Evidence map›Paper›PMID 26111464›Full record

ReviewSeminars in hematology2015

Epigenetic Therapy in Acute Myeloid Leukemia: Current and Future Directions.

Tae Kon Kim, Steven D Gore, Amer M Zeidan

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Targeting and Monitoring Acute Myeloid Leukaemia with Nucleophosmin-1 (International journal of molecular sciences · 2023
    Review
  11. Article
  12. N6-Adenosine Methylation (mJournal of cardiovascular translational research · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Knockout OfBlood and lymphatic cancer : targets and therapy · 2019
    Article
  19. Article
  20. Pharmacological Inhibition of LSD1 for Cancer Treatment.Molecules (Basel, Switzerland) · 2018
    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

3 authors at 2 institutions in 1 country.

Tae Kon KimSection of Hematology, Department of Internal Medicine, Yale University School of Medicine, and Smilow Cancer Hospital at Yale-New Haven Hospital, New Haven, CT.
Steven D GoreSection of Hematology, Department of Internal Medicine, Yale University School of Medicine, and Smilow Cancer Hospital at Yale-New Haven Hospital, New Haven, CT.
Amer M ZeidanSection of Hematology, Department of Internal Medicine, Yale University School of Medicine, and Smilow Cancer Hospital at Yale-New Haven Hospital, New Haven, CT. Electronic address: amer.zeidan@yale.edu.
Yale New Haven Hospital · USYale University · US

Funding

Targeting Epigenomics in Myeloid NeoplasmsK24CA111717 · NCI · YALE UNIVERSITY · PI GORE, STEVEN D · 2005 to 2015
$1.7M
NCI NIH HHS K24 CA111717
6 · The paper itself

Abstract

Epigenetic modifications affect gene expression without changes in the actual DNA sequence. Two of the most important mechanisms include DNA methylation and histone tail modifications (especially acetylation and methylation). Epigenetic modulation is a part of normal physiologic development; its dysregulation is an important mechanism of pathogenesis of some cancers, including acute myeloid leukemia (AML). Despite significant progress in understanding the pathogenesis of AML, therapeutic options remain quite limited. Technological advances have facilitated understanding of aberrant DNA methylation and histone methylation/acetylation as key elements in the development of AML and uncovered several recurrent mutations in genes important for epigenetic regulation. However, much remains to be learned about how to exploit this knowledge for epigenetic therapeutic targeting. Currently, no epigenetic therapy is approved for the treatment of AML, although two DNA methyltransferase inhibitors (azacitidine and decitabine) are commonly used in clinical practice. Among the other epigenetic modifiers undergoing research in AML, the histone deacetylase inhibitors are the most studied. Other promising drugs, such as inhibitors of histone methylation (eg, EZH2 and DOT1L inhibitors), inhibitors of histone demethylases (eg, LSD1 inhibitors), inhibitors of bromodomain-containing epigenetic "reader" BET proteins, and inhibitors of mutant isocitrate dehydrogenases, are at early stages of clinical evaluation.

Indexed as

Epigenesis, GeneticAnimalsDNA MethylationHistone Deacetylase InhibitorsHumansLeukemia, Myeloid, AcuteMutationHistone Deacetylase Inhibitors

Identifiers

PMID26111464
PMCPMC5785931
OpenAlexW2164892300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.