Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (749 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, g-csf is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Factor, Granulocyte Colony-Stimulating; Granulocyte Colony Stimulating Factor; Colony-Stimulating Factor, Granulocyte; Colony Stimulating Factor, Granulocyte; Myeloid Growth Factor; Factor, Myeloid Growth; Growth Factor, Myeloid; G-CSF.
Where it fits in the MeSH classification
- Broader topics
- Colony-Stimulating Factors
- Narrower topics
- Filgrastim; Lenograstim
- See also
- Receptors, Granulocyte Colony-Stimulating Factor
Related concepts
- G-Csf
Research landscape
PubMed indexes 17,676 records tagged with the MeSH heading “Granulocyte Colony-Stimulating Factor” (counts retrieved 2026-10-31). 2,129 of them (12.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,851 records.
Reviews account for 2,050 records (11.6%) and meta-analyses for 164. Randomized controlled trials number 1,089 (6.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,851 |
| 2000-2009 | 5,235 |
| 2010-2019 | 4,461 |
| 2020 onward | 2,129 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,050 | 11.6% |
| Meta-analyses | 164 | 0.9% |
| Randomized controlled trials | 1,089 | 6.2% |
Method: PubMed query "Granulocyte Colony-Stimulating Factor"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Effect of granulocyte colony-stimulating factor on toxicities after CAR T cell therapy for lymphoma and myeloma | 2022 | Research article Design not recorded in structured metadata | 51 | cc by PMID 36316312 · DOI · PMC9622902 |
| Intrauterine G-CSF Administration in Recurrent Implantation Failure (RIF): An Rct | 2020 | Randomized controlled trial Design not recorded in structured metadata | 44 | cc by PMID 32198409 · DOI · PMC7083859 |
| Granulocyte Colony-Stimulating Factor-Primed Unmanipulated Haploidentical Blood and Marrow Transplantation | 2019 | Review article Design not recorded in structured metadata | 44 | cc by PMID 31749802 · DOI · PMC6842971 |
| OLFM4 promotes intrahepatic cholangiocarcinoma progression through a PKM2-glycolysis-histone lactylation feedback loop | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42910221 · DOI · PMC13685613 |
Effect of granulocyte colony-stimulating factor on toxicities after CAR T cell therapy for lymphoma and myeloma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Chimeric antigen receptor T cells (CAR T) are groundbreaking therapies but may cause significant toxicities including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and cytopenias.
- Closing excerpt
- Future trials should clarify the optimal G-CSF strategy to improve outcomes after CAR T.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (205 words)
Chimeric antigen receptor T cells (CAR T) are groundbreaking therapies but may cause significant toxicities including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and cytopenias. Granulocyte colony-stimulating factor (G-CSF) is often used to mitigate neutropenia after CAR T, but there is no consensus recommended strategy due to hypothesized, but largely unknown risks of exacerbating toxicities. To investigate the impact of G-CSF, we retrospectively analyzed 197 patients treated with anti-CD19 CAR T for lymphoma and 47 patients treated with anti-BCMA CAR T for multiple myeloma. In lymphoma, 140 patients (71%) received prophylactic G-CSF before CAR T (mostly pegylated G-CSF) and were compared with 57 patients (29%) treated with G-CSF after CAR T or not exposed. Prophylactic G-CSF was associated with faster neutrophil recovery (3 vs. 4 days, P < 0.01) but did not reduce recurrent neutropenia later. Prophylactic G-CSF was associated with increased grade ≥2 CRS (HR 2.15, 95% CI 1.11-4.18, P = 0.02), but not ICANS. In multiple myeloma, prophylactic G-CSF was not used; patients were stratified by early G-CSF exposure (≤2 days vs. ≥3 days after CAR T or no exposure), with no significant difference in toxicities. Future trials should clarify the optimal G-CSF strategy to improve outcomes after CAR T.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36316312 · DOI · PMC9622902
Intrauterine G-CSF Administration in Recurrent Implantation Failure (RIF): An Rct [2]
Abstract reading summary — source excerpts
- Opening excerpt
- This study investigates the effects of intrauterine G-CSF on endometrial thickness, clinical pregnancy rate and live birth rate in a recurrent implantation failure (RIF) group with normal endometrium.
