Evidence map›Paper›PMID 22469984›Full record

ArticleOncogene2013

The Polycomb complex PRC2 supports aberrant self-renewal in a mouse model of MLL-AF9;Nras(G12D) acute myeloid leukemia.

J Shi, E Wang, J Zuber, A Rappaport, M Taylor, C Johns, S W Lowe, C R Vakoc

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Polycomb Repressive Complex 2 in Oncology.Cancer treatment and research · 2023
    Article
  9. Article
  10. Article
  11. A PRC2-Kdm5b axis sustains tumorigenicity of acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. HCK maintains the self-renewal of leukaemia stem cells via CDK6 in AML.Journal of experimental & clinical cancer research : CR · 2021
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

19 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

8 authors at 2 institutions in 2 countries.

J ShiCold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
E Wang
J Zuber
A Rappaport
M Taylor
C Johns
S W Lowe
C R Vakoc
Cold Spring Harbor Laboratory · USResearch Institute of Molecular Pathology · AT

Funding

CSHL Watson School of Biological SciencesT32GM065094 · NIGMS · COLD SPRING HARBOR LABORATORY · PI GANN, ALEXANDER · 2002 to 2021
$4.8M
Howard Hughes Medical InstituteIntramural NIH HHSNIGMS NIH HHS T32 GM065094
6 · The paper itself

Abstract

The Trithorax and Polycomb groups of chromatin regulators are critical for cell-lineage specification during normal development; functions that often become deregulated during tumorigenesis. As an example, oncogenic fusions of the Trithorax-related protein mixed lineage leukemia (MLL) can initiate aggressive leukemias by altering the transcriptional circuitry governing hematopoietic cell differentiation, a process that requires multiple epigenetic pathways to implement. Here we used shRNA screening to identify chromatin regulators uniquely required in a mouse model of MLL-fusion acute myeloid leukemia, which revealed a role for the Polycomb repressive complex 2 (PRC2) in maintenance of this disease. shRNA-mediated suppression of PRC2 subunits Eed, Suz12 or Ezh1/Ezh2 led to proliferation arrest and differentiation of leukemia cells, with a minimal impact on growth of several non-transformed hematopoietic cell lines. The requirement for PRC2 in leukemia is partly because of its role in direct transcriptional repression of genes that limit the self-renewal potential of hematopoietic cells, including Cdkn2a. In addition to implicating a role for PRC2 in the pathogenesis of MLL-fusion leukemia, our results suggest, more generally, that Trithorax and Polycomb group proteins can cooperate with one another to maintain aberrant lineage programs in cancer.

Indexed as

Cell ProliferationAmino Acid SubstitutionAnimalsAspartic AcidDisease Models, AnimalGenes, rasGlycineHumansLeukemia, Myeloid, AcuteMiceMice, TransgenicModels, BiologicalMutation, MissenseOncogene Proteins, FusionPolycomb-Group ProteinsPolycomb Repressive Complex 2Aspartic AcidGlycineMLL-AF9 fusion protein, mouseOncogene Proteins, FusionPolycomb-Group ProteinsPolycomb Repressive Complex 2Suz12 protein, mouse

Identifiers

PMID22469984
PMCPMC4102143
OpenAlexW2118325816

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.