Evidence map›Paper›PMID 24220695›Full record

ArticleBritish journal of cancer2014

Granulocyte colony-stimulating factor receptor signalling via Janus kinase 2/signal transducer and activator of transcription 3 in ovarian cancer.

J Kumar, F W Fraser, C Riley, N Ahmed, D R McCulloch, A C Ward

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Tuning of G-CSFR signaling by de novo-designed agonists.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  2. γδCellular & molecular immunology · 2025
    Article
  3. Article
  4. JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

J Kumar1] School of Medicine, Deakin University, Geelong, Victoria 3216, Australia [2] Strategic Research Centre in Molecular and Medical Research, Deakin University, Geelong, Victoria 3216, Australia.
F W Fraser1] School of Medicine, Deakin University, Geelong, Victoria 3216, Australia [2] Strategic Research Centre in Molecular and Medical Research, Deakin University, Geelong, Victoria 3216, Australia.
C RileyWomen's Cancer Research Centre, Royal Women's Hospital, Parkville, Victoria 3052, Australia.
N Ahmed1] Women's Cancer Research Centre, Royal Women's Hospital, Parkville, Victoria 3052, Australia [2] Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria 3052, Australia.
D R McCulloch1] School of Medicine, Deakin University, Geelong, Victoria 3216, Australia [2] Strategic Research Centre in Molecular and Medical Research, Deakin University, Geelong, Victoria 3216, Australia.
A C Ward1] School of Medicine, Deakin University, Geelong, Victoria 3216, Australia [2] Strategic Research Centre in Molecular and Medical Research, Deakin University, Geelong, Victoria 3216, Australia.
Deakin University · AURoyal Women's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOvarian cancer remains a major cause of cancer mortality in women, with only limited understanding of disease aetiology at the molecular level. Granulocyte colony-stimulating factor (G-CSF) is a key regulator of both normal and emergency haematopoiesis, and is used clinically to aid haematopoietic recovery following ablative therapies for a variety of solid tumours including ovarian cancer.

methodsThe expression of G-CSF and its receptor, G-CSFR, was examined in primary ovarian cancer samples and a panel of ovarian cancer cell lines, and the effects of G-CSF treatment on proliferation, migration and survival were determined.

resultsG-CSFR was predominantly expressed in high-grade serous ovarian epithelial tumour samples and a subset of ovarian cancer cell lines. Stimulation of G-CSFR-expressing ovarian epithelial cancer cells with G-CSF led to increased migration and survival, including against chemotherapy-induced apoptosis. The effects of G-CSF were mediated by signalling via the downstream JAK2/STAT3 pathway.

conclusionThis study suggests that G-CSF has the potential to impact on ovarian cancer pathogenesis, and that G-CSFR expression status should be considered in determining appropriate therapy.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, Ovarian EpithelialCell Growth ProcessesCell Line, TumorCell MovementCisplatinFemaleGranulocyte Colony-Stimulating FactorHumansInterleukin-6Janus Kinase 2Neoplasm GradingNeoplasms, Glandular and EpithelialOvarian NeoplasmsPaclitaxelAntineoplastic AgentsCisplatinGranulocyte Colony-Stimulating FactorInterleukin-6Janus Kinase 2PaclitaxelReceptors, Colony-Stimulating FactorSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24220695
PMCPMC3887286
OpenAlexW2048113014

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.