Evidence map›Paper›PMID 25693834›Full record

ReviewNature reviews. Cancer2015

DNMT3A in haematological malignancies.

Liubin Yang, Rachel Rau, Margaret A Goodell

Abstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
291citing papers in PubMed, 2 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

291 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Multidomain interaction governs the filamentous assembly of the dominant-negative DNMT3A R882H mutant.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Double jeopardy: howFrontiers in cell and developmental biology · 2026
    Review
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231 more citing papers are in PubMed but not listed here.

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.

Liubin Yang1] Department of Molecular and Human Genetics, Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA. [2].
Rachel Rau1] Department of Pediatrics, Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA. [2].
Margaret A Goodell1] Department of Molecular and Human Genetics, Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA. [2] Department of Pediatrics, Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA.

Funding

Tissue ResourceP50CA126752 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MALCOLM K. BRENNER, HELEN E HESLOP · 2007 to 2026
$51.4M
PEDIATRIC ONCOLOGY CLINICAL RESEARCH TRAINING PROGRAMK12CA090433 · NCI · BAYLOR COLLEGE OF MEDICINE · PI CARL E ALLEN, Donald W. Parsons · 2002 to 2026
$18.5M
REGULATION OF HEMATOPOIETIC PROGENITORS BY DE NOVO DNA METHYLATIONR01DK092883 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2012 to 2024
$7.4M
DNMT3A in Development of Hematologic MalignanciesR01CA183252 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MARGARET A. GOODELL · 2014 to 2026
$7.1M
PROGRAM IN HUMAN MOLECULAR GENETICST32GM008307 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SHAULSKY, GAD · 1990 to 2020
$6.6M
Regulation of Hematopoietic Progenitors by de novo DNA MethylationR56DK092883 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2011 to 2011
$344k
NCI NIH HHS CA183252NCI NIH HHS K12 CA090433NCI NIH HHS P50 CA126752NCI NIH HHS R01 CA183252NIDDK NIH HHS DK092883NIDDK NIH HHS R01 DK092883NIDDK NIH HHS R56 DK092883NIGMS NIH HHS T32 GM008307
6 · The paper itself

Abstract

DNA methylation patterns are disrupted in various malignancies, suggesting a role in the development of cancer, but genetic aberrations directly linking the DNA methylation machinery to malignancies were rarely observed, so this association remained largely correlative. Recently, however, mutations in the gene encoding DNA methyltransferase 3A (DNMT3A) were reported in patients with acute myeloid leukaemia (AML), and subsequently in patients with various other haematological malignancies, pointing to DNMT3A as a critically important new tumour suppressor. Here, we review the clinical findings related to DNMT3A, tie these data to insights from basic science studies conducted over the past 20 years and present a roadmap for future research that should advance the agenda for new therapeutic strategies.

Indexed as

DNA MethylationDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AGene Expression Regulation, NeoplasticHematologic NeoplasmsHumansLeukemia, Myeloid, AcuteMutationPrognosisDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, human

Identifiers

PMID25693834
PMCPMC5814392

What OpenQuestion holds

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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.