukemia (CMML) is an aggressive hematopoietic malignancy that arises from hematopoietic stem and progenitor cells (HSPCs). Patients with CMML are frequently treated with epigenetic therapeutic approaches, in particular the hypomethylating agents (HMAs), azacitidine (Aza) and decitabine (Dec). Although HMAs are believed to mediate their efficacy via re-expression of hypermethylated tumor suppressors, knowledge about relevant HMA targets is scarce. As silencing of tumor-suppressive micro-RNAs (miRs) by promoter hypermethylation is a crucial step in malignant transformation, we asked for a role of miRs in HMA efficacy in CMML.
RESULTS
Initially, we performed genome-wide miR-expression profiling in a Kras
CONCLUSIONS
Taken together, we report decreased expression of miR-125a in CMML and delineate its relevance as mediator of HMA efficacy within this neoplasia.
Identifiants
pubmed: 33407852
doi: 10.1186/s13148-020-00979-2
pii: 10.1186/s13148-020-00979-2
pmc: PMC7789782
doi:
Substances chimiques
Antimetabolites, Antineoplastic
0
RNA, Messenger
0
Decitabine
776B62CQ27
Azacitidine
M801H13NRU
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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