Evidence map›Paper›PMID 22897849›Full record

ArticleCancer cell2012

ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression.

Omar Abdel-Wahab, Mazhar Adli, Lindsay M LaFave, Jie Gao, Todd Hricik, Alan H Shih, Suveg Pandey, Jay P Patel, Young Rock Chung, Richard Koche and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 378 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
378citing papers in PubMed, 2 pooled it
27.9field-weighted citation impact, top 1% 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

378 citing papers in PubMed, 2 syntheses or guidelines pooled it, 588 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. TruncatingbioRxiv : the preprint server for biology · 2026
    Article
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  18. The Role and Impact of Non-driver Gene Mutations in Myelofibrosis.Current hematologic malignancy reports · 2026
    Review
  19. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
  20. Article

318 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

21 authors at 7 institutions in 1 country.

Omar Abdel-WahabHuman Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.
Mazhar Adli
Lindsay M LaFave
Jie Gao
Todd Hricik
Alan H Shih
Suveg Pandey
Jay P Patel
Young Rock Chung
Richard Koche
Fabiana Perna
Xinyang Zhao
Jordan E Taylor
Christopher Y Park
Martin Carroll
Ari Melnick
Stephen D Nimer
Jacob D Jaffe
Iannis Aifantis
Bradley E Bernstein
Ross L Levine
Memorial Sloan Kettering Cancer Center · USBroad Institute · USCornell University · USHoward Hughes Medical Institute · USUniversity of Alabama at Birmingham · USUniversity of Miami · USUniversity of Pennsylvania · US

Funding

The Cell-Of-Origin of Human CancersU54CA143798 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MICHOR, FRANZISKA · 2009 to 2014
$11.2M
Expansion of Cardiac and Hematopoietic Pregenitors by Wnt and NotchU01HL100395 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BERNSTEIN, IRWIN D, MOON, RANDALL TODD · 2009 to 2015
$8.4M
Role of TET2 mutations in malignant transformation and acute myeloid leukemiaR01CA173636 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI AIFANTIS, IANNIS, LEVINE, ROSS L · 2013 to 2022
$6.3M
Regulation of hematopoietic stem cell differentiationR01CA105129 · NCI · UNIVERSITY OF CHICAGO · PI AIFANTIS, IANNIS · 2005 to 2014
$2.8M
Genetic Dissection of Acute Myeloid Leukemia.R01CA169784 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI AIFANTIS, IANNIS, LEVINE, ROSS L · 2014 to 2018
$1.8M
Role of ASXL1 mutations in myeloid malignanciesK08CA160647 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ABDEL-WAHAB, OMAR · 2011 to 2015
$849k
Howard Hughes Medical InstituteNCI NIH HHS 1K08CA160647-01NCI NIH HHS K08 CA160647NCI NIH HHS R01 CA105129NCI NIH HHS R01 CA169784NCI NIH HHS R01 CA173636NCI NIH HHS U54 CA143798NHLBI NIH HHS 5U01HL100395
6 · The paper itself

Abstract

Recurrent somatic ASXL1 mutations occur in patients with myelodysplastic syndrome, myeloproliferative neoplasms, and acute myeloid leukemia, and are associated with adverse outcome. Despite the genetic and clinical data implicating ASXL1 mutations in myeloid malignancies, the mechanisms of transformation by ASXL1 mutations are not understood. Here, we identify that ASXL1 mutations result in loss of polycomb repressive complex 2 (PRC2)-mediated histone H3 lysine 27 (H3K27) tri-methylation. Through integration of microarray data with genome-wide histone modification ChIP-Seq data, we identify targets of ASXL1 repression, including the posterior HOXA cluster that is known to contribute to myeloid transformation. We demonstrate that ASXL1 associates with the PRC2, and that loss of ASXL1 in vivo collaborates with NRASG12D to promote myeloid leukemogenesis.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingHematopoietic SystemHistonesHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMethylationMiceASXL1 protein, humanBAP1 protein, humanDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesHomeodomain ProteinsHoxA proteinPolycomb-Group ProteinsPolycomb Repressive Complex 2ras ProteinsRepressor ProteinsTranscription FactorsTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID22897849
PMCPMC3422511
OpenAlexW1992320498

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.