Evidence map›Paper›PMID 22937757›Full record

ReviewCancer science2012

Contribution of GATA1 dysfunction to multi-step leukemogenesis.

Ritsuko Shimizu, Masayuki Yamamoto

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Exploring the Leukemogenic Potential of GATA-1Antioxidants (Basel, Switzerland) · 2021
    Article
  4. Article
  5. Article
  6. Derepression of the DNA Methylation Machinery of theMolecular and cellular biology · 2017
    Article
  7. Article
  8. SCL/TAL1-mediated transcriptional network enhances megakaryocytic specification of human embryonic stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    Article
  9. Article
  10. Article
  11. Article
  12. 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

2 authors at 1 institution in 1 country.

Ritsuko ShimizuDepartment of Molecular Hematology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Masayuki Yamamoto
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammals, hematopoietic homeostasis is maintained by a fine-tuned balance among the self-renewal, proliferation, differentiation and survival of hematopoietic stem cells and their progenies. Each process is also supported by the delicate balance of the expression of multiple genes specific to each process. GATA1 is a transcription factor that comprehensively regulates the genes that are important for the development of erythroid and megakaryocytic cells. Accumulating evidence supports the notion that defects in GATA1 function are intimately linked to hematopoietic disorders. In particular, the somatic mutation of the GATA1 gene, which leads to the production of N-terminally truncated GATA1, contributes to the genesis of transient myeloproliferative disorder and acute megakaryoblastic leukemia in infants with Down syndrome. Similarly, a mutation in the GATA1 regulatory region that reduces GATA1 expression is involved in the onset of erythroid leukemia in mice. In both cases, the accumulation of immature progenitor cells caused by GATA1 dysregulation underlies the pathogenesis of the leukemia. This review provides a summary of multi-step leukemogenesis with a focus on GATA1 dysfunction.

Indexed as

AnimalsCell LineageDown SyndromeErythropoiesisGATA1 Transcription FactorGene ExpressionHumansLeukemia, Erythroblastic, AcuteLeukemia, Megakaryoblastic, AcuteGATA1 Transcription Factor

Identifiers

PMID22937757
PMCPMC7659349
OpenAlexW2050985416

What OpenQuestion holds

Textmetadata
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.