Evidence map›Paper›PMID 29484447›Full record

ReviewCellular and molecular life sciences : CMLS2018

Enhancer DNA methylation in acute myeloid leukemia and myelodysplastic syndromes.

Leonidas Benetatos, George Vartholomatos

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Double jeopardy: howFrontiers in cell and developmental biology · 2026
    Review
  4. Association of Intergenic and IntragenicInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Epialleles and epiallelic heterogeneity in hematological malignancies.Medical oncology (Northwood, London, England) · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Enhancers and MYC interplay in hematopoiesis.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  20. Review
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 at 1 institution in 1 country.

Leonidas BenetatosBlood Bank, Preveza General Hospital, Preveza, Greece. benetatosleon@yahoo.com.
George VartholomatosMolecular Biology Laboratory, Ioannina University Hospital, Ioannina, Greece.
University Hospital of Ioannina · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation (CpG methylation) exerts an important role in normal differentiation and proliferation of hematopoietic stem cells and their differentiated progeny, while it has also the ability to regulate myeloid versus lymphoid fate. Mutations of the epigenetic machinery are observed in hematological malignancies including acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) resulting in hyper- or hypo-methylation affecting several different pathways. Enhancers are cis-regulatory elements which promote transcription activation and are characterized by histone marks including H3K27ac and H3K4me1/2. These gene subunits are target gene expression 'fine-tuners', are differentially used during the hematopoietic differentiation, and, in contrast to promoters, are not shared by the different hematopoietic cell types. Although the interaction between gene promoters and DNA methylation has extensively been studied, much less is known about the interplay between enhancers and DNA methylation. In hematopoiesis, DNA methylation at enhancers has the potential to discriminate between fetal and adult erythropoiesis, and also is a regulatory mechanism in granulopoiesis through repression of neutrophil-specific enhancers in progenitor cells during maturation. The interplay between DNA methylation at enhancers is disrupted in AML and MDS and mainly hyper-methylation at enhancers raising early during myeloid lineage commitment is acquired during malignant transformation. Interactions between mutated epigenetic drivers and other oncogenic mutations also affect enhancers' activity with final result, myeloid differentiation block. In this review, we have assembled recent data regarding DNA methylation and enhancers' activity in normal and mainly myeloid malignancies.

Indexed as

DNA MethylationEnhancer Elements, GeneticAnimalsEpigenesis, GeneticHumansLeukemia, Myeloid, AcuteMutationMyelodysplastic SyndromesAMLDNA methyltransferasesHematopoietic stem cellsHistone marksMDSTranscription factors

Identifiers

PMID29484447
PMCPMC11105366
OpenAlexW2791754076

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.