Evidence map›Paper›PMID 27789332›Full record

ReviewExperimental hematology2017

Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.

Pankaj Dwivedi, Kenneth D Greis

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 3 syntheses or guidelines pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. PF-06881893 (Nivestym™), a Filgrastim Biosimilar, Versus US-Licensed Filgrastim Reference Product (US-NeupogenBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2019
    Trial
  6. Article
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  8. The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  9. Article
  10. Article
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  12. Review
  13. Tuning of G-CSFR signaling by de novo-designed agonists.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  18. Review
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24 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Pankaj DwivediDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH.
Kenneth D GreisDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH. Electronic address: ken.greis@uc.edu.
University of Cincinnati Medical Center · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
Enhanced proteomics capabilities for quantitation of proteins with a triple quadS10RR027015 · NCRR · UNIVERSITY OF CINCINNATI · PI GREIS, KENNETH DONALD · 2010 to 2010
$426k
NCRR NIH HHS S10 RR027015NIEHS NIH HHS P30 ES006096
6 · The paper itself

Abstract

Granulocyte colony-stimulating factor is a hematopoietic cytokine that stimulates neutrophil production and hematopoietic stem cell mobilization by initiating the dimerization of homodimeric granulocyte colony-stimulating factor receptor. Different mutations of CSF3R have been linked to a unique spectrum of myeloid disorders and related malignancies. Myeloid disorders caused by the CSF3R mutations include severe congenital neutropenia, chronic neutrophilic leukemia, and atypical chronic myeloid leukemia. In this review, we provide an analysis of granulocyte colony-stimulating factor receptor, various mutations, and their roles in the severe congenital neutropenia, chronic neutrophilic leukemia, and malignant transformation, as well as the clinical implications and some perspective on approaches that could expand our knowledge with respect to the normal signaling mechanisms and those associated with mutations in the receptor.

Indexed as

Signal TransductionAnimalsCell Transformation, NeoplasticCongenital Bone Marrow Failure SyndromesGenetic Predisposition to DiseaseHumansJanus KinasesLeukemia, Myeloid, AcuteLeukemia, Neutrophilic, ChronicMAP Kinase Signaling SystemMutationNeutropeniaPhosphatidylinositol 3-KinasesProtein BindingProtein Interaction Domains and MotifsProto-Oncogene Proteins c-aktJanus KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Granulocyte Colony-Stimulating FactorSTAT Transcription Factors

Identifiers

PMID27789332
PMCPMC5241233
OpenAlexW2538288310

What OpenQuestion holds

Textmetadata
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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.