Journal articles: 'Granulocyte colony stimulating factor (G-CSF)'

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Lieschke, Graham J. "Granulocyte colony stimulating factor (G-CSF)." Australian Prescriber 17, no. 4 (October 1, 1994): 96–99. http://dx.doi.org/10.18773/austprescr.1994.100.

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Schaafsma, MR, JH Falkenburg, N. Duinkerken, J. Van Damme, BW Altrock, R. Willemze, and WE Fibbe. "Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor." Blood 74, no. 7 (November 15, 1989): 2398–404. http://dx.doi.org/10.1182/blood.v74.7.2398.2398.

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Abstract Interleukin-1 (IL-1) was found to act synergistically with granulocyte- macrophage colony-stimulating factor (GM-CSF) on granulocytic colony growth of normal human bone marrow cells, depleted of mononuclear phagocytes and T lymphocytes. Using CD34/HLA-DR-enriched bone marrow cells we demonstrated that this activity of IL-1 was not a direct action on hematopoietic progenitor cells, but an effect of an intermediate factor produced by residual accessory cells in response to IL-1. Neutralization experiments using an anti-IL-6 antiserum showed that IL-1-induced IL-6 did not contribute to the observed synergy. Furthermore, IL-6 by itself had neither a direct stimulatory effect on CFU-GM colony growth, nor did it act synergistically with GM-CSF on granulocytic or monocytic colony formation. Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1-induced G-CSF production was responsible for the synergy with GM-CSF. Using combinations of G-CSF and GM-CSF this synergistic activity could be detected at concentrations of G-CSF as low as 0.1 ng/mL (10 U/mL). Our results indicate that IL-1, but not IL-6, stimulates the GM-CSF- dependent proliferation of relatively mature myeloid progenitor cells in the presence of small numbers of accessory cells.

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Schaafsma, MR, JH Falkenburg, N. Duinkerken, J. Van Damme, BW Altrock, R. Willemze, and WE Fibbe. "Interleukin-1 synergizes with granulocyte-macrophage colony-stimulating factor on granulocytic colony formation by intermediate production of granulocyte colony-stimulating factor." Blood 74, no. 7 (November 15, 1989): 2398–404. http://dx.doi.org/10.1182/blood.v74.7.2398.bloodjournal7472398.

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Interleukin-1 (IL-1) was found to act synergistically with granulocyte- macrophage colony-stimulating factor (GM-CSF) on granulocytic colony growth of normal human bone marrow cells, depleted of mononuclear phagocytes and T lymphocytes. Using CD34/HLA-DR-enriched bone marrow cells we demonstrated that this activity of IL-1 was not a direct action on hematopoietic progenitor cells, but an effect of an intermediate factor produced by residual accessory cells in response to IL-1. Neutralization experiments using an anti-IL-6 antiserum showed that IL-1-induced IL-6 did not contribute to the observed synergy. Furthermore, IL-6 by itself had neither a direct stimulatory effect on CFU-GM colony growth, nor did it act synergistically with GM-CSF on granulocytic or monocytic colony formation. Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1-induced G-CSF production was responsible for the synergy with GM-CSF. Using combinations of G-CSF and GM-CSF this synergistic activity could be detected at concentrations of G-CSF as low as 0.1 ng/mL (10 U/mL). Our results indicate that IL-1, but not IL-6, stimulates the GM-CSF- dependent proliferation of relatively mature myeloid progenitor cells in the presence of small numbers of accessory cells.

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Collins, Steven J., Jon Ulmer, Louise E. Purton, and Gretchen Darlington. "Multipotent hematopoietic cell lines derived from C/EBPα(−/−) knockout mice display granulocyte macrophage–colony-stimulating factor, granulocyte– colony-stimulating factor, and retinoic acid–induced granulocytic differentiation." Blood 98, no. 8 (October 15, 2001): 2382–88. http://dx.doi.org/10.1182/blood.v98.8.2382.

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Abstract The transcription factor C/EBPα is an important mediator of granulocyte differentiation and regulates the expression of multiple granulocyte-specific genes including the granulocyte–colony-stimulating factor (G-CSF) receptor, neutrophil elastase, and myeloperoxidase. Indeed C/EBPα knockout mice display a profound block in granulocyte differentiation. To study this block in granulocytic differentiation in more detail, retroviral vector-mediated transduction of a dominant-negative retinoic acid receptor was used to establish hematopoietic growth factor–dependent, lympho-myeloid progenitor cell lines from the fetal livers of both the C/EBPα knockout animals (C/EBPα(−/−)) and their heterozygous littermates (C/EBPα(+/−)). Surprisingly, the C/EBPα(−/−) cell lines displayed significant spontaneous granulocytic differentiation, and this differentiation was markedly enhanced when the cells were stimulated with granulocyte macrophage (GM)–CSF. This GM-CSF–mediated differentiation was associated with the up-regulation of G-CSF receptor mRNA, and the combination of GM-CSF and G-CSF generated more than 95% mature neutrophils in the C/EBPα(−/−) cultures. The addition of all-transretinoic acid also enhanced this granulocytic differentiation of the cultured C/EBPα(−/−) cells, indicating that the activated retinoic acid receptors can enhance granulocytic differentiation through a molecular pathway that is independent of C/EBPα. These studies clearly indicate that terminal granulocytic differentiation associated with the up-regulation of C/EBPα-responsive genes can occur in the absence of C/EBPα, and they indicate the existence of multiple independent molecular pathways potentially used by primitive hematopoietic precursors that can lead to the development of mature granulocytes.

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Cetean, Sînziana, Călin Căinap, Anne-Marie Constantin, Simona Căinap, Alexandra Gherman, Luminița Oprean, Adriana Hangan, and Radu Oprean. "The importance of the granulocyte-colony stimulating factor in oncology." Medicine and Pharmacy Reports 88, no. 4 (September 20, 2015): 468–72. http://dx.doi.org/10.15386/cjmed-531.

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Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein, the second CSF, sharing some common effects with granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin-3 (IL-3) and interleukin-5 (IL-5). G-CSF is mainly produced by fibroblasts and endothelial cells from bone marrow stroma and by immunocompetent cells (monocytes, macrophages). The receptor for G-CSF (G-CSFR) is part of the cytokine and hematopoietin receptor superfamily and G-CSFR mutations cause severe congenital neutropenia.The main action of G-CSF - G-CSFR linkage is stimulation of the production, mobilization, survival and chemotaxis of neutrophils, but there are many other G-CSF effects: growth and migration of endothelial cells, decrease of norepinephrine reuptake, increase in osteoclastic activity and decrease in osteoblast activity.In oncology, G-CSF is utilized especially for the primary prophylaxis of chemotherapy-induced neutropenia, but it can be used for hematopoietic stem cell transplantation, it can produce monocytic differentiation of some myeloid leukemias and it can increase some drug resistance.The therapeutic indications of G-CSF are becoming more and more numerous: non neutropenic patients infections, reproductive medicine, neurological disturbances, regeneration therapy after acute myocardial infarction and of skeletal muscle, and hepatitis C therapy.

