Evidence map›Paper›PMID 24373928›Full record

ArticleExperimental hematology2014

Clonal-level responses of functionally distinct hematopoietic stem cells to trophic factors.

Cates Mallaney, Alok Kothari, Andrew Martens, Grant A Challen

Abstract read
In one paragraph

Article in Experimental hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

4 authors at 2 institutions in 1 country.

Cates MallaneyDivision of Oncology, Section of Molecular Oncology, Department of Internal Medicine, Washington University in St. Louis, St. Louis, MO.
Alok KothariDepartment of Pediatrics, Washington University in St. Louis, St. Louis, MO.
Andrew MartensDivision of Oncology, Section of Molecular Oncology, Department of Internal Medicine, Washington University in St. Louis, St. Louis, MO.
Grant A ChallenDivision of Oncology, Section of Molecular Oncology, Department of Internal Medicine, Washington University in St. Louis, St. Louis, MO. Electronic address: gchallen@DOM.wustl.edu.
Molecular Oncology (United States) · USWashington University in St. Louis · US

Funding

DNA Methylation Control Hematopoietic Stem Cell Lineage DifferentiationR00DK084259 · NIDDK · WASHINGTON UNIVERSITY · PI CHALLEN, GRANT ANTHONY · 2012 to 2014
$734k
DNA Methylation Control Hematopoietic Stem Cell Lineage DifferentiationK99DK084259 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHALLEN, GRANT ANTHONY · 2010 to 2011
$182k
NIDDK NIH HHS K99 DK084259NIDDK NIH HHS R00 DK084259
6 · The paper itself

Abstract

Recent findings from several groups have identified distinct classes of hematopoietic stem cells (HSCs) in the bone marrow, each with inherent functional biases in terms of their differentiation, self-renewal, proliferation, and lifespan. It has previously been demonstrated that myeloid- and lymphoid-biased HSCs can be prospectively enriched based on their degree of Hoechst dye efflux. In the present study, we used differential Hoechst efflux to enrich lineage-biased HSC subtypes and analyzed their functional potentials. Despite similar outputs in vitro, bone marrow transplantation assays revealed contrasting lineage differentiation in vivo. To stratify the molecular differences underlying these contrasting functional potentials at the clonal level, single-cell gene expression analysis was performed using the Fluidigm BioMark system and revealed dynamic expression of genes including Meis1, CEBP/α, Sfpi1, and Dnmt3a. Finally, single-cell gene expression analysis was used to unravel the opposing proliferative responses of lineage-biased HSCs to the growth factor TGF-β1, revealing a potential role for the cell cycle inhibitor Cdkn1c as molecular mediator. This work lends further credence to the concept of HSC heterogeneity, and it presents unprecedented molecular resolution of the HSC response to trophic factors using single-cell gene expression analysis.

Indexed as

Cell ProliferationAllograftsAnimalsBone Marrow TransplantationCCAAT-Enhancer-Binding ProteinsCell DifferentiationCyclin-Dependent Kinase Inhibitor p57Gene Expression RegulationHematopoietic Stem CellsHomeodomain ProteinsIntercellular Signaling Peptides and ProteinsMiceMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1CCAAT-Enhancer-Binding ProteinsCdkn1c protein, mouseCEBPA protein, mouseCyclin-Dependent Kinase Inhibitor p57Homeodomain ProteinsIntercellular Signaling Peptides and ProteinsMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Tgfb1 protein, mouseTrans-ActivatorsTransforming Growth Factor beta1

Identifiers

PMID24373928
PMCPMC4004675
OpenAlexW2079609582

What OpenQuestion holds

Textmetadata
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.