- Closing excerpt
- The intervention of administration G-CSF into the uterine cavity in RIF patients with normal endometrium, did not alter the endometrial thickness, clinical pregnancy rates, or live birth rates.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (262 words)
This study investigates the effects of intrauterine G-CSF on endometrial thickness, clinical pregnancy rate and live birth rate in a recurrent implantation failure (RIF) group with normal endometrium. This study was designed as a prospective randomized controlled trial with the involvement of 157 RIF group pati; ents. The RIF group was formed on the basis of the RIF criteria: "The failure to achieve a clinical pregnancy after the transfer of at least four good-quality embryos in a minimum of three fresh or frozen cycles to a woman under the age of 40 years. The study sample included 82 patients in the G-CSF group who received G-CSF once a day on hCG. The procedure was performed by administering 30 mIU of Leucostim®(Filgrastim [G-CSF] 30 mIU/mL; DEM Medical, Dong-A; South Korea) through slow infusion into the endometrial cavity using a soft embryo transfer catheter. Normal saline of 1 mL was infused into the endometrial cavity in the same way in 75 patients in the control group. The standard ICSI procedure was used for all patients, and fresh cycle embryos were transferred on the third or fifth day. No statistically significant difference was identified in clinical pregnancy rates, miscarriage rates and live birth rates between the G-CSF group and the control group (p = 0.112, p = 0.171, p = 0.644, respectively), and no difference was observed between the two groups regarding endometrial thickness (p = 0.965). The intervention of administration G-CSF into the uterine cavity in RIF patients with normal endometrium, did not alter the endometrial thickness, clinical pregnancy rates, or live birth rates.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32198409 · DOI · PMC7083859
Granulocyte Colony-Stimulating Factor-Primed Unmanipulated Haploidentical Blood and Marrow Transplantation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Granulocyte colony-stimulating factor (G-CSF), a growth factor for neutrophils, has been successfully used for stem cell mobilization and T cell immune tolerance induction.
- Closing excerpt
- The application of G-CSF-primed allografts in other haploidentical modalities is also discussed.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Granulocyte colony-stimulating factor (G-CSF), a growth factor for neutrophils, has been successfully used for stem cell mobilization and T cell immune tolerance induction. The establishment of G-CSF-primed unmanipulated haploidentical blood and marrow transplantation (The Beijing Protocol) has achieved outcomes for the treatment of acute leukemia, myelodysplastic syndrome, and severe aplastic anemia with haploidentical allografts comparable to those of human leukocyte antigen (HLA)-matched sibling donor transplantation. Currently, G-CSF-mobilized bone marrow and/or peripheral blood stem cell sources have been widely used in unmanipulated haploidentical transplant settings. In this review, we summarize the roles of G-CSF in inducing T cell immune tolerance. We discuss the recent advances in the Beijing Protocol, mainly focusing on strategies that have been used to improve transplant outcomes in cases of poor graft function, virus infections, and relapse. The application of G-CSF-primed allografts in other haploidentical modalities is also discussed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31749802 · DOI · PMC6842971
OLFM4 promotes intrahepatic cholangiocarcinoma progression through a PKM2-glycolysis-histone lactylation feedback loop [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolic reprogramming is increasingly recognized as a key characteristic of intrahepatic cholangiocarcinoma (ICC) initiation and progression.