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Brown, TJ, J. Liu, C. Brashem-Stein, and M. Shoyab. "Regulation of granulocyte colony-stimulating factor and granulocyte- macrophage colony-stimulating factor expression by oncostatin M." Blood 82, no. 1 (July 1, 1993): 33–37. http://dx.doi.org/10.1182/blood.v82.1.33.bloodjournal82133.

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Oncostatin M (OM) is structurally and functionally related to a subclass of hematopoietic cytokines including leukemia-inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), granulocyte colony- stimulating factor (G-CSF), and interleukin-6 (IL-6). Using human endothelial cells (HEC) as a model for cytokine regulation of hematopoietic growth factor expression, we tested OM as an inducer of colony-stimulating activity. Colony-forming cell assays supplemented with culture supernatants from OM-treated HEC contained a threefold increase in colony-forming unit granulocyte-macrophage colonies. Specific immunoassay (enzyme-linked immunosorbent assay) of culture supernatants indicated that OM treatment of HEC resulted in a dose- and time-dependent increase in the accumulation of G-CSF and granulocyte- macrophage CSF (GM-CSF) (> 28-fold). The ED50 for OM induction of G-CSF and GM-CSF protein expression was 17 and 7 pmol/L, respectively. Increased protein expression was associated with a similar increase in steady-state expression of G-CSF and GM-CSF mRNA. Furthermore, a period of 12 to 24 hours elapsed before there were measurable increases in CSF expression, suggesting that OM may stimulate CSF production through a mechanism requiring the synthesis or activation of a secondary mediating factor or pathway. These findings provide the first evidence that OM may regulate myelopoiesis by inducing the cellular expression of hematopoietic growth factors.

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Morinaga, Ryota, Takashi Kawahara, Shinnosuke Kuroda, Yoshiaki Inayama, and Hiroji Uemura. "Granulocyte Colony-Stimulating Factor-Producing Bladder Cancer." Case Reports in Oncology 12, no. 2 (August 6, 2019): 603–7. http://dx.doi.org/10.1159/000502174.

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Granulocyte colony-stimulating factor (G-CSF)-producing bladder cancer is rare, with only 75 cases reported in Japan. A 67-year-old woman was referred to our institution for the further examination of gross hematuria. Cystoscopy revealed a 7-cm bladder tumor. The initial white blood cell count was 17,100/μL, and a transurethral resected specimen showed G-CSF expression. CT revealed that the tumor had invaded the colon. As the patient had uncontrollable schizophrenia, radical cystectomy was abandoned. We herein report a case of G-CSF-producing bladder tumor.

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Paszko-Patej, G., D. Sienkiewicz, B. Okurowska-Zawada, and W. Kułak. "Granulocyte colony-stimulating factor potential use in the treatment of children with cerebral palsy." Progress in Health Sciences 7, no. 1 (May 19, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.1882.

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Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the blood. Recent studies demonstrated the presence of CSF-receptor (G-CSFR) system in the brain and spinal cord, and their roles in neuroprotection and neural tissue repair, as well as improvement in functional recovery. G-CSF exerts neuroprotective actions through the inhibition of apoptosis and inflammation, and the stimulation of neurogenesis. This review highlights recent studies on the potential use of G-CSF in cerebral palsy.

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Chakraborty, Arup, Eric R. Hentzen, Scott M. Seo, and C. Wayne Smith. "Granulocyte colony-stimulating factor promotes adhesion of neutrophils." American Journal of Physiology-Cell Physiology 284, no. 1 (January 1, 2003): C103—C110. http://dx.doi.org/10.1152/ajpcell.00165.2002.

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Granulocyte colony stimulating factor (G-CSF) is well known for its ability to drive the maturation and mobilization of neutrophils. G-CSF also appears to have the potential to activate functions of mature neutrophils, influencing recruitment at sites of inflammation and tissue injury. We investigated the ability of G-CSF to stimulate adhesion of isolated blood neutrophils. G-CSF induced significant adherence to intercellular adhesion molecule (ICAM)-1 that was both macrophage antigen-1 (Mac-1) and leukocyte function-associated antigen-1 dependent. The kinetics of G-CSF-stimulated adhesion to ICAM-1 peaked at 11 min without detectable surface upregulation of Mac-1. This was in marked contrast to chemokines, in which peak activation of adhesion is seen within 1 min of stimulation. In contrast to chemokine-induced adhesion, G-CSF stimulation was not inhibited by pertussis toxin. G-CSF also augmented the attachment of neutrophils to activated human umbilical vein endothelial cells (HUVEC) through specific effects on neutrophils, because HUVEC appear to lack functional G-CSF receptors.

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Kitching, A. Richard, Xiao Ru Huang, Amanda L. Turner, Peter G. Tipping, Ashley R. Dunn, and Stephen R. Holdsworth. "The Requirement for Granulocyte-Macrophage Colony-Stimulating Factor and Granulocyte Colony-Stimulating Factor in Leukocyte-Mediated Immune Glomerular Injury." Journal of the American Society of Nephrology 13, no. 2 (February 2002): 350–58. http://dx.doi.org/10.1681/asn.v132350.

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ABSTRACT. Proliferative glomerulonephritis in humans is characterized by the presence of leukocytes in glomeruli. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) can potentially stimulate or affect T cell, macrophage, and neutrophil function. To define the roles of GM-CSF and G-CSF in leukocyte-mediated glomerulonephritis, glomerular injury was studied in mice genetically deficient in either GM-CSF (GM-CSF −/− mice) or G-CSF (G-CSF −/− mice). Two models of glomerulonephritis were studied: neutrophil-mediated heterologous-phase anti-glomerular basement membrane (GBM) glomerulonephritis and T cell/macrophage-mediated crescentic autologous-phase anti-GBM glomerulonephritis. Both GM-CSF −/− and G-CSF −/− mice were protected from heterologous-phase anti-GBM glomerulonephritis compared with genetically normal (CSF WT) mice, with reduced proteinuria and glomerular neutrophil numbers. However, only GM-CSF −/− mice were protected from crescentic glomerular injury in the autologous phase, whereas G-CSF −/− mice were not protected and in fact had increased numbers of T cells in glomeruli. Humoral responses to the nephritogenic antigen were unaltered by deficiency of either GM-CSF or G-CSF, but glomerular T cell and macrophage numbers, as well as dermal delayed-type hypersensitivity to the nephritogenic antigen, were reduced in GM-CSF −/− mice. These studies demonstrate that endogenous GM-CSF plays a role in experimental glomerulonephritis in both the autologous and heterologous phases of injury.

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Broudy, V. C., K. Kaushansky, J. M. Harlan, and J. W. Adamson. "Interleukin 1 stimulates human endothelial cells to produce granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor." Journal of Immunology 139, no. 2 (July 15, 1987): 464–68. http://dx.doi.org/10.4049/jimmunol.139.2.464.

