Evidence map›Paper›PMID 37071125›Full record

ArticleThe Journal of experimental medicine2023

Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs.

Takako Yokomizo-Nakano, Ai Hamashima, Sho Kubota, Jie Bai, Supannika Sorin, Yuqi Sun, Kenta Kikuchi, Mihoko Iimori, Mariko Morii, Akinori Kanai and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. 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
2.0field-weighted citation impact, top 12% 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, 7 citations in OpenAlex.

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  9. Stem cell regulation and dynamics in myeloid malignancies.International journal of hematology · 2023
    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

16 authors at 5 institutions in 3 countries.

Takako Yokomizo-NakanoLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0003-3879-7046
Ai HamashimaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-1683-4443
Sho KubotaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0001-6119-1259
Jie BaiLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-7485-4450
Supannika SorinLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-5075-0139
Yuqi SunLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0003-0942-8241
Kenta KikuchiLaboratory of Chromatin Organization in Immune Cell Development, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-6084-7559
Mihoko IimoriLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0001-6777-4770
Mariko MoriiLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-2814-4087
Akinori KanaiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.ORCID 0000-0003-1555-6768
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 , Tokyo, Japan.ORCID 0000-0001-9410-8992
Gang HuangDepartment of Cell Systems & Anatomy, Department of Pathology and Laboratory Medicine, UT Health San Antonio, Joe R. and Teresa Lozano Long School of Medicine, Mays Cancer Center at UT Health San Antonio, San Antonio, TX, USA.ORCID 0000-0002-5457-5358
Daisuke KurotakiLaboratory of Chromatin Organization in Immune Cell Development, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-4728-0113
Hitoshi TakizawaLaboratory of Stem Cell Stress, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0002-5276-5430
Hirotaka MatsuiDepartment of Molecular Laboratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-6266-3227
Goro SashidaLaboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University , Kumamoto, Japan.ORCID 0000-0003-2318-5987
Kumamoto University · JPThe University of Tokyo · JPChiba University · JPKhon Kaen University · THThe University of Texas Health Science Center at San Antonio · US

Funding

The Role of HIF1A-DNMT3A axis in AML1/ETO-Driven Acute MyelogenousLeukemiaR01CA248019 · NCI · UNIVERSITY OF MINNESOTA · PI LIU, SHUJUN · 2021 to 2025
$3.2M
NCI NIH HHS R01 CA248019
6 · The paper itself

Abstract

Aberrant innate immune signaling in myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cells (HSPCs) has been implicated as a driver of the development of MDS. We herein demonstrated that a prior stimulation with bacterial and viral products followed by loss of the Tet2 gene facilitated the development of MDS via up-regulating the target genes of the Elf1 transcription factor and remodeling the epigenome in hematopoietic stem cells (HSCs) in a manner that was dependent on Polo-like kinases (Plk) downstream of Tlr3/4-Trif signaling but did not increase genomic mutations. The pharmacological inhibition of Plk function or the knockdown of Elf1 expression was sufficient to prevent the epigenetic remodeling in HSCs and diminish the enhanced clonogenicity and the impaired erythropoiesis. Moreover, this Elf1-target signature was significantly enriched in MDS HSPCs in humans. Therefore, prior infection stress and the acquisition of a driver mutation remodeled the transcriptional and epigenetic landscapes and cellular functions in HSCs via the Trif-Plk-Elf1 axis, which promoted the development of MDS.

Indexed as

DioxygenasesMyelodysplastic SyndromesAdaptor Proteins, Vesicular TransportDNA-Binding ProteinsGene Expression RegulationHematopoietic Stem CellsHumansTranscription FactorsAdaptor Proteins, Vesicular TransportDioxygenasesDNA-Binding ProteinsTET2 protein, humanTranscription Factors

Identifiers

PMID37071125
PMCPMC10120406
OpenAlexW4366241068

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.