Evidence map›Paper›PMID 40995689›Full record

ReviewEpigenomics2025

Novel approaches to the use of hypomethylating agents in myeloid malignancies.

Justin Cheng, Casey O'Connell

Abstract readReview
In one paragraph

Review in Epigenomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Justin ChengKeck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0001-7665-3911
Casey O'ConnellJane Anne Nohl Division of Hematology and Center for the Study of Blood Diseases, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-8404-6078

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic dysregulation has been increasingly understood to be a key factor in the development of myeloid malignancies, often acting alongside genetic alterations to disrupt normal hematopoiesis. The inherent reversibility of epigenetic changes has provided an excellent opportunity for therapeutic intervention. Hypomethylating agents (HMA) preferentially alter gene expression in heavily methylated malignant myeloid cells by inhibiting DNA methyltransferases thereby altering gene expression. They have since become foundation therapies in myelodysplastic syndrome (MDS) and in older patients with acute myeloid leukemia (AML). However, complete responses to HMA monotherapy are limited and usually non-durable. In recent years, novel approaches have been sought to overcome resistance and expand the role of epigenetic therapies in MDS and AML as well as in less well-studied myeloid malignancies such as myeloproliferative neoplasms (MPNs) and MDS/MPN overlap syndromes. Combination regimens that synergistically pair HMAs or other epigenetically active therapeutics with agents targeting apoptosis, cellular metabolism, and immune evasion have also shown early promise in improving patient outcomes. Oral formulations of HMAs have made maintenance strategies more convenient and tolerable for patients, with demonstrated benefits in AML and ongoing investigations in MDS and post-transplant settings. This review will explore these novel therapeutic strategies in the treatment of myeloid malignancies.

Indexed as

DNA MethylationEpigenesis, GeneticLeukemia, Myeloid, AcuteMyelodysplastic SyndromesMyeloproliferative DisordersHumansAMLCancer epigeneticsdrug combinationsHMAsMDSmyeloid neoplasms

Identifiers

PMID40995689
PMCPMC12562737

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.