Granulocyte colony stimulating factor (G-CSF)

Produced by monocytes, macrophages, T cells, fibroblasts, and endothelial cells and regulates the production of granulocytes in the bone marrow and affects neutrophil proliferation.

causes proliferation and differentiation of hematopoetic stem cells and progenitor cells, generating polymorphonuclear neutrophils via precursor stages of myeloblasts, promyelocyte,myelocyte, meta-myelocyte and bands.

Granulocyte colony stimulating factors are used to increase production of granulocytes and neutrophils for myeloid count recovery, and they have been shown to reduce the risk of duration of febrile neutropenia.

G-CSF is a growth factor for neutrophils and may act by increasing the activity of neutrophil-derived proteases such as neutrophil elastase in the bone marrow leading to proteolytic degradation of SDF-1. 

The complex of the ligand-receptor recruits tyrosine kinases including the Janus kinase (JAK) signal transducers and activators of transcription proteins.

Induces a shift toward long lasting type 2 immune reactivity, impairs IL-12 production by Th2 inducing dendritic cells, decreases IL-12 receptor expression by IL-4 and IL-10 producing CD4+ cells and decreases IFN-gamma and IL-4 production.

When used for primary prophylaxis, which refers to their use in the time. after the first cycle of cancer patient’s chemotherapy but before the development of neutropenia, they reduce the risk, severity, and duration of febrile neutropenia.

Therapy associated with at least a 50% reduction in the incidence of febrile neutropenia during each chemotherapy cycle.

If the risk of febrile neutropenia is approximately 17 – 20% then G-CSF may become a cost-saving therapy.

Utilized to mobilize stem cells for blood stem cell transplantation.

Increases circulating progenitors 10 to 100 fold.

Peripheral blood stem cells (PBSC) enumerated by CD34 determination has largely replaced bone marrow as a source of both autologous and allogeneic stem cells.

Reduces chemotherapy induced mucositis.

Most commonly reported toxicity is musculoskeletal pain.

No long term benefit after allogeneic stem cell transplantation to promote hematologic recovery.

Reduces neutropenic complications, including febrile neutropenia, infection, infection associated mortality, in patients undergoing chemotherapy.

Enables an increase in the delivery of chemotherapy dose intensity.

Use should be considered for patients undergoing chemotherapy who have a 20% or greater risk of febrile neutropenia.

Meta-analyses show that when G-CSF is initiated in the first cycle of chemotherapy there is a significant reduction in early mortality.

Patients who receive treatment with G-CSF primary prophylaxis receive greater chemotherapy relative does intensity than patients who did not receive such prophylaxis.

Mobilization of peripheral blood stem cells with G-CSF varies to-three fold, and 10 to 20% of patients with multiple myeloma or lymphoma fail to collect enough CD34 cells to support hematopoietic transplantation.

Five days of G-CSF is not inferior to 7/10 days as primary prophylaxis of chemotherapy induced febrile neutropenia in early breast cancer.

Patients treated with G-CSF may have a peripheral blast count size 40% of circulating leukocytes.

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