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Abstract Endothelial cells are a potent source of hematopoietic growth factors when stimulated by soluble products of monocytes. Interleukin 1 (IL 1) is released by activated monocytes and is a mediator of the inflammatory response. We determined whether purified recombinant human IL 1 could stimulate cultured human umbilical vein endothelial cells to release hematopoietic growth factors. As little as 1 U/ml of IL 1 stimulated growth factor production by the endothelial cells, and increasing amounts of IL 1 enhanced growth factor production in a dose-dependent manner. Growth factor production increased within 2 to 4 hr and remained elevated for more than 48 hr. To investigate the molecular basis for these findings, oligonucleotide probes for granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), and multi-CSF were hybridized to poly(A)-containing RNA prepared from unstimulated and IL 1-stimulated endothelial cells. Significant levels of GM-CSF and G-CSF, but not M-CSF or multi-CSF, mRNA were detected in the IL 1-stimulated endothelial cells. Biological assays performed on the IL 1-stimulated endothelial cell-conditioned medium confirmed the presence of both GM- and G-CSF. These results demonstrate that human recombinant IL 1 can stimulate endothelial cells to release GM-CSF and G-CSF, and provide a mechanism by which IL 1 could modulate both granulocyte production and function during the course of an inflammatory response.

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Suzumura, Kazuhiro, Yuji Iimuro, Tadamichi Hirano, Yasukane Asano, Nobukazu Kuroda, Toshihiro Okada, Shogo Tanaka, Keiji Nakasho, and Jiro Fujimoto. "Granulocyte Colony-Stimulating Factor–Producing Cholangiocellular Carcinoma." International Surgery 100, no. 1 (January 1, 2015): 123–27. http://dx.doi.org/10.9738/intsurg-d-13-00183.1.

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Abstract A 61-year-old female was admitted to our hospital with epigastric pain and fever. The laboratory data showed severe inflammatory reactions. Computed tomography revealed an irregular tumor in the left hepatic lobe and swelling of lymph nodes. 18F-fluorodeoxy-glucose positron emission tomography (FDG-PET) showed high uptake by the tumor, with diffuse uptake in the spine. Based on the elevated leukocyte count and FDG-PET findings, the patient was diagnosed with a granulocyte colony-stimulating factor (G-CSF)-producing tumor (G-CSF, 213 pg/mL). We performed left trisegmentectomy of the liver, bile duct resection, and lymph node dissection. Histologically, the tumor was a poorly differentiated adenocarcinoma with some lymph nodes metastasis. Immunohistochemical staining of the tumor cells was positive for G-CSF. Therefore, the tumor was diagnosed as G-CSF–producing cholangiocellular carcinoma. The inflammatory reactions and serum G-CSF level transiently improved immediately after surgery. However, 1 month later, the leukocyte count and serum G-CSF level increased again, and recurrence was observed in the remnant liver. The patient died 3 months after the operation. G-CSF–producing cholangiocellular carcinoma is rare. This tumor progresses rapidly, and surgical treatment for advanced condition should be carefully selected.

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Raynor, B. Denise, Penny Clark, and Patrick Duff. "Granulocyte Colony-Stimulating Factor in Amniotic Fluid." Infectious Diseases in Obstetrics and Gynecology 3, no. 4 (1995): 140–44. http://dx.doi.org/10.1155/s1064744995000482.

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Objective: The purpose of this study was to determine if granulocyte colony-stimulating factor (G-CSF) is normally present in amniotic fluid and then to determine if amniotic-fluid G-CSF levels are affected by labor and intrauterine infection.Methods: Amniotic fluid was collected from 35 patients in 4 groups: no labor, early labor, late labor, and labor plus chorioamnionitis. G-CSF levels were measured by enzyme-linked immunosorbent assay (ELISA).Results: The mean amniotic-fluid G-CSF concentrations prior to labor were lower than during labor (0.49 ± 0.25 ng/ml for prior to labor vs. 1.83 ± 1.0 ng/ml for labor, P < 0.001). With chorioamnionitis, the mean levels were elevated compared with normal labor (25.0 ± 4.8 ng/ml for chorioamnionitis vs. 1.83 ± 1.0 ng/ml for normal labor, P < 0.0001). In early and late labor, G-CSF was higher than prior to labor (0.49 ± 0.25 ng/ml for no labor vs. 1.48 ± 1.0 ng/ml for early labor, P < 0.02, vs. 2.2 ± 0.8 ng/ml for late labor, P < 0.0005). The mean concentrations in early and late labor were not different.Conclusions: G-CSF is present in amniotic fluid and increased with labor. When labor is complicated by chorioamnionitis, G-CSF is significantly elevated.

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Suzumura, Kazuhiro, Yuji Iimuro, Yasukane Asano, Nobukazu Kuroda, Tadamichi Hirano, Junichi Yamanaka, Toshihiro Okada, Tomohiro Okamoto, Ikuko Torii, and Jiro Fujimoto. "Granulocyte-Colony Stimulating Factor–Producing Gallbladder Carcinoma." International Surgery 99, no. 5 (September 1, 2014): 577–83. http://dx.doi.org/10.9738/intsurg-d-13-00129.1.

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Abstract A 78-year-old man was admitted to our hospital with right upper abdominal pain and fever. His general condition was poor. The laboratory data showed severe inflammatory reactions. Computed tomography revealed an irregular tumor in the gallbladder. 18F-fluorodeoxy-glucose positron emission tomography (FDG-PET) showed high uptake by the tumor, with diffuse uptake in the spine. Based on the elevated leukocyte count and FDG-PET findings, a granulocyte-colony stimulating factor (G-CSF)–producing tumor was diagnosed (G-CSF 120 pg/mL). We performed cholecystectomy with central bisegmentectomy of the liver, lymph node dissection and right hemicolectomy. Histologically, the tumor was an adenosquamous cell carcinoma of the gallbladder. Immunohistochemical staining of the tumor cells was positive for G-CSF. Postoperatively, the general condition of the patient was improved. The fever subsided, the leukocyte count and serum G-CSF level normalized, and FDG-PET showed no uptake in the spine postoperatively. The patient showed no signs of recurrence at 27 months after undergoing surgery. FDG-PET is a useful method for diagnosing G-CSF–producing gallbladder carcinoma. Aggressive curative resection for G-CSF–producing gallbladder carcinoma may improve patients' general condition and prognosis.

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Budel, LM, IP Touw, R. Delwel, and B. Lowenberg. "Granulocyte colony-stimulating factor receptors in human acute myelocytic leukemia." Blood 74, no. 8 (December 1, 1989): 2668–73. http://dx.doi.org/10.1182/blood.v74.8.2668.2668.