- Closing excerpt
- Collectively, these findings support targeting OLFM4 as a promising therapeutic strategy for ICC management.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (140 words)
Metabolic reprogramming is increasingly recognized as a key characteristic of intrahepatic cholangiocarcinoma (ICC) initiation and progression. Among these metabolic alterations, glycolysis is central for supporting tumor growth. Elucidating the precise molecular mechanisms of glycolysis in ICC is critical for developing precision therapies. Here, comprehensive integrative analyses revealed that olfactomedin 4 (OLFM4) is upregulated in ICC specimens and is associated with adverse patient outcomes. Mechanistically, OLFM4 promotes ICC progression by recruiting ubiquitin specific peptidase 10 (USP10) to stabilize pyruvate kinase M2 (PKM2). This interaction enhances glycolysis and lactate production, thereby elevating histone lactylation, with a prominent impact on H3K18 lactylation (H3K18la). Consequently, H3K18la positively regulates OLFM4 transcription, establishing a positive glycolysis-histone lactylation feedback loop. Notably, tiliroside, a candidate pharmacological inhibitor of OLFM4, demonstrated antitumor efficacy in ICC. Collectively, these findings support targeting OLFM4 as a promising therapeutic strategy for ICC management.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42910221 · DOI · PMC13685613
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article 2010 update of EORTC guidelines for the use of granulocyte-colony stimulating factor to reduce the incidence of chemotherapy-induced febrile neutropenia in adult patients with lymphoproliferative disorders and solid tumours [5]
- Research article Recommendations for the Use of WBC Growth Factors: American Society of Clinical Oncology Clinical Practice Guideline Update [6]
- Research article Granulocyte colony-stimulating factor: molecular mechanisms of action during steady state and 'emergency' hematopoiesis [7]
- Research article G-CSF and GM-CSF in Neutropenia [8]
- Research article G-CSF: a key regulator of neutrophil production, but that's not all! [9]
- Research article G-CSF: From granulopoietic stimulant to bone marrow stem cell mobilizing agent [10]
References
- Miller KC, Johnson PC, Abramson JS, Soumerai JD, Yee AJ, Branagan AR, et al.. Effect of granulocyte colony-stimulating factor on toxicities after CAR T cell therapy for lymphoma and myeloma. . 2022. PMID 36316312 · DOI · PMC9622902
- Kalem Z, Namli Kalem M, Bakirarar B, Kent E, Makrigiannakis A, Gurgan T. Intrauterine G-CSF Administration in Recurrent Implantation Failure (RIF): An Rct. . 2020. PMID 32198409 · DOI · PMC7083859
- Chang YJ, Zhao XY, Huang XJ. Granulocyte Colony-Stimulating Factor-Primed Unmanipulated Haploidentical Blood and Marrow Transplantation. . 2019. PMID 31749802 · DOI · PMC6842971
- Liu S, Cao K, Chen C, Xu X, Shan J, Li C, et al.. OLFM4 promotes intrahepatic cholangiocarcinoma progression through a PKM2-glycolysis-histone lactylation feedback loop. . 2026. PMID 42910221 · DOI · PMC13685613
- Aapro MS, Bohlius J, Cameron DA, Dal Lago L, Donnelly JP, Kearney N, et al.. 2010 update of EORTC guidelines for the use of granulocyte-colony stimulating factor to reduce the incidence of chemotherapy-induced febrile neutropenia in adult patients with lymphoproliferative disorders and solid tumours. Eur J Cancer. 2011. PMID 21095116 · DOI
- Smith TJ, Bohlke K, Lyman GH, Carson KR, Crawford J, Cross SJ, et al.. Recommendations for the Use of WBC Growth Factors: American Society of Clinical Oncology Clinical Practice Guideline Update. J Clin Oncol. 2015. PMID 26169616 · DOI
- Panopoulos AD, Watowich SS. Granulocyte colony-stimulating factor: molecular mechanisms of action during steady state and 'emergency' hematopoiesis. Cytokine. 2008. PMID 18400509 · DOI · PMC2852428
- Mehta HM, Malandra M, Corey SJ. G-CSF and GM-CSF in Neutropenia. J Immunol. 2015. PMID 26254266 · DOI · PMC4741374
- Roberts AW. G-CSF: a key regulator of neutrophil production, but that's not all!. Growth Factors. 2005. PMID 16019425 · DOI
- Bendall LJ, Bradstock KF. G-CSF: From granulopoietic stimulant to bone marrow stem cell mobilizing agent. Cytokine Growth Factor Rev. 2014. PMID 25131807 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.