Evidence map›Paper›PMID 16105753›Full record

ReviewInternational journal of hematology2005

Runx1/AML1 in normal and abnormal hematopoiesis.

Tetsuya Yamagata, Kazuhiro Maki, Kinuko Mitani

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.0field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Prognostic Value of RUNX1 Mutations in AML: A Meta-AnalysisAsian Pacific journal of cancer prevention : APJCP · 2018
    Pooled it
  2. Article
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  6. Review
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  8. GermlineEJHaem · 2023
    Article
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  14. Review
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  17. Osteoclast activators are elevated in intervertebral disks with Modic changes among patients operated for herniated nucleus pulposus.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2016
    Article
  18. Article
  19. Article
  20. Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.International journal of hematology · 2013
    Article
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

3 authors at 2 institutions in 2 countries.

Tetsuya YamagataSection on Immunology and Immunogenetics, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Kazuhiro Maki
Kinuko Mitani
Dokkyo University · JPJoslin Diabetes Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Runx1/AML1 (also known as CBFA2 and PEBP23B) is a Runt family transcription factor critical for normal hematopoiesis. Runx1 forms a heterodimer with CBF3 and binds to the consensus PEBP2 sequence through the Runt domain. Runx1 enhances gene transcription by interacting with transcriptional coactivators such as p300 and CREB-binding protein. However, Runx1 can also suppress gene transcription by interacting with transcriptional corepressors, including mSin3A, TLE (mammalian homolog of Groucho), and histone deacetylases. Runx1 not only is critical for definitive hematopoiesis in the fetus but also is required for normal megakaryocytic maturation and T-lymphocyte and B-lymphocyte development in adult mice. Runx1 has been identified in leukemia-associated chromosomal translocations, including t(8;21) (Runx1-ETO/MTG8), t(16;21) (Runx1-MTG16), t(3;21) (Runx1-Evi1), t(12;21) (TEL-Runx1), and t(X;21) (Runx1-Fog2). The molecular mechanism of leukemogenesis by these fusion proteins is discussed. Various mutant mice expressing these fusion proteins have been created. However, expression of the fusion protein is not sufficient by itself to cause leukemia and likely requires additional events for leukemogenesis. Point mutations in a Runx1 allele cause haploinsufficiency and a biallelic null for Runx1, which are associated with familial platelet disorder with a propensity for acute myeloid leukemia (FPD/AML) and AML-M0, respectively. Thus, the correct protein structure and the precise dosage of Runx1 are essential for the maintenance of normal hematopoiesis.

Indexed as

AnimalsCore Binding Factor Alpha 2 SubunitFetal DevelopmentHematopoiesisHumansLeukemiaMicePoint MutationTranscription, GeneticTranslocation, GeneticCore Binding Factor Alpha 2 SubunitRUNX1 protein, human

Identifiers

PMID16105753
OpenAlexW1989182431

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.