Evidence map›Paper›PMID 32381577›Full record

ArticleHaematologica2021

The ASXL1-G643W variant accelerates the development of CEBPA mutant acute myeloid leukemia.

Teresa D'Altri, Anna S Wilhelmson, Mikkel B Schuster, Anne Wenzel, Adrija Kalvisa, Sachin Pundhir, Anne Meldgaard Hansen, Bo T Porse

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022
    Review
  12. Review
  13. Article
  14. Review
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 1 country.

Teresa D'AltriThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Anna S WilhelmsonThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Mikkel B SchusterThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Anne WenzelThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Adrija KalvisaThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Sachin PundhirThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Anne Meldgaard HansenThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Bo T PorseThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.
Rigshospitalet · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ASXL1 is one of the most commonly mutated genes in myeloid malignancies, including Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML). In order to further our understanding of the role of ASXL1 lesions in malignant hematopoiesis, we generated a novel knock-in mouse model carrying the most frequent ASXL1 mutation identified in MDS patients, p.G643WfsX12. Mutant mice did not display any major hematopoietic defects nor developed any apparent hematological disease. In AML patients, ASXL1 mutations co-occur with mutations in CEBPA and we therefore generated compound Cebpa and Asxl1 mutated mice. Using a transplantation model, we found that the mutated Asxl1 allele significantly accelerated disease development in a CEBPA mutant context. Importantly, we demonstrated that, similar to the human setting, Asxl1 mutated mice responded poorly to chemotherapy. This model therefore constitutes an excellent experimental system for further studies into the clinically important question of chemotherapy resistance mediated by mutant ASXL1.

Indexed as

Leukemia, Myeloid, AcuteMyelodysplastic SyndromesMyeloproliferative DisordersAnimalsCCAAT-Enhancer-Binding ProteinsHematopoiesisHumansMiceMutationRepressor ProteinsASXL1 protein, humanAsxl1 protein, mouseCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCEBPA protein, mouseRepressor Proteins

Identifiers

PMID32381577
PMCPMC8017816
OpenAlexW3022914228

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.