Evidence map›Paper›PMID 32009100›Full record

ArticleInternal medicine (Tokyo, Japan)2021

Molecular Pathogenesis and Treatment of Myelodysplastic Syndromes.

Hideaki Nakajima

Open access · diamondAbstract read
In one paragraph

Article in Internal medicine (Tokyo, Japan), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

1 author at 1 institution in 1 country.

Hideaki NakajimaDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Japan.
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) are clonal hematological disorders arising from hematopoietic stem cells that have accumulated various genetic abnormalities. MDS are heterogeneous in nature but uniformly characterized by chronic and progressive cytopenia from ineffective hematopoiesis, dysplasia in single or multiple lineages, and transformation to acute leukemia in a subset of patients. The genomic landscape revealed by next-generation sequencing has provided a comprehensive picture of the molecular pathways involved in MDS pathogenesis. Recurrent mutational targets in MDS are the genes involved in RNA splicing, DNA methylation, histone modification, transcription, signal transduction, cohesin complex and DNA repair. Sequential acquisition of mutations in these sets of genes serves as a driver for the initiation, clonal evolution and progression of MDS. Based on these findings, novel agents targeting driver mutations of MDS are currently under development and expected to improve the clinical outcome of MDS in the coming decades.

Indexed as

Leukemia, Myeloid, AcuteMyelodysplastic SyndromesDNA MethylationHumansMutationRNA SplicingepigenomegenomeMDSmolecular pathogenesismyelodysplastic syndromestreatment

Identifiers

PMID32009100
PMCPMC7835461
OpenAlexW3004220419

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.