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Abstract The binding of granulocyte colony-stimulating factor (G-CSF) to normal and human acute myeloid leukemia (AML) cells was investigated with radiolabeled recombinant human G-CSF (rhG-CSF). In all 14 cases of primary AML specific receptors for G-CSF were demonstrated on purified blast cells. The average numbers of G-CSF receptors ranged from very low to 428 receptors per cell (mean). Normal granulocytes showed G-CSF binding sites on their surface at higher densities (703 to 1,296 sites per cell). G-CSF receptors appeared to be of a single affinity type with a dissociation constant (kd) ranging between 214 and 378 pmol/L for AML blasts and 405 to 648 pmol/L for granulocytes. In 12 of 14 cases, including those with relatively low specific binding, G-CSF was a potent inducer of DNA synthesis of blasts in vitro; therefore, apparently relatively few receptors are required to permit activation of AML cell growth. However, in two cases cell cycling was not activated in response to G-CSF despite G-CSF receptor availability. The results show that G-CSF receptors of high affinity are frequently expressed on the blasts of human AML, but their presence may not be a strict indicator of the proliferative responsiveness of the cells to G- CSF.

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Budel, LM, IP Touw, R. Delwel, and B. Lowenberg. "Granulocyte colony-stimulating factor receptors in human acute myelocytic leukemia." Blood 74, no. 8 (December 1, 1989): 2668–73. http://dx.doi.org/10.1182/blood.v74.8.2668.bloodjournal7482668.

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The binding of granulocyte colony-stimulating factor (G-CSF) to normal and human acute myeloid leukemia (AML) cells was investigated with radiolabeled recombinant human G-CSF (rhG-CSF). In all 14 cases of primary AML specific receptors for G-CSF were demonstrated on purified blast cells. The average numbers of G-CSF receptors ranged from very low to 428 receptors per cell (mean). Normal granulocytes showed G-CSF binding sites on their surface at higher densities (703 to 1,296 sites per cell). G-CSF receptors appeared to be of a single affinity type with a dissociation constant (kd) ranging between 214 and 378 pmol/L for AML blasts and 405 to 648 pmol/L for granulocytes. In 12 of 14 cases, including those with relatively low specific binding, G-CSF was a potent inducer of DNA synthesis of blasts in vitro; therefore, apparently relatively few receptors are required to permit activation of AML cell growth. However, in two cases cell cycling was not activated in response to G-CSF despite G-CSF receptor availability. The results show that G-CSF receptors of high affinity are frequently expressed on the blasts of human AML, but their presence may not be a strict indicator of the proliferative responsiveness of the cells to G- CSF.

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Nakajima, Hideaki, and James N. Ihle. "Granulocyte colony-stimulating factor regulates myeloid differentiation through CCAAT/enhancer-binding protein ε." Blood 98, no. 4 (August 15, 2001): 897–905. http://dx.doi.org/10.1182/blood.v98.4.897.h8000897_897_905.

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Granulocyte colony-stimulating factor (G-CSF) is a major cytokine that regulates proliferation and differentiation of myeloid cells, although the underlying mechanisms by which G-CSF controls myeloid differentiation are largely unknown. Differentiation of hematopoietic cells is regulated by lineage-specific transcription factors, and gene-targeting studies previously revealed the critical roles of CCAAT/enhancer-binding protein (C/EBP) α and C/EBPε, respectively, in the early and mid-late stages of granulocyte differentiation. The expression of C/EBPε in 32Dcl3 cells and FDCP1 cells expressing mutant G-CSF receptors was examined and it was found that G-CSF up-regulates C/EBPε. The signal for this expression required the region containing the first tyrosine residue of G-CSF receptor. Dominant-negative signal transducers and activators of transcription 3 blocked G-CSF–induced granulocytic differentiation in 32D cells but did not block induction of C/EBPε, indicating that these proteins work in different pathways. It was also found that overexpression of C/EBPε greatly facilitated granulocytic differentiation by G-CSF and, surprisingly, that expression of C/EBPε alone was sufficient to make cells differentiate into morphologically and functionally mature granulocytes. Overexpression of c-myc inhibits differentiation of hematopoietic cells, but the molecular mechanisms of this inhibition are not fully understood. In 32Dcl3 cells overexpressing c-myc that do not differentiate by means of G-CSF, induction of C/EBPε is completely abrogated. Ectopic expression of C/EBPε in these cells induced features of differentiation, including changes in nuclear morphologic characteristics and the appearance of granules. These data show that C/EBPε constitutes a rate-limiting step in G-CSF–regulated granulocyte differentiation and that c-myc antagonizes G-CSF–induced myeloid differentiation, at least partly by suppressing induction of C/EBPε.

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Bregni, M., S. Siena, M. Di Nicola, A. Dodero, F. Peccatori, F. Ravagnani, G. Danesini, A. Laffranchi, G. Bonadonna, and A. M. Gianni. "Comparative effects of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor after high-dose cyclophosphamide cancer therapy." Journal of Clinical Oncology 14, no. 2 (February 1996): 628–35. http://dx.doi.org/10.1200/jco.1996.14.2.628.

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PURPOSE We compared hematologic and clinical effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) after treatment with high-dose cyclophosphamide (HD-CTX, 7 g/m2), given as the first phase of a high-dose sequential chemotherapy program that includes a myeloablative therapy with mobilized progenitor cell autografting. PATIENTS AND METHODS Forty-nine consecutive patients with non-Hodgkin's lymphoma, Hodgkin's disease, or poor-prognosis breast cancer received GM-CSF (n = 27) or G-CSF (n = 22) after HD-CTX in two consecutive, nonrandomized studies. Cytokines were administered in continuous intravenous (i.v.) infusion for 14 to 15 days at a median dose of 5.5 and 10 micrograms/kg/d, respectively, starting 24 hours after HD-CTX. RESULTS Neutrophil recovery was faster with G-CSF administration (11.5 v 13.2 days; P = .01), whereas platelet counts recovered more rapidly with GM-CSF (13.7 v 16.6 days; P = .01). Prophylactic platelet transfusions were administered more frequently to patients treated with G-CSF than with GM-CSF (66% v 22% of the patients; P = .02). No clinically significant difference was observed between the two groups concerning days of absolute neutropenia or neutropenic fever. Both cytokines reduced the time to eligibility for subsequent chemotherapy administration compared with historical controls not given cytokine (14 to 16 v 20 days). Both cytokines increased circulation of hematopoietic progenitors. Most side effects were World Health Organization (WHO) median grade 1 to 2, were more frequent during GM-CSF than during G-CSF treatment, and were reversible by simple supportive measures and/or by dose reduction or suspension of the cytokine. Permanent suspension of cytokine administration was never required in either group. CONCLUSION GM-CSF or G-CSF administration after HD-CTX reduces hematologic toxicity of high-dose chemotherapy and induces circulation of large amounts of hematopoietic progenitors suitable for autografting in cancer patients.

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Takahama, Hideto, Rie Itoh, Chiyuki Inoue-Komatsu, Shuichi Furusawa, Hisashi Takahashi, and Masako Mizoguchi. "Granulocyte Colony-Stimulating Factor (G-CSF) and Granulocyte Macrophage Colony-Stimulating Factor (GM-CSF) in Behçet's Disease." Journal of Dermatology 21, no. 8 (August 1994): 546–52. http://dx.doi.org/10.1111/j.1346-8138.1994.tb01792.x.

