ReviewFrontiers in oncology2022
A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.
Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed.
- Rewiring glucose metabolism in pancreatic cancer by natural compounds: implications for immune evasion and therapeutic targets.Molecular biology reports · 2026Review
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- Successful conversion therapy for presumed granulocyte colony-stimulating factor-producing hepatocellular carcinoma: a case report.Frontiers in oncology · 2026Article
- Silver nanoparticles at sub-cytotoxic levels increase enteric pathogen invasion by compromising intestinal epithelial barrier integrity.Frontiers in cellular and infection microbiology · 2026Article
- Efficiency and safety of five different agents forFrontiers in molecular biosciences · 2026Article
- Atypical chronic myeloid leukemia: From diagnosis to molecular features and therapeutic options.HemaSphere · 2025Review
- A new STAT3-based potency assay for human G-CSF analog therapeutics.Journal of pharmaceutical and biomedical analysis · 2025Article
- Tuning of G-CSFR signaling by de novo-designed agonists.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.Cancer cell international · 2025Review
- Group B Streptococci lyse endothelial cells to infect the brain in a zebrafish meningitis model.PLoS biology · 2025Article
- Cancer-associated fibroblasts secrete CSF3 to promote TNBC progression via enhancing PGM2L1-dependent glycolysis reprogramming.Cell death & disease · 2025Article
- SOX2-Dependent Wound Repair Signature Triggers Prohealing Outcome in Hyperglycemic Wounds.The Journal of investigative dermatology · 2025Article
- Distribution of different classes of CSF3R mutations and co-mutational pattern in 360 myeloid neoplasia.Annals of hematology · 2025Article
- FRA1 controls acinar cell plasticity during murine KrasDevelopmental cell · 2024Article
- A strategy to design protein-based antagonists against type I cytokine receptors.PLoS biology · 2024Article
- Advancing drug-response prediction using multi-modal and -omics machine learning integration (MOMLIN): a case study on breast cancer clinical data.Briefings in bioinformatics · 2024Article
- Potential diagnostic and drug target markers in glioblastoma.Scientific reports · 2024Article
- Gene Expression ofInternational journal of molecular sciences · 2024Article
- Interaction of the intestinal cytokines-JAKs-STAT3 and 5 axes with RNA N6-methyladenosine to promote chronic inflammation-induced colorectal cancer.Frontiers in oncology · 2024Review
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Granulocyte colony-stimulating factor receptor (GCSFR) is a critical regulator of granulopoiesis. Studies have shown significant upregulation of GCSFR in a variety of cancers and cell types and have recognized GCSFR as a cytokine receptor capable of influencing both myeloid and non-myeloid immune cells, supporting pro-tumoral actions. This systematic review aims to summarize the available literature examining the mechanisms that control GCSFR signaling, regulation, and surface expression with emphasis on how these mechanisms may be dysregulated in cancer. Experiments with different cancer cell lines from breast cancer, bladder cancer, glioma, and neuroblastoma are used to review the biological function and underlying mechanisms of increased GCSFR expression with emphasis on actions related to tumor proliferation, migration, and metastasis, primarily acting through the JAK/STAT pathway. Evidence is also presented that demonstrates a differential physiological response to aberrant GCSFR signal transduction in different organs. The lifecycle of the receptor is also reviewed to support future work defining how this signaling axis becomes dysregulated in malignancies.
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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.