Evidence map›Paper›PMID 18400509›Full record

ReviewCytokine2008

Granulocyte colony-stimulating factor: molecular mechanisms of action during steady state and 'emergency' hematopoiesis.

Athanasia D Panopoulos, Stephanie S Watowich

Registry-linked trialAbstract readReview
In one paragraph

Review in Cytokine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03395028 (Granulocyte-Colony Stimulating Factor Adjunct Therapy for Biliary Atresia), which is not on this map. Cited by 203 papers.

0numbers the graph read from it
0cells of the map it votes in
203citing 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.

NCT03395028 early_phase1completednot on this mapstarted 2018, after this paper: background citation

Granulocyte-Colony Stimulating Factor Adjunct Therapy for Biliary Atresia

TypeinterventionalSponsorHolterman, Ai-Xuan, M.D.Ran2018 to 2020Enrolled6ConditionsBiliary AtresiaArmsGranulocyte Colony-Stimulating Factor
3 · Its place in the literature

Who cites it

203 citing papers in PubMed.

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  8. Cas9eLife · 2026
    Article
  9. Multi-dimensional plasma proteomic profiling elucidates molecular mechanisms and pathophysiological networks in pediatric severe traumatic brain injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  10. Review
  11. Review
  12. Article
  13. Review
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  15. Article
  16. Association ofAnnals of laboratory medicine · 2026
    Article
  17. Article
  18. A new STAT3-based potency assay for human G-CSF analog therapeutics.Journal of pharmaceutical and biomedical analysis · 2025
    Article
  19. Article
  20. Article

143 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.

Athanasia D PanopoulosDepartment of Immunology and Center for Cancer Immunology Research, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, PO Box 301402, Unit 902, Houston, TX 77030, USA.
Stephanie S Watowich

Funding

Training Program in Cancer ImmunobiologyT32CA009598 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ALLISON, JAMES P · 1988 to 2014
$4.9M
MOLECULAR MECHANISMS CYTOKINE RECEPTOR SIGNALINGR01CA077447 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI WATOWICH, STEPHANIE S · 1998 to 2000
$250k
NCI NIH HHS CA77447NCI NIH HHS R01 CA077447NCI NIH HHS T32 CA009598NCI NIH HHS T32-CA-09598-16
6 · The paper itself

Abstract

Neutrophils are phagocytes whose principal function is to maintain anti-bacterial immunity. Neutrophils ingest and kill invading bacteria, releasing cytotoxic, chemotactic and inflammatory mediators at sites of infection. This serves to control the immediate host immune response and attract other cells, such as macrophages and dendritic cells, which are important for establishing long-term adaptive immunity. Neutrophils thus contribute to both the initiation and the maintenance of inflammation at sites of infection. Aberrant neutrophil activity is deleterious; suppressed responses can cause extreme susceptibility to infection while overactivation can lead to excessive inflammation and tissue damage. This review will focus on neutrophil regulation by granulocyte colony-stimulating factor (G-CSF), the principal cytokine controlling neutrophil development and function. The review will emphasize the molecular aspects of G-CSF-driven granulopoiesis in steady state (healthy) conditions and during demand-driven or 'emergency' conditions elicited by infection or clinical administration of G-CSF. Understanding the molecular control of granulopoiesis will aid in the development of new approaches designed to treat disorders of neutrophil production and function.

Indexed as

AnimalsBacterial InfectionsCell ProliferationGene Expression RegulationGranulocyte Colony-Stimulating FactorHumansInterleukin-17MiceMyelopoiesisNeutropeniaNeutrophil ActivationReceptors, Granulocyte Colony-Stimulating FactorSignal TransductionGranulocyte Colony-Stimulating FactorInterleukin-17Receptors, Granulocyte Colony-Stimulating Factor

Identifiers

PMID18400509
PMCPMC2852428

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.