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Ferrero, D., C. Tarella, R. Badoni, D. Caracciolo, G. Bellone, A. Pileri, and E. Gallo. "Granulocyte-macrophage colony-stimulating factor requires interaction with accessory cells or granulocyte-colony stimulating factor for full stimulation of human myeloid progenitors." Blood 73, no. 2 (February 1, 1989): 402–5. http://dx.doi.org/10.1182/blood.v73.2.402.402.

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Abstract Human recombinant GM-CSF (rGM-CSF) was tested on highly purified and fractionated CFU-GM subsets. The fractionation was performed with the DS1–1 monoclonal antibody (MoAb), which distinguishes early and late CFU-GM. On whole bone marrow cells, rGM-CSF had a colony-stimulating activity comparable to that of known sources of CSFs, ie, the supernatant (SN) of TPA 30–1 or 5637 cell lines, used as control. A greatly reduced activity was observed when CFU-GM were depleted of phagocytizing and E rosetting cells (colony growth of 27% as compared with control). On fractionated CFU-GM, the rGM-CSF activity was even more reduced on both early and late progenitors (18% and 6% of colony growth, respectively). However, when rGM-CSF was used together with rG- CSF at suboptimal concentrations, the colony growth reached values analogous to that of control cultures. A synergistic interaction between rGM-CSF and rG-CSF in stimulating either early or late myeloid progenitors was observed. The results suggest that the activity of rGM- CSF on CFU-GM is mainly exerted through cooperation with accessory cells. r-G-CSF is one of the factors that can synergistically cooperate with r-GM-CSF in the myelopoietic stimulation.

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Ferrero, D., C. Tarella, R. Badoni, D. Caracciolo, G. Bellone, A. Pileri, and E. Gallo. "Granulocyte-macrophage colony-stimulating factor requires interaction with accessory cells or granulocyte-colony stimulating factor for full stimulation of human myeloid progenitors." Blood 73, no. 2 (February 1, 1989): 402–5. http://dx.doi.org/10.1182/blood.v73.2.402.bloodjournal732402.

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Human recombinant GM-CSF (rGM-CSF) was tested on highly purified and fractionated CFU-GM subsets. The fractionation was performed with the DS1–1 monoclonal antibody (MoAb), which distinguishes early and late CFU-GM. On whole bone marrow cells, rGM-CSF had a colony-stimulating activity comparable to that of known sources of CSFs, ie, the supernatant (SN) of TPA 30–1 or 5637 cell lines, used as control. A greatly reduced activity was observed when CFU-GM were depleted of phagocytizing and E rosetting cells (colony growth of 27% as compared with control). On fractionated CFU-GM, the rGM-CSF activity was even more reduced on both early and late progenitors (18% and 6% of colony growth, respectively). However, when rGM-CSF was used together with rG- CSF at suboptimal concentrations, the colony growth reached values analogous to that of control cultures. A synergistic interaction between rGM-CSF and rG-CSF in stimulating either early or late myeloid progenitors was observed. The results suggest that the activity of rGM- CSF on CFU-GM is mainly exerted through cooperation with accessory cells. r-G-CSF is one of the factors that can synergistically cooperate with r-GM-CSF in the myelopoietic stimulation.

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White, Scott M., Mark H. Alarcon, and David J. Tweardy. "Inhibition of granulocyte colony-stimulating factor–mediated myeloid maturation by low level expression of the differentiation-defective class IV granulocyte colony-stimulating factor receptor isoform." Blood 95, no. 11 (June 1, 2000): 3335–40. http://dx.doi.org/10.1182/blood.v95.11.3335.

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Abstract In acute myeloid leukemia (AML), granulocyte colony-stimulating factor receptor (G-CSFR) proliferative and maturational signaling pathways are uncoupled. Seven human G-CSFR mRNA isoforms exist, named class I through class VII. The 183-amino acid cytosolic domain of the class I isoform provides all signaling activities. The class IV isoform is “differentiation defective” because the carboxy-terminal 87 amino acids are replaced with 34 amino acids of novel sequence. In more than 50% of AML samples, the class IV/class I G-CSFR mRNA ratio is aberrantly elevated compared to normal CD34+ bone marrow cells. We hypothesized that the increased relative expression of class IV G-CSFR in AML uncouples proliferative and maturational G-CSFR signaling pathways. To test this, we transfected the G-CSF–responsive murine cell line 32Dcl3 with class IV G-CSFR cDNA. After 10 days of G-CSF stimulation, clones expressing class IV G-CSFR had greater percentages of myeloblasts and promyelocytes than controls (53% ± 13% versus 3% ± 2%). Differential counts over time demonstrated delayed G-CSF–driven maturation in 5 class IV-expressing clones, with 2 clones demonstrating a subpopulation that completely failed to differentiate. Heterologous class IV expression did not affect G-CSF–dependent proliferation. Class IV/murine G-CSFR mRNA ratios after 24 hours of G-CSF stimulation for 3 of the 5 clones (range, 0.090 to 0.245; mean, 0.152 ± 0.055) are within the range of class IV/class I mRNA ratios seen in patients with AML. This indicates that aberrantly increased relative class IV G-CSFR expression seen in AML can uncouple G-CSFR proliferative and maturational signaling pathways.

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White, Scott M., Mark H. Alarcon, and David J. Tweardy. "Inhibition of granulocyte colony-stimulating factor–mediated myeloid maturation by low level expression of the differentiation-defective class IV granulocyte colony-stimulating factor receptor isoform." Blood 95, no. 11 (June 1, 2000): 3335–40. http://dx.doi.org/10.1182/blood.v95.11.3335.011k23_3335_3340.

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In acute myeloid leukemia (AML), granulocyte colony-stimulating factor receptor (G-CSFR) proliferative and maturational signaling pathways are uncoupled. Seven human G-CSFR mRNA isoforms exist, named class I through class VII. The 183-amino acid cytosolic domain of the class I isoform provides all signaling activities. The class IV isoform is “differentiation defective” because the carboxy-terminal 87 amino acids are replaced with 34 amino acids of novel sequence. In more than 50% of AML samples, the class IV/class I G-CSFR mRNA ratio is aberrantly elevated compared to normal CD34+ bone marrow cells. We hypothesized that the increased relative expression of class IV G-CSFR in AML uncouples proliferative and maturational G-CSFR signaling pathways. To test this, we transfected the G-CSF–responsive murine cell line 32Dcl3 with class IV G-CSFR cDNA. After 10 days of G-CSF stimulation, clones expressing class IV G-CSFR had greater percentages of myeloblasts and promyelocytes than controls (53% ± 13% versus 3% ± 2%). Differential counts over time demonstrated delayed G-CSF–driven maturation in 5 class IV-expressing clones, with 2 clones demonstrating a subpopulation that completely failed to differentiate. Heterologous class IV expression did not affect G-CSF–dependent proliferation. Class IV/murine G-CSFR mRNA ratios after 24 hours of G-CSF stimulation for 3 of the 5 clones (range, 0.090 to 0.245; mean, 0.152 ± 0.055) are within the range of class IV/class I mRNA ratios seen in patients with AML. This indicates that aberrantly increased relative class IV G-CSFR expression seen in AML can uncouple G-CSFR proliferative and maturational signaling pathways.

