Evidence map›Paper›PMID 29400094›Full record

ReviewExpert review of hematology2018

GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.

Te Ling, John D Crispino, Maria Zingariello, Fabrizio Martelli, Anna Rita Migliaccio

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. SF3B1 mutant-induced missplicing of MAP3K7 causes anemia in myelodysplastic syndromes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Frontiers in genetics · 2021
    Article
  15. Article
  16. Article
  17. GATA1 gets personal.Haematologica · 2020
    Article
  18. Review
  19. Mutations in the zebrafishBlood advances · 2019
    Article
  20. 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

5 authors at 4 institutions in 2 countries.

Te Linga Division of Hematology/Oncology , Northwestern University , Chicago , IL , USA.
John D Crispinoa Division of Hematology/Oncology , Northwestern University , Chicago , IL , USA.
Maria Zingariellob Department of Medicine , Campus Biomedico , Rome , Italy.
Fabrizio Martellic National Center for Drug Research and Evaluation, Istituto Superiore di Sanità , Roma , Italy.
Anna Rita Migliacciod Department of Biomedical and Neuromotorial Sciences , Alma Mater University , Bologna , Italy.
Northwestern University · USIstituto Superiore di Sanità · ITUniversità Campus Bio-Medico · ITUniversity of Bologna · IT

Funding

Tissue BankP01CA108671 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Ronald Hoffman · 2006 to 2026
$82.0M
GATA1 Mutation in Defective ErythropoiesisR01DK101329 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CRISPINO, JOHN D · 2013 to 2017
$1.7M
NCI NIH HHS P01 CA108671NIDDK NIH HHS R01 DK101329
6 · The paper itself

Abstract

introductionGATA1, the founding member of a family of transcription factors, plays important roles in the development of hematopoietic cells of several lineages. Although loss of GATA1 has been known to impair hematopoiesis in animal models for nearly 25 years, the link between GATA1 defects and human blood diseases has only recently been realized. Areas covered: Here the current understanding of the functions of GATA1 in normal hematopoiesis and how it is altered in disease is reviewed. GATA1 is indispensable mainly for erythroid and megakaryocyte differentiation. In erythroid cells, GATA1 regulates early stages of differentiation, and its deficiency results in apoptosis. In megakaryocytes, GATA1 controls terminal maturation and its deficiency induces proliferation. GATA1 alterations are often found in diseases involving these two lineages, such as congenital erythroid and/or megakaryocyte deficiencies, including Diamond Blackfan Anemia (DBA), and acquired neoplasms, such as acute megakaryocytic leukemia (AMKL) and the myeloproliferative neoplasms (MPNs). Expert commentary: Since the first discovery of GATA1 mutations in AMKL, the number of diseases that are associated with impaired GATA1 function has increased to include DBA and MPNs. With respect to the latter, we are only just now appreciating the link between enhanced JAK/STAT signaling, GATA1 deficiency and disease pathogenesis.

Indexed as

Anemia, Diamond-BlackfanHematologic NeoplasmsLeukemia, Megakaryoblastic, AcutePrimary MyelofibrosisAnimalsCell DifferentiationCell ProliferationErythroid CellsGATA1 Transcription FactorHematopoiesisHumansMegakaryocytesNeoplasm ProteinsSignal TransductionGATA1 protein, humanGATA1 Transcription FactorNeoplasm Proteinscongenital anemiaserythropoiesisGATA1myelofibrosismyeloproliferative disordersribosome deficiencies

Identifiers

PMID29400094
PMCPMC6108178
OpenAlexW2790231673

What OpenQuestion holds

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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.