Evidence map›Paper›PMID 41315211›Full record

ArticleNature communications2025

Chromatin accessibility in stem cells unveils progressive transcriptional alterations in myelodysplastic syndrome.

Motohiko Oshima, Naoya Takayama, Yaeko Nakajima-Takagi, Daisuke Shinoda, Naoki Itokawa, Shuhei Kurosawa, Satoshi Kaito, Takahiro Kamiya, Yuta Yamada, Shohei Andoh and 23 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. 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
–field-weighted citation impact
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.

  1. Review
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

33 authors.

Motohiko Oshima *Division 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.
Naoya Takayama *Department of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0001-6867-1677
Yaeko Nakajima-TakagiDivision 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.
Daisuke ShinodaDivision 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.
Naoki ItokawaDivision 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 http://orcid.org/0000-0002-2091-4948
Shuhei KurosawaDivision 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 http://orcid.org/0000-0001-6426-6770
Satoshi KaitoDivision 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 http://orcid.org/0000-0001-7966-291X
Takahiro KamiyaDivision 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 http://orcid.org/0000-0003-3080-3747
Yuta YamadaDivision 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.
Shohei AndohDivision 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.
Kensuke KayamoriDivision 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 http://orcid.org/0000-0001-6140-3135
Sudip Kumar PaulDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0009-0000-3131-0042
Maria Alejandra KanashiroDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0009-0006-0689-9717
Tomoya MutoDepartment of Hematology, Chiba University Hospital, Chiba, Japan.
Shokichi TsukamotoDepartment of Hematology, Chiba University Hospital, Chiba, Japan.ORCID http://orcid.org/0000-0003-4314-893X
Emiko SakaidaDepartment of Hematology, Chiba University Hospital, Chiba, Japan.ORCID http://orcid.org/0000-0002-7254-1928
Eriko SatoDepartment of Hematology, Juntendo University Nerima Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4159-2834
Nozomi YusaDepartment of Hematology and Oncology, Research Hospital, The Institute of Medical Science, the University of Tokyo, Tokyo, Japan.
Kazuaki YokoyamaDepartment of Hematology and Oncology, Research Hospital, The Institute of Medical Science, the University of Tokyo, Tokyo, Japan.
Yasuhito NannyaDepartment of Hematology and Oncology, Research Hospital, The Institute of Medical Science, the University of Tokyo, Tokyo, Japan.
Seiya ImotoDivision of Health Medical Intelligence, Human Genome Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Bahityar RahmutullaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0002-6980-5515
Kiyoshi YamaguchiDivision of Clinical Genome Research, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2113-4369
Yoichi FurukawaDivision of Clinical Genome Research, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Noriko DokiHematology Division, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8661-3179
Koji EtoDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0002-5863-7122
Kei NishikawaDepartment of Oncology and Hematology, Edogawa Hospital, Tokyo, Japan.
Ye DingDepartment of Oncology and Hematology, Edogawa Hospital, Tokyo, Japan.
Tomohiro MyojoDepartment of Oncology and Hematology, Edogawa Hospital, Tokyo, Japan.
Yuka HaradaDepartment of Clinical Laboratory, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4550-3176
Hironori HaradaLaboratory of Oncology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9401-5470
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. 03aiwama@ims.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0001-9410-8992

Funding

Japan Agency for Medical Research and Development (AMED) 18ck0106401h0001Japan Agency for Medical Research and Development (AMED) 21zf0127003h0001MEXT | Japan Society for the Promotion of Science (JSPS) 19H05653MEXT | Japan Society for the Promotion of Science (JSPS) 19H05746MEXT | Japan Society for the Promotion of Science (JSPS) 21K08366MEXT | Japan Society for the Promotion of Science (JSPS) 24H00066MEXT | Japan Society for the Promotion of Science (JSPS) 24K11554
6 · The paper itself

Abstract

Myelodysplastic syndrome (MDS) originates from hematopoietic stem cell (HSC) clones with acquired gene mutations. However, the molecular characteristics of MDS stem cells remain poorly understood. Here, we show that the chromatin accessibility profiles of MDS stem cells more accurately reflect disease status than those of progenitor cells and reveal the process of stem cell alterations during disease progression. Characterization of differentially accessible regions (DARs) shows that MDS stem cells acquire progenitor-like chromatin accessibility during disease progression, leading to disruption of the normal stem-progenitor hierarchy. Profiling of transcription factor-binding motifs at DARs further uncovers precocious activation of myeloid transcriptional networks in MDS stem cells, with a concurrent loss of HSC-associated regulatory programs. In particular, increased chromatin accessibility at CEBP target sites represents the myeloid reprogramming status of MDS stem cells. Newly developed "progenitor scores" based on chromatin accessibility stratify disease status and correlate well with prognosis. These findings indicate that chromatin landscapes of MDS stem cells define their cell-autonomous behavior and contribute to disease progression.

Indexed as

ChromatinHematopoietic Stem CellsMyelodysplastic SyndromesTranscription, GeneticDisease ProgressionFemaleGene Regulatory NetworksHumansMaleTranscription FactorsChromatinTranscription Factors

Identifiers

PMID41315211
PMCPMC12663188

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Registered trials

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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.