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Tian, SS, P. Lamb, HM Seidel, RB Stein, and J. Rosen. "Rapid activation of the STAT3 transcription factor by granulocyte colony-stimulating factor." Blood 84, no. 6 (September 15, 1994): 1760–64. http://dx.doi.org/10.1182/blood.v84.6.1760.1760.

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Abstract Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates proliferation and differentiation of progenitor cells of neutrophils by signaling through its receptor (G-CSFR). Although the G- CSFR belongs to the cytokine receptor superfamily, which lacks an intracellular kinase domain, G-CSF-induced tyrosine phosphorylation of cellular proteins is critical for its biologic activities. We report here that JAK1 and JAK2 tyrosine kinases are tyrosine phosphorylated in response to G-CSF induction. We also demonstrate that the DNA-binding protein STAT3 (also called the acute-phase response factor [APRF], activated by interleukin-6) is an early target of G-CSF-induced tyrosine phosphorylation. G-CSF induces two DNA-binding complexes; the major complex contains tyrosine phosphorylated STAT3 protein and the minor complex appears to be a heterodimer of the STAT1 (previously p91, a component of DNA-binding complexes activated by interferons) and STAT3 proteins. Antiphosphotyrosine antibody interferes with the DNA binding activity of activated STAT3, indicating that tyrosine phosphorylation of STAT3 is important for the DNA binding activity. These results identify a signal transduction pathway activated in response to G-CSF and provide a mechanism for the rapid modulation of gene expression by G-CSF.

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Tian, SS, P. Lamb, HM Seidel, RB Stein, and J. Rosen. "Rapid activation of the STAT3 transcription factor by granulocyte colony-stimulating factor." Blood 84, no. 6 (September 15, 1994): 1760–64. http://dx.doi.org/10.1182/blood.v84.6.1760.bloodjournal8461760.

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Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates proliferation and differentiation of progenitor cells of neutrophils by signaling through its receptor (G-CSFR). Although the G- CSFR belongs to the cytokine receptor superfamily, which lacks an intracellular kinase domain, G-CSF-induced tyrosine phosphorylation of cellular proteins is critical for its biologic activities. We report here that JAK1 and JAK2 tyrosine kinases are tyrosine phosphorylated in response to G-CSF induction. We also demonstrate that the DNA-binding protein STAT3 (also called the acute-phase response factor [APRF], activated by interleukin-6) is an early target of G-CSF-induced tyrosine phosphorylation. G-CSF induces two DNA-binding complexes; the major complex contains tyrosine phosphorylated STAT3 protein and the minor complex appears to be a heterodimer of the STAT1 (previously p91, a component of DNA-binding complexes activated by interferons) and STAT3 proteins. Antiphosphotyrosine antibody interferes with the DNA binding activity of activated STAT3, indicating that tyrosine phosphorylation of STAT3 is important for the DNA binding activity. These results identify a signal transduction pathway activated in response to G-CSF and provide a mechanism for the rapid modulation of gene expression by G-CSF.

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26

Takahashi, Momoko, Chihiro Kondoh, and Toshimi Takano. "The history of Granulocyte-colony stimulating factor." Drug Delivery System 32, no. 2 (2017): 134–42. http://dx.doi.org/10.2745/dds.32.134.

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27

Chung, Joonho, Moon Hang Kim, Yong Je Yoon, Kil Hwan Kim, So Ra Park, and Byung Hyune Choi. "Effects of granulocyte colony–stimulating factor and granulocyte-macrophage colony–stimulating factor on glial scar formation after spinal cord injury in rats." Journal of Neurosurgery: Spine 21, no. 6 (December 2014): 966–73. http://dx.doi.org/10.3171/2014.8.spine131090.

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Object This study investigated the effects of granulocyte colony–stimulating factor (G-CSF) on glial scar formation after spinal cord injury (SCI) in rats and compared the therapeutic effects between G-CSF and granulocytemacrophage colony–stimulating factor (GM-CSF) to evaluate G-CSF as a potential substitute for GM-CSF in clinical application. Methods Rats were randomly assigned to 1 of 4 groups: a sham-operated group (Group 1), an SCI group without treatment (Group 2), an SCI group treated with G-CSF (Group 3), and an SCI group treated with GM-CSF (Group 4). G-CSF and GM-CSF were administered via intraperitoneal injection immediately after SCI. The effects of G-CSF and GM-CSF on functional recovery, glial scar formation, and axonal regeneration were evaluated and compared. Results The rats in Groups 3 and 4 showed better functional recovery and more decreased cavity sizes than those in Group 2 (p < 0.05). Both G-CSF and GM-CSF suppressed intensive expression of glial fibrillary acidic protein around the cavity at 4 weeks and reduced the expression of chondroitin sulfate proteoglycans (p < 0.05). Also, early administration of G-CSF and GM-CSF protected axon fibers from destructive injury and facilitated axonal regeneration. There were no significant differences in comparisons of functional recovery, glial scar formation, and axonal regeneration between G-CSF and GM-CSF. Conclusions G-CSF suppressed glial scar formation after SCI in rats, possibly by restricting the expression of glial fibrillary acidic protein and chondroitin sulfate proteoglycans, which might facilitate functional recovery from SCI. GM-CSF and G-CSF had similar effects on glial scar formation and functional recovery after SCI, suggesting that G-CSF can potentially be substituted for GM-CSF in the treatment of SCI.

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Corcione, A., MV Corrias, S. Daniele, S. Zupo, M. Spriano, and V. Pistoia. "Expression of granulocyte colony-stimulating factor and granulocyte colony-stimulating factor receptor genes in partially overlapping monoclonal B-cell populations from chronic lymphocytic leukemia patients." Blood 87, no. 7 (April 1, 1996): 2861–69. http://dx.doi.org/10.1182/blood.v87.7.2861.bloodjournal8772861.

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B lymphocytes were purified from the peripheral blood of 30 B-cell chronic lymphocytic leukemia (B-CLL) patients and tested for the ability to produce granulocyte colony-stimulating factor (G-CSF) in vitro. Fifteen Staphylococcus aureus Cowan I (SAC)-stimulated, but not unstimulated, B-cell suspensions produced G-CSF in short-term cultures. Accordingly, G-CSF mRNA was detected only in SAC-stimulated B cells. Five CLL B-cell fractions that released G-CSF following exposure to SAC were also incubated with CD40 or anti-mu antibodies in the presence or absence of recombinant (r) interleukin-2 (IL-2) or IL-4. The 5 cell suspensions produced G-CSF only on culture with CD40 monoclonal antibody in combination with rIL-2 or rIL-4. CD5+ B lymphocytes, which represent the normal counterparts of most B-CLL proliferations, did not produce G-CSF under any of the above culture conditions. G-CSF produced by leukemic B lymphocytes was biologically active, because conditioned media of SAC-stimulated cells supported the in vitro growth of myeloid colonies from normal bone marrow progenitors. The colony stimulating activity of CLL B-cell supernatants was ascribed to both G-CSF and granulocyte-macrophage colony stimulating factor. G-CSF receptors (G- CSFRs) were detected on freshly isolated B lymphocytes from 7 of 11 B- CLL patients; 5 of these cell suspensions produced G-CSF in culture, whereas 2 did not. rG-CSF rescued 3 of the 7 G-CSFR+ cell fractions from spontaneous apoptosis but had no effect on their in vitro proliferation.

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Barber, K. E., P. S. Crosier, and J. D. Watson. "The differential inhibition of hemopoietic growth factor activity by cytotoxins and interferon-gamma." Journal of Immunology 139, no. 4 (August 15, 1987): 1108–12. http://dx.doi.org/10.4049/jimmunol.139.4.1108.

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Abstract The effects of recombinant human tumor necrosis factor (TNF), lymphotoxin (LT), and interferon-gamma (IFN-gamma) on the growth of human hemopoietic progenitor cells in clonal culture have been examined. Colony growth was induced by using granulocyte colony-stimulating factor (G-CSF), or granulocyte-macrophage colony-stimulating factor (GM-CSF). A suppressive effect of TNF, LT, and IFN-gamma on the development of granulocyte, macrophage, and mixed granulocyte/macrophage colonies was shown. Suppression of colonies formed after stimulation with G-CSF was greater than that observed after stimulation with GM-CSF. In the presence of a monoclonal antibody to TNF, or polyclonal antibodies to either LT or IFN-gamma, the inhibitory effect of the molecule to which the antibody was directed was abrogated. These findings suggest that progenitor cells responsive to G-CSF or GM-CSF have different sensitivities to the effects of TNF, LT, and IFN-gamma. Defining the interactions of growth factors and inhibitors should increase understanding of mechanisms underlying diseases associated with suppression of normal hemopoiesis, and in predicting the effects in vivo of these bioregulatory molecules in clinical medicine.

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Uemura, Yoshiki, Makoto Kobayashi, Hideshi Nakata, Tetsuya Kubota, and Hirokuni Taguchi. "Role of Protein Kinase C in Expression of Granulocyte Colony Stimulating Factor and Granulocyte-Macrophage Colony Stimulating Factor in Lung Cancer Cells." Blood 104, no. 11 (November 16, 2004): 4210. http://dx.doi.org/10.1182/blood.v104.11.4210.4210.

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Abstract Many cases of tumors that produce granulocyte-colony stimulating factor (G-CSF) or granulocyte macrophage-colony stimulating factor (GM-CSF) have been reported. However, the biological properties regulatory mechanisms of the overproduction of G-CSFor GM-CSF by tumor cells are not well known. We present the role of protein kinase C (PKC) pathways in the constitutive expression of G-CSF and GM-CSF by lung cancer cells. We previously established two lung cancer cell lines, OKa-C-1 and MI-4, that constitutively produce an abundant dose of G-CSF and GM-CSF. We showed that the PKC activator; phorbol 12-myristate 13-acetate (PMA) stimulated the production of GM-CSF in a dose-dependent manner and inversely reduced G-CSF in the cell lines. These effects of PMA were antagonized by PKC inhibitor; staurosporine. The induction of GM-CSF expression by PMA was mediated through the activations of nuclear factor (NF)-kB activation. The induction of G-CSF expression by staurosporine was mediated through p44/42 mitogen-activated protein kinase (MAPK) pathway signaling. PMA accelerated cell growth and inhibited cell death in the cell line. Whereas staurosporine acted inversely. GM-CSF induced by PMA might stimulate cell growth and suppress cell death. G-CSF expression by staurosporine appears to be related to the activation of p44/42 MAPK, and GM-CSF by PMA to NF-kB in OKa-C-1 and MI-4 cells. Figure Figure

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31

Villunger, Andreas, Lorraine A. O'Reilly, Nils Holler, Jerry Adams, and Andreas Strasser. "FAS Ligand, Bcl-2, Granulocyte Colony-Stimulating Factor, and p38 Mitogen-Activated Protein Kinase." Journal of Experimental Medicine 192, no. 5 (August 28, 2000): 647–58. http://dx.doi.org/10.1084/jem.192.5.647.

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The short life span of granulocytes, which limits many inflammatory responses, is thought to be influenced by the Bcl-2 protein family, death receptors such as CD95 (Fas/APO-1), stress-activated protein kinases such as p38 mitogen-activated protein kinase (MAPK), and proinflammatory cytokines like granulocyte colony-stimulating factor (G-CSF). To clarify the roles of these various regulators in granulocyte survival, we have investigated the spontaneous apoptosis of granulocytes in culture and that induced by Fas ligand or chemotherapeutic drugs, using cells from normal, CD95-deficient lpr, or vav-bcl-2 transgenic mice. CD95-induced apoptosis, which required receptor aggregation by recombinant Fas ligand or the membrane-bound ligand, was unaffected by G-CSF treatment or Bcl-2 overexpression. Conversely, spontaneous and drug-induced apoptosis occurred normally in lpr granulocytes but were suppressed by G-CSF treatment or Bcl-2 overexpression. Although activation of p38 MAPK has been implicated in granulocyte death, their apoptosis actually was markedly accelerated by specific inhibitors of this kinase. These results suggest that G-CSF promotes granulocyte survival largely through the Bcl-2–controlled pathway, whereas CD95 regulates a distinct pathway to apoptosis that is not required for either their spontaneous or drug-induced death. Moreover, p38 MAPK signaling contributes to granulocyte survival rather than their apoptosis.

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Akiyama, Akihito, Yuhei Ohkubo, Fumihiko Hokoishi, Takaaki Ito, Akira Tsuchiya, and Hiroshi Kusama. "BLADDER CARCINOMA PRODUCTING GRANULOCYTE COLONY STIMULATING FACTOR (G-CSF)." Japanese Journal of Urology 85, no. 7 (1994): 1135–38. http://dx.doi.org/10.5980/jpnjurol1989.85.1135.

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33

Oster, W., A. Lindemann, R. Mertelsmann, and F. Herrmann. "Granulocyte-macrophage colony-stimulating factor (CSF) and multilineage CSF recruit human monocytes to express granulocyte CSF." Blood 73, no. 1 (January 1, 1989): 64–67. http://dx.doi.org/10.1182/blood.v73.1.64.64.

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Abstract We assessed the capacity of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) and multilineage (Multi)-CSF to induce release of granulocyte-CSF (G-CSF) by highly purified peripheral blood monocyte (Mo) preparations. Our results reveal that GM-CSF and Multi-CSF, either alone or in a synergistic concert, activate Mo to transcribe G-CSF messenger (m) RNA and release biologically active G- CSF protein into their culture supernatants. G-CSF had no regulatory effect on Mo expression of cytoplasmic G-CSF mRNA levels and G-CSF protein secretion by itself. These differential actions of CSFs provide further insight into self-regulatory mechanisms within the growth factor hierarchy system.

