Evidence map›Paper›PMID 29694893›Full record

ArticleCell reports2018

SETDB2 Links E2A-PBX1 to Cell-Cycle Dysregulation in Acute Leukemia through CDKN2C Repression.

Chiou-Hong Lin, Stephen Hon-Kit Wong, Jason H Kurzer, Corina Schneidawind, Michael C Wei, Jesús Duque-Afonso, Johan Jeong, Xuhui Feng, Michael L Cleary

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. Review
  9. Review
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  11. Comprehensive summary: the role of PBX1 in development and cancers.Frontiers in cell and developmental biology · 2024
    Review
  12. Article
  13. Article
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  15. Article
  16. Mediator subunit MED1 is required for E2A-PBX1-mediated oncogenic transcription and leukemic cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Review
  18. Article
  19. Article
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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

9 authors at 4 institutions in 2 countries.

Chiou-Hong LinDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Stephen Hon-Kit WongDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: honkit@stanford.edu.
Jason H KurzerDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Corina SchneidawindDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Hematology and Oncology, University Hospital Tuebingen, Tuebingen, Germany.
Michael C WeiDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jesús Duque-AfonsoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Hematology and Oncology, University Medical Center Freiburg, Freiburg, Germany.
Johan JeongDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Xuhui FengKrannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Michael L ClearyDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: mcleary@stanford.edu.
Stanford University · USIndiana University School of MedicineUniversity Medical Center Freiburg · DEUniversity of Tübingen · DE

Funding

Spectrum Stanford Center for clinical and Translational Research and EducationUL1TR001085 · NCATS · STANFORD UNIVERSITY · PI CULLEN, MARK RICHARD, GREENBERG, HARRY BERNARD · 2013 to 2017
$37.1M
Functional and Translational Epigenomics of Acute Lymphoblastic LeukemiaR01CA214888 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 2018 to 2023
$1.8M
NCATS NIH HHS UL1 TR001085NCI NIH HHS R01 CA214888
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) is associated with significant morbidity and mortality, necessitating further improvements in diagnosis and therapy. Targeted therapies directed against chromatin regulators are emerging as promising approaches in preclinical studies and early clinical trials. Here, we demonstrate an oncogenic role for the protein lysine methyltransferase SETDB2 in leukemia pathogenesis. It is overexpressed in pre-BCR

Indexed as

Cell CycleBasic Helix-Loop-Helix ProteinsCell Line, TumorCyclin-Dependent Kinase Inhibitor p18Histone-Lysine N-MethyltransferaseHumansNeoplastic Stem CellsPre-B-Cell Leukemia Transcription Factor 1Precursor Cell Lymphoblastic Leukemia-LymphomaBasic Helix-Loop-Helix ProteinsCDKN2C protein, humanCyclin-Dependent Kinase Inhibitor p18Histone-Lysine N-MethyltransferasePBX1 protein, humanPre-B-Cell Leukemia Transcription Factor 1SETD2 protein, humanTCF3 protein, humanacute leukemiaCDKN2Ccell-cycle inhibitionE2A-PBX1preB-ALLSETDB2

Identifiers

PMID29694893
PMCPMC5963704
OpenAlexW2802028035

What OpenQuestion 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 OpenQuestion graph.