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ABSTRACT: 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 KrasG12D-induced CMML mouse model
SUBMITTER: Berg JL
PROVIDER: S-EPMC7789782 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature