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granulocyte colony-stimulating factor (G-CSF). This article focuses on the long-term benefits and risks associated with G-CSF therapy, including data for other myeloid factors, as available. Chemotherapy-Induced Neutropenia G-CSF reduces neutropenic

treatment delays, and subsequently compromise disease control and overall survival. 2 – 6 The myeloid growth factors (MGFs), including granulocyte colony-stimulating factor (G-CSF), have been shown to decrease the risk of neutropenic complications

, chemotherapy agents, or cycle length; (2) received prophylactic granulocyte colony-stimulating factor (G-CSF) within 4 days of chemotherapy initiation and/or antibiotics prophylaxis dispensed between 3 days before and 10 days after first chemotherapy

-metHuG-CSF): the first 10 years . Blood 1996 ; 88 : 1907 – 1929 . 2. Spiekermann K Roesler J Emmendoerffer A . Functional features of neutrophils induced by G-CSF and GM-CSF treatment: differential effects and clinical implications . Leukemia 1997

Hematol 1989 ; 26 : 7 – 14 . 15 Dale DC Bonilla MA Davis MW . A randomized controlled phase III trial of recombinant human G-CSF for treatment of severe chronic neutropenia . Blood 1993 ; 181 : 2496 – 2502 . 16 Smith TJ

: AC, anthracycline/cyclophosphamide; CMF, cyclophosphamide/methotrexate/fluorouracil; doc, docetaxel; G-CSF, granulocyte colony-stimulating factor; pts, patients; T, paclitaxel; TC, docetaxel/cyclophosphamide; TCH, docetaxel

identified prophylactic granulocyte colony-stimulating factor (G-CSF) administration during the first cycle. 24 The primary outcome of analysis was death within 30 days from chemotherapy initiation. The secondary outcome was hospitalization. We also

cost. 2 Prophylactic use of recombinant human granulocyte colony-stimulating factors (G-CSFs), such as filgrastim or pegfilgrastim, can significantly reduce FN risk and FN-related costs. 3 – 5 The risk of developing FN depends on patient and disease

of the protected marrow microenvironment, rendering them more susceptible to chemotherapy. One preclinical study found that granulocyte colony-stimulating factor (G-CSF) reduced the viability of AML cells in vitro when cocultured with HS-5 stroma

dosing of cytokines and receptor antagonists. Granulocyte colony-stimulating factor (G-CSF) causes release of proteases, including neutrophil elastase, which cleaves CXCR4 and VCAM-1, 8 , 9 and elevated levels of metalloproteinases, including MMP-2 (that