Evidence map›Paper›PMID 30706327›Full record

ReviewInternational journal of hematology2019

Deregulated Polycomb functions in myeloproliferative neoplasms.

Goro Sashida, Motohiko Oshima, Atsushi Iwama

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. The Disordered Region of ASXL1 Acts as an Auto-Regulator Through Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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 1 country.

Goro SashidaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0003-2318-5987
Motohiko OshimaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Atsushi IwamaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. 03aiwama@ims.u-tokyo.ac.jp.
The University of Tokyo · JPKumamoto University · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology #22118004Ministry of Education, Culture, Sports, Science and Technology #26115002
6 · The paper itself

Abstract

Polycomb proteins function in the maintenance of gene silencing via post-translational modifications of histones and chromatin compaction. Genetic and biochemical studies have revealed that the repressive function of Polycomb repressive complexes (PRCs) in transcription is counteracted by the activating function of Trithorax-group complexes; this balance fine-tunes the expression of genes critical for development and tissue homeostasis. The function of PRCs is frequently dysregulated in various cancer cells due to altered expression or recurrent somatic mutations in PRC genes. The tumor suppressive functions of EZH2-containing PRC2 and a PRC2-related protein ASXL1 have been investigated extensively in the pathogenesis of hematological malignancies, including myeloproliferative neoplasms (MPN). BCOR, a component of non-canonical PRC1, suppresses various hematological malignancies including MPN. In this review, we focus on recent findings on the role of PRCs in the pathogenesis of MPN and the therapeutic impact of targeting the pathological functions of PRCs in MPN.

Indexed as

Bromodomain Containing ProteinsCell Cycle ProteinsCell Transformation, NeoplasticEnhancer of Zeste Homolog 2 ProteinGain of Function MutationGene Expression Regulation, NeoplasticHematopoiesisHistone CodeHistone-Lysine N-MethyltransferaseHumansMolecular Targeted TherapyMyeloid-Lymphoid Leukemia ProteinMyeloproliferative DisordersNeoplasm ProteinsPolycomb-Group ProteinsPolycomb Repressive Complex 2ASXL1 protein, humanBCOR protein, humanBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsEnhancer of Zeste Homolog 2 ProteinEZH1 protein, humanEZH2 protein, humanHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsPolycomb-Group ProteinsPolycomb Repressive Complex 2Proto-Oncogene ProteinsRepressor ProteinsTranscription FactorsASXL1BCORBRD4 inhibitionDNA methylationEZH2

Identifiers

PMID30706327
OpenAlexW2913406522

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.