Evidence map›Paper›PMID 37520699›Full record

ArticleiScience2023

Progressive disruption of hematopoietic architecture from clonal hematopoiesis to MDS.

Michèle C Buck, Lisa Bast, Judith S Hecker, Jennifer Rivière, Maja Rothenberg-Thurley, Luisa Vogel, Dantong Wang, Immanuel Andrä, Fabian J Theis, Florian Bassermann and 4 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.5field-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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. 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

14 authors at 5 institutions in 1 country.

Michèle C BuckTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Lisa BastHelmholtz Zentrum München-German Research Center for Environmental Health, Institute of Computational Biology, Neuherberg, Germany.
Judith S HeckerTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Jennifer RivièreTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Maja Rothenberg-ThurleyUniversity Hospital, Ludwig-Maximilians-University, Department of Medicine III, Laboratory for Leukemia Diagnostics, Munich, Germany.
Luisa VogelTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Dantong WangHelmholtz Zentrum München-German Research Center for Environmental Health, Institute of Computational Biology, Neuherberg, Germany.
Immanuel AndräTechnical University of Munich, Microbiology Institute, Munich, Germany.
Fabian J TheisHelmholtz Zentrum München-German Research Center for Environmental Health, Institute of Computational Biology, Neuherberg, Germany.
Florian BassermannTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Klaus H MetzelerUniversity Hospital, Ludwig-Maximilians-University, Department of Medicine III, Laboratory for Leukemia Diagnostics, Munich, Germany.
Robert A J OostendorpTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Carsten MarrHelmholtz Zentrum München-German Research Center for Environmental Health, Institute of Computational Biology, Neuherberg, Germany.
Katharina S GötzeTechnical University of Munich (TUM), School of Medicine, Department of Medicine III, Munich, Germany.
Technical University of Munich · DEGerman Cancer Research Center · DEHelmholtz Zentrum München · DELudwig-Maximilians-Universität München · DEUniversity Hospital Leipzig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) describes the age-related acquisition of somatic mutations in hematopoietic stem/progenitor cells (HSPC) leading to clonal blood cell expansion. Although CHIP mutations drive myeloid malignancies like myelodysplastic syndromes (MDS) it is unknown if clonal expansion is attributable to changes in cell type kinetics, or involves reorganization of the hematopoietic hierarchy. Using computational modeling we analyzed differentiation and proliferation kinetics of cultured hematopoietic stem cells (HSC) from 8 healthy individuals, 7 CHIP, and 10 MDS patients. While the standard hematopoietic hierarchy explained HSPC kinetics in healthy samples, 57% of CHIP and 70% of MDS samples were best described with alternative hierarchies. Deregulated kinetics were found at various HSPC compartments with high inter-individual heterogeneity in CHIP and MDS, while altered HSC rates were most relevant in MDS. Quantifying kinetic heterogeneity in detail, we show that reorganization of the HSPC compartment is already detectable in the premalignant CHIP state.

Indexed as

Computational molecular modellingDiseaseExperimental systems for structural biology

Identifiers

PMID37520699
PMCPMC10382887
OpenAlexW4383743446

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.