Evidence map›Paper›PMID 26609488›Full record

ArticleAmerican journal of cancer research2015

The histone methyltransferase DOT1L: regulatory functions and a cancer therapy target.

Matthew Wong, Patsie Polly, Tao Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  6. Epigenetic Targeting in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Role of Histone Modifications in Kidney Fibrosis.Medicina (Kaunas, Lithuania) · 2024
    Review
  13. Review
  14. Article
  15. Resistance Mechanisms in Pediatric B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Matthew WongChildren's Cancer Institute Australia for Medical Research Randwick NSW 2031, Australia.
Patsie PollyDepartment of Pathology and Inflammation and Infection Research Centre, School of Medical Sciences, UNSW Australia Kensington NSW 2052, Australia.
Tao LiuChildren's Cancer Institute Australia for Medical Research Randwick NSW 2031, Australia ; School of Women's & Children's Health, University of New South Wales Randwick NSW 2031, Australia.
Children's Cancer Institute Australia · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DOT1L is a unique histone methyltransferase that targets the histone H3 lysine 79 (H3K79) residue for mono-, di- and tri- methylation. Histone H3K79 mono- and di-methylation results in active gene transcription, while H3K79 tri-methylation is associated with gene repression. DOT1L has a critical role in regulating gene transcription, development, cell cycle progression, somatic reprogramming and DNA damage repair. DOT1L interacts with Mixed Lineage Leukemia (MLL) fusion proteins, leading to enhanced H3K79 methylation, maintenance of open chromatin, overexpression of downstream oncogenes and leukemogenesis. Importantly, small molecule DOT1L inhibitors have been recently developed, and one of the DOT1L inhibitors is already under investigation in a Phase I clinical trial in patients with MLL fusion gene-driven leukemia.

Indexed as

DOT1LDOT1L inhibitorsgene transcriptionhistone methylationmixed lineage leukemia

Identifiers

PMID26609488
PMCPMC4633909
OpenAlexW2173162468

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.