Evidence map›Paper›PMID 27694924›Full record

ArticleLeukemia2017

Impact of combinatorial dysfunctions of Tet2 and Ezh2 on the epigenome in the pathogenesis of myelodysplastic syndrome.

N Hasegawa, M Oshima, G Sashida, H Matsui, S Koide, A Saraya, C Wang, T Muto, K Takane, A Kaneda and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Deregulated Polycomb functions in myeloproliferative neoplasms.International journal of hematology · 2019
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Environmental Deflection: The Impact of Toxicant Exposures on the Aging Epigenome.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    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

14 authors at 4 institutions in 2 countries.

N HasegawaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
M OshimaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
G SashidaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
H MatsuiDepartment of Molecular Laboratory Medicine, Kumamoto University, Kumamoto, Japan.
S KoideDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
A SarayaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
C WangDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
T MutoDepartment of Hematology, Chiba University Hospital, Chiba, Japan.
K TakaneDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
A KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K ShimodaDepartment of Gastroenterology and Hematology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
C NakasekoDepartment of Hematology, Chiba University Hospital, Chiba, Japan.
K YokoteDepartment of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
A IwamaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University · JPChiba University Hospital · JPKumamoto University · JPUniversity of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic inactivating mutations in epigenetic regulators are frequently found in combination in myelodysplastic syndrome (MDS). However, the mechanisms by which combinatory mutations in epigenetic regulators promote the development of MDS remain unknown. Here we performed epigenomic profiling of hematopoietic progenitors in MDS mice hypomorphic for Tet2 following the loss of the polycomb-group gene Ezh2 (Tet2

Indexed as

Epigenesis, GeneticGene Expression RegulationAnimalsBase SequenceBinding SitesCpG IslandsDioxygenasesDisease Models, AnimalDNA-Binding ProteinsDNA MethylationEnhancer Elements, GeneticEnhancer of Zeste Homolog 2 ProteinHematopoiesisMiceMice, KnockoutMice, TransgenicDioxygenasesDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinNuclear Receptor Subfamily 4, Group A, Member 2Proto-Oncogene ProteinsRepressor ProteinsTET2 protein, humanTranscription Factors

Identifiers

PMID27694924
OpenAlexW2528548385

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.