Evidence map›Paper›PMID 33770496›Full record

ArticleStem cell reports2021

Reconciling Flux Experiments for Quantitative Modeling of Normal and Malignant Hematopoietic Stem/Progenitor Dynamics.

Munetomo Takahashi, Melania Barile, Richard H Chapple, Yu-Jung Tseng, Daisuke Nakada, Katrin Busch, Ann-Kathrin Fanti, Petter Säwén, David Bryder, Thomas Höfer and 1 more

Abstract read
In one paragraph

Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

11 authors.

Munetomo TakahashiWellcome and MRC Cambridge Stem Cell Institute, University of Cambridge, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge CB2 0AW, UK; Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Melania BarileWellcome and MRC Cambridge Stem Cell Institute, University of Cambridge, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge CB2 0AW, UK. Electronic address: mb2338@cam.ac.uk.
Richard H ChappleDepartment of Molecular & Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Yu-Jung TsengDepartment of Molecular & Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Daisuke NakadaDepartment of Molecular & Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Katrin BuschDivision of Cellular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Ann-Kathrin FantiDivision of Cellular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Petter SäwénDivision for Molecular Hematology at Institute for Experimental Medical Sciences, Lund University, Lund, Sweden.
David BryderDepartment of Microbiology and Immunology at the Institute of Biomedicine, Göteborg, Sweden.
Thomas HöferDivision of Theoretical Systems Biology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. Electronic address: t.hoefer@dkfz.de.
Berthold GöttgensWellcome and MRC Cambridge Stem Cell Institute, University of Cambridge, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, Cambridge CB2 0AW, UK. Electronic address: bg200@cam.ac.uk.

Funding

Cancer Research UK 21762Cancer Research UK C1163/A21762Medical Research Council MR/S036113/1Wellcome Trust 206328/Z/17/Z
6 · The paper itself

Abstract

Hematopoiesis serves as a paradigm for how homeostasis is maintained within hierarchically organized cell populations. However, important questions remain as to the contribution of hematopoietic stem cells (HSCs) toward maintaining steady state hematopoiesis. A number of in vivo lineage labeling and propagation studies have given rise to contradictory interpretations, leaving key properties of stem cell function unresolved. Using processed flow cytometry data coupled with a biology-driven modeling approach, we show that in vivo flux experiments that come from different laboratories can all be reconciled into a single unifying model, even though they had previously been interpreted as being contradictory. We infer from comparative analysis that different transgenic models display distinct labeling efficiencies across a heterogeneous HSC pool, which we validate by marker gene expression associated with HSC function. Finally, we show how the unified model of HSC differentiation can be used to simulate clonal expansion in the early stages of leukemogenesis.

Indexed as

Models, BiologicalAnimalsBiomarkersCarcinogenesisCell Self RenewalGuanine Nucleotide Exchange FactorsHematopoietic Stem CellsIntegrasesKineticsLeukemiaMice, TransgenicReceptor, TIE-2Staining and LabelingBiomarkersCre recombinaseFGD5 protein, mouseGuanine Nucleotide Exchange FactorsIntegrasesReceptor, TIE-2cell behaviourcell dynamicsfate mappinghematopoietic stem cellskineticsmathematical modelingreconcile different published data

Identifiers

PMID33770496
PMCPMC8072066

What OpenQuestion holds

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LicenceCC BY
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.