Evidence map›Paper›PMID 23681919›Full record

ArticleStem cells (Dayton, Ohio)2013

KIT receptor gain-of-function in hematopoiesis enhances stem cell self-renewal and promotes progenitor cell expansion.

Shayu Deshpande, Benedikt Bosbach, Yasemin Yozgat, Christopher Y Park, Malcolm A S Moore, Peter Besmer

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. New C3H KitScientific reports · 2022
    Article
  6. Article
  7. Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  8. Article
  9. Functional Analysis ofFrontiers in genetics · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. 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

6 authors at 1 institution in 1 country.

Shayu DeshpandeDevelopmental Biology, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Benedikt Bosbach
Yasemin Yozgat
Christopher Y Park
Malcolm A S Moore
Peter Besmer
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
SPORE in Soft Tissue SarcomaP50CA140146 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SPRIGGS, DAVID R · 2010 to 2014
$11.1M
PI 3-KINASE AND KIT RECEPTOR SIGNALINGR01HL055748 · NHLBI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BESMER, PETER · 1997 to 2012
$4.0M
A Mouse Model for Human Gastrointestinal Stromal TumorR01CA102774 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BESMER, PETER · 2004 to 2014
$3.4M
ROLE OF KIT IN GAMETOGENESISR01HD038908 · NICHD · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BESMER, PETER · 2000 to 2004
$1.4M
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA140146NCI NIH HHS P50-CA140146NCI NIH HHS R01 CA102774NCI NIH HHS R01-CA102774NHLBI NIH HHS R01 HL055748NHLBI NIH HHS R01-HL55748NICHD NIH HHS R01 HD038908
6 · The paper itself

Abstract

The KIT receptor tyrosine kinase has important roles in hematopoiesis. We have recently produced a mouse model for imatinib resistant gastrointestinal stromal tumor (GIST) carrying the Kit(V558Δ) and Kit(T669I) (human KIT(T670I) ) mutations found in imatinib-resistant GIST. The Kit(V558Δ;T669I/+) mice developed microcytic erythrocytosis with an increase in erythroid progenitor numbers, a phenotype previously seen only in mouse models of polycythemia vera with alterations in Epo or Jak2. Significantly, the increased hematocrit observed in Kit(V558Δ;T669I/+) mice normalized upon splenectomy. In accordance with increased erythroid progenitors, myeloerythroid progenitor numbers were also elevated in the Kit(V558Δ;T669I/+) mice. Hematopoietic stem cell (HSC) numbers in the bone marrow (BM) of Kit(V558Δ;T669I/+) mice were unchanged in comparison to wild-type mice. However, increased HSC numbers were observed in fetal livers and the spleen and peripheral blood of adult Kit(V558Δ;T669I/+) mice. Importantly, HSC from Kit(V558Δ;T669I/+) BM had a competitive advantage over wild-type HSC. In response to 5-fluorouracil treatment, elevated numbers of dividing Lin(-) Sca(+) cells were found in the Kit(V558Δ;T669I/+) BM compared to wild type. Our study demonstrates that signaling from the Kit(V558Δ;T669I/+) receptor has important consequences in hematopoiesis enhancing HSC self-renewal and resulting in increased erythropoiesis.

Indexed as

AnimalsCell Growth ProcessesDisease Models, AnimalErythroid CellsFemaleFluorouracilHematopoiesisHematopoietic Stem CellsMaleMiceMice, Inbred C57BLProto-Oncogene Proteins c-kitSignal TransductionFluorouracilProto-Oncogene Proteins c-kitErythroid progenitorsHematopoietic stem cellsSelf-renewalSignal transduction

Identifiers

PMID23681919
PMCPMC3775897
OpenAlexW1549722835

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.