Evidence map›Paper›PMID 30423295›Full record

ArticleCancer cell2018

JARID2 Functions as a Tumor Suppressor in Myeloid Neoplasms by Repressing Self-Renewal in Hematopoietic Progenitor Cells.

Hamza Celik, Won Kyun Koh, Ashley C Kramer, Elizabeth L Ostrander, Cates Mallaney, Daniel A C Fisher, Jingyu Xiang, William C Wilson, Andrew Martens, Alok Kothari and 7 more

Abstract read
In one paragraph

Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
  7. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Evaluation of Acute Myeloid Leukemia Genomes using Genomic Proximity Mapping.medRxiv : the preprint server for health sciences · 2024
    Article
  15. Article
  16. Article
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  18. Review
  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

17 authors at 2 institutions in 1 country.

Hamza CelikDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Won Kyun KohDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Ashley C KramerDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Elizabeth L OstranderDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Cates MallaneyDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Daniel A C FisherDivision of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jingyu XiangDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
William C WilsonDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Andrew MartensDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Alok KothariDepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
Gregory FishbergerDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Eric TycksenGenome Technology Access Center, Department of Genetics, Washington University in St. Louis, St. Louis, MO 63110, USA.
Darja KarpovaDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Eric J DuncavageDepartment of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Youngsook LeeDepartment of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison, WI 53705, USA.
Stephen T OhDivision of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Grant A ChallenDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Developmental, Regenerative and Stem Cell Biology Program, Division of Biology and Biomedical Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: gchallen@dom.wustl.edu.
Washington University in St. Louis · USUniversity of Wisconsin–Madison · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
PRE-AND POSTGRADUATE TRAINING IN MOLECULAR HEMATOLOGYT32HL007088 · NHLBI · WASHINGTON UNIVERSITY · PI Grant Anthony Challen, Stephen Oh · 1985 to 2026
$14.1M
MOLECULAR ONCOLOGY TRAINING GRANTT32CA113275 · NCI · WASHINGTON UNIVERSITY · PI Matthew J Walter · 2006 to 2026
$5.7M
The role of histone demethylase Kdm6b in normal hematopoiesisF31DK111058 · NIDDK · WASHINGTON UNIVERSITY · PI MALLANEY, CATES · 2016 to 2018
$69k
The Contribution of Inflammatory Stress to Clonal HematopoiesisF31DK114951 · NIDDK · WASHINGTON UNIVERSITY · PI OSTRANDER, ELIZABETH LEIGH · 2018 to 2019
$39k
NCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1 TR002345NCI NIH HHS P30 CA091842NCI NIH HHS T32 CA113275NHLBI NIH HHS T32 HL007088NIDDK NIH HHS F31 DK111058NIDDK NIH HHS F31 DK114951
6 · The paper itself

Abstract

How specific genetic lesions contribute to transformation of non-malignant myeloproliferative neoplasms (MPNs) and myelodysplastic syndromes (MDSs) to secondary acute myeloid leukemia (sAML) are poorly understood. JARID2 is lost by chromosomal deletions in a proportion of MPN/MDS cases that progress to sAML. In this study, genetic mouse models and patient-derived xenografts demonstrated that JARID2 acts as a tumor suppressor in chronic myeloid disorders. Genetic deletion of Jarid2 either reduced overall survival of animals with MPNs or drove transformation to sAML, depending on the timing and context of co-operating mutations. Mechanistically, JARID2 recruits PRC2 to epigenetically repress self-renewal pathways in hematopoietic progenitor cells. These studies establish JARID2 as a bona fide hematopoietic tumor suppressor and highlight potential therapeutic targets.

Indexed as

AnimalsCell Line, TumorCell Self RenewalCell Transformation, NeoplasticCRISPR-Cas SystemsFemaleGene DeletionGene Knockdown TechniquesGenes, Tumor SuppressorHumansLeukemia, Myeloid, AcuteMaleMiceMice, Inbred C57BLMice, KnockoutMyelodysplastic SyndromesJARID2 protein, humanJarid2 protein, mouseMYCN protein, mouseN-Myc Proto-Oncogene ProteinPolycomb Repressive Complex 2RUNX1 Translocation Partner 1 ProteinJARID2myelodysplastic syndromesmyeloproliferative neoplasmspolycomb repressive complex 2secondary acute myeloid leukemia

Identifiers

PMID30423295
PMCPMC6237100
OpenAlexW2900824724

What OpenQuestion holds

Textmetadata
LicenceTDM
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.