Evidence map›Paper›PMID 22823977›Full record

ReviewBMC cancer2012

Myeloid malignancies: mutations, models and management.

Anne Murati, Mandy Brecqueville, Raynier Devillier, Marie-Joelle Mozziconacci, Véronique Gelsi-Boyer, Daniel Birnbaum

Open access · goldAbstract readReview
In one paragraph

Review in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. SystemicProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. CHIPing Away at Proteomics to Find Correlations with Myeloid Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  13. Article
  14. Review
  15. Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. CAR T-Cell Therapy in Hematological Malignancies.International journal of molecular sciences · 2021
    Review

10 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

6 authors at 3 institutions in 1 country.

Anne MuratiCentre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR1068 Inserm, Institut Paoli-Calmettes, 27 Bd, Leï Roure, BP 30059, Marseille, 13273, France.
Mandy Brecqueville
Raynier Devillier
Marie-Joelle Mozziconacci
Véronique Gelsi-Boyer
Daniel Birnbaum
Centre de Recherche en Cancérologie de Marseille · FRInserm · FRInstitut Paoli-Calmettes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid malignant diseases comprise chronic (including myelodysplastic syndromes, myeloproliferative neoplasms and chronic myelomonocytic leukemia) and acute (acute myeloid leukemia) stages. They are clonal diseases arising in hematopoietic stem or progenitor cells. Mutations responsible for these diseases occur in several genes whose encoded proteins belong principally to five classes: signaling pathways proteins (e.g. CBL, FLT3, JAK2, RAS), transcription factors (e.g. CEBPA, ETV6, RUNX1), epigenetic regulators (e.g. ASXL1, DNMT3A, EZH2, IDH1, IDH2, SUZ12, TET2, UTX), tumor suppressors (e.g. TP53), and components of the spliceosome (e.g. SF3B1, SRSF2). Large-scale sequencing efforts will soon lead to the establishment of a comprehensive repertoire of these mutations, allowing for a better definition and classification of myeloid malignancies, the identification of new prognostic markers and therapeutic targets, and the development of novel therapies. Given the importance of epigenetic deregulation in myeloid diseases, the use of drugs targeting epigenetic regulators appears as a most promising therapeutic approach.

Indexed as

MutationCell Transformation, NeoplasticHumansLeukemia, MyeloidModels, BiologicalMyelodysplastic SyndromesMyeloproliferative Disorders

Identifiers

PMID22823977
PMCPMC3418560
OpenAlexW2009127763

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.