Evidence map›Paper›PMID 27627705›Full record

ArticleCancer science2016

EWSR1/ELF5 induces acute myeloid leukemia by inhibiting p53/p21 pathway.

Akifumi Endo, Daisuke Tomizawa, Yuki Aoki, Tomohiro Morio, Shuki Mizutani, Masatoshi Takagi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. A positive feedback circuit between RN7SK snRNA and mMolecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. [Advances in the mouse models of myeloid leukemia].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2019
    Review
  11. Article
  12. [Screening and verification of key genes in T-cell acute lymphoblastic leukemia].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  13. 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

6 authors at 2 institutions in 1 country.

Akifumi EndoDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Daisuke TomizawaDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Yuki AokiDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Tomohiro MorioDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Shuki MizutaniDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Masatoshi TakagiDepartment of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Tokyo Medical and Dental University · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ewing sarcoma breakpoint region 1 (EWSR1) gene is known to fuse with various partner genes to promote the development of the Ewing sarcoma family of tumors and other sarcomas. In contrast, the association of EWSR1 chimeric fusion genes with leukemia has rarely been reported. We identified a novel EWSR1-associated chimeric fusion gene in a patient with acute myeloid leukemia harboring 46, XY, t (11; 22) (p13; q12) karyotype abnormality. The patient was refractory to intensified chemotherapy including hematopoietic stem cell transplantation. Total RNA paired-end sequencing identified a novel chimeric fusion gene as EWSR1/ELF5, a member of the E26 transformation-specific transcription factor family. Transduction of EWSR1/ELF5 to NIH3T3 cells induced transformation by attenuating with the p53/p21-dependent pathway. The injection of EWSR1/ELF5-transduced NIH3T3 cells into NSG-SCID mice systematically induced the development of tumors in vivo. These results revealed the oncogenic potency of EWSR1/ELF5.

Indexed as

Signal TransductionAnimalsCalmodulin-Binding ProteinsCell Line, TransformedCell Line, TumorCell Transformation, NeoplasticChild, PreschoolChromosome BandingDisease Models, AnimalDNA-Binding ProteinsFemaleGene ExpressionGene Expression ProfilingHumansIn Situ Hybridization, FluorescenceLeukemia, Myeloid, AcuteCalmodulin-Binding ProteinsDNA-Binding ProteinsELF5 protein, humanEWSR1 protein, humanOncogene Proteins, FusionProto-Oncogene Proteins c-etsProto-Oncogene Proteins p21(ras)RNA-Binding Protein EWSRNA-Binding ProteinsTranscription FactorsTumor Suppressor Protein p53Acute myelogenous leukemiaELF5EWSR1senescenceTP53

Identifiers

PMID27627705
PMCPMC5198945
OpenAlexW2520500565

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.