Evidence map›Paper›PMID 23538751›Full record

ArticleLeukemia2013

Global H3K4me3 genome mapping reveals alterations of innate immunity signaling and overexpression of JMJD3 in human myelodysplastic syndrome CD34+ cells.

Y Wei, R Chen, S Dimicoli, C Bueso-Ramos, D Neuberg, S Pierce, H Wang, H Yang, Y Jia, H Zheng and 7 more

Abstract read
In one paragraph

Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 87 citations in OpenAlex.

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  20. Histone H3K27me3 demethylases regulate human Th17 cell development and effector functions by impacting on metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

17 authors at 5 institutions in 2 countries.

Y WeiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
R Chen
S Dimicoli
C Bueso-Ramos
D Neuberg
S Pierce
H Wang
H Yang
Y Jia
H Zheng
Z Fang
M Nguyen
I Ganan-Gomez
B Ebert
R Levine
H Kantarjian
G Garcia-Manero
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · USMemorial Sloan Kettering Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA100632
6 · The paper itself

Abstract

The molecular bases of myelodysplastic syndromes (MDS) are not fully understood. Trimethylated histone 3 lysine 4 (H3K4me3) is present in promoters of actively transcribed genes and has been shown to be involved in hematopoietic differentiation. We performed a genome-wide H3K4me3 CHIP-Seq (chromatin immunoprecipitation coupled with whole genome sequencing) analysis of primary MDS bone marrow (BM) CD34+ cells. This resulted in the identification of 36 genes marked by distinct higher levels of promoter H3K4me3 in MDS. A majority of these genes are involved in nuclear factor (NF)-κB activation and innate immunity signaling. We then analyzed expression of histone demethylases and observed significant overexpression of the JmjC-domain histone demethylase JMJD3 (KDM6b) in MDS CD34+ cells. Furthermore, we demonstrate that JMJD3 has a positive effect on transcription of multiple CHIP-Seq identified genes involved in NF-κB activation. Inhibition of JMJD3 using shRNA in primary BM MDS CD34+ cells resulted in an increased number of erythroid colonies in samples isolated from patients with lower-risk MDS. Taken together, these data indicate the deregulation of H3K4me3 and associated abnormal activation of innate immunity signals have a role in the pathogenesis of MDS and that targeting these signals may have potential therapeutic value in MDS.

Indexed as

Chromosome MappingAntigens, CD34Blotting, WesternBone MarrowChromatin ImmunoprecipitationHistonesHumansImmunity, InnateImmunoenzyme TechniquesJumonji Domain-Containing Histone DemethylasesLysineMyelodysplastic SyndromesNF-kappa BPromoter Regions, GeneticReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionAntigens, CD34HistonesJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanLysineNF-kappa BRNA, Messenger

Identifiers

PMID23538751
PMCPMC4476310
OpenAlexW2091193918

What OpenQuestion holds

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LicenceTDM
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.