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Oster, W., A. Lindemann, R. Mertelsmann, and F. Herrmann. "Granulocyte-macrophage colony-stimulating factor (CSF) and multilineage CSF recruit human monocytes to express granulocyte CSF." Blood 73, no. 1 (January 1, 1989): 64–67. http://dx.doi.org/10.1182/blood.v73.1.64.bloodjournal73164.

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We assessed the capacity of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) and multilineage (Multi)-CSF to induce release of granulocyte-CSF (G-CSF) by highly purified peripheral blood monocyte (Mo) preparations. Our results reveal that GM-CSF and Multi-CSF, either alone or in a synergistic concert, activate Mo to transcribe G-CSF messenger (m) RNA and release biologically active G- CSF protein into their culture supernatants. G-CSF had no regulatory effect on Mo expression of cytoplasmic G-CSF mRNA levels and G-CSF protein secretion by itself. These differential actions of CSFs provide further insight into self-regulatory mechanisms within the growth factor hierarchy system.

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35

Shetty, Pradnya Devdas, Nikita Lad, Pallavi Vishwekar, and Mamta Vijay Shivtare. "Granulocyte colony stimulating factor in COS-IUI cycles." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 8, no. 4 (March 26, 2019): 1463. http://dx.doi.org/10.18203/2320-1770.ijrcog20191200.

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Background: An unresolved assisted reproductive technique problem is the unresponsive, thin endometrium. Approximately 0.6%-0.8% of patients do not reach the minimum thickness. Using endometrial co culture, G-CSF>130pg/mL was associated with significantly improved pregnancy rate in ART cycles. This is a retrospective study that included all unexplained infertility cycles with controlled ovulation stimulation –IUI protocols. Aim was to note the effects of G-CSF on thin endometrium and pregnancy rate in G-CSF administered COS-IUI cycles.Methods: This study was done in the IVF department of Dr D Y Patil University, Navi Mumbai, India. Thin endometrium was defined as ET<7mm on transvaginal ultrasound. Clomiphene citrate was used for ovulation induction in strengths of 100mg or 50mg on day 2 of their cycle based on the antral follicle count. Trigger used was injection 10,000µg urinary hCG. On the same day when the trigger injection was given, 300 units G-CSF was instilled into the uterus. Post 36 hours IUI was done under aseptic precautions .After 16 days β-hCG levels were done to determine whether there is a pregnancy.Results: In present study,200 COS-IUI cycles were analysed.50 cycles showed a thin endometrium and in them G-CSF was used. The chemical pregnancy rates was 32%, the intrauterine pregnancy rate was 28%, ectopic pregnancy rate was 4%.Conclusions: Present study concluded that G-CSF increases ET significantly in COS-IUI cycles in the event of thin endometrium. In view of small cohort size further larger randomized controlled trials may be required to substantiate the above conclusions.

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Lee, MY, K. Kaushansky, SA Judkins, JL Lottsfeldt, A. Waheed, and RK Shadduck. "Mechanisms of tumor-induced neutrophilia: constitutive production of colony-stimulating factors and their synergistic actions." Blood 74, no. 1 (July 1, 1989): 115–22. http://dx.doi.org/10.1182/blood.v74.1.115.115.

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Abstract Transplantation of a murine mammary carcinoma (CE maca) into mice induces marked granulocytosis and hypercalcemia secondary to excessive bone resorption. Such responses are not induced by another murine mammary carcinoma Bc66. In order to understand the mechanisms of these unique phenomena, we analyzed mRNA of tumor cells for expression of murine granulopoietic growth factors and studied interactions of tumor- derived factors using antiserum to a growth factor in vitro and in vivo. The Northern blot analysis of CE tumor clones revealed the expression of granulocyte colony stimulating factor (G-CSF) and macrophage colony stimulating factor (M-CSF), but no other CSF genes, while the Bc66 clone expressed only M-CSF. The G-CSF and M-CSF gene expression in CE tumor clones was accompanied by secretion of these proteins in culture. The granulocyte stimulating activity of CE tumor- derived G-CSF or recombinant human G-CSF was markedly enhanced by purified M-CSF in vitro. Significant but variable neutrophilia was observed in mice inoculated with CE tumor clones. Anti-M-CSF treatment of CE tumor-bearing mice significantly reduced neutrophilia, but did not affect hypercalcemia. These studies document that G-CSF and M-CSF are produced constitutively from the CE maca, and G-CSF is likely responsible for granulocytosis induced by this tumor. G-CSF and M-CSF function synergistically in granulocyte stimulation in vitro and this synergism may also play a role in marked granulocytosis of tumor- bearing animals, providing further evidence of the effect of CSFs in vivo.

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Lee, MY, K. Kaushansky, SA Judkins, JL Lottsfeldt, A. Waheed, and RK Shadduck. "Mechanisms of tumor-induced neutrophilia: constitutive production of colony-stimulating factors and their synergistic actions." Blood 74, no. 1 (July 1, 1989): 115–22. http://dx.doi.org/10.1182/blood.v74.1.115.bloodjournal741115.

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Transplantation of a murine mammary carcinoma (CE maca) into mice induces marked granulocytosis and hypercalcemia secondary to excessive bone resorption. Such responses are not induced by another murine mammary carcinoma Bc66. In order to understand the mechanisms of these unique phenomena, we analyzed mRNA of tumor cells for expression of murine granulopoietic growth factors and studied interactions of tumor- derived factors using antiserum to a growth factor in vitro and in vivo. The Northern blot analysis of CE tumor clones revealed the expression of granulocyte colony stimulating factor (G-CSF) and macrophage colony stimulating factor (M-CSF), but no other CSF genes, while the Bc66 clone expressed only M-CSF. The G-CSF and M-CSF gene expression in CE tumor clones was accompanied by secretion of these proteins in culture. The granulocyte stimulating activity of CE tumor- derived G-CSF or recombinant human G-CSF was markedly enhanced by purified M-CSF in vitro. Significant but variable neutrophilia was observed in mice inoculated with CE tumor clones. Anti-M-CSF treatment of CE tumor-bearing mice significantly reduced neutrophilia, but did not affect hypercalcemia. These studies document that G-CSF and M-CSF are produced constitutively from the CE maca, and G-CSF is likely responsible for granulocytosis induced by this tumor. G-CSF and M-CSF function synergistically in granulocyte stimulation in vitro and this synergism may also play a role in marked granulocytosis of tumor- bearing animals, providing further evidence of the effect of CSFs in vivo.

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Sicinska, Ewa, Young-Mi Lee, Judith Gits, Hirokazu Shigematsu, Qunyan Yu, Vivienne I. Rebel, Yan Geng, et al. "Essential Role for Cyclin D3 in Granulocyte Colony-Stimulating Factor-Driven Expansion of Neutrophil Granulocytes." Molecular and Cellular Biology 26, no. 21 (September 5, 2006): 8052–60. http://dx.doi.org/10.1128/mcb.00800-06.

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ABSTRACT The proliferation of neutrophil granulocyte lineage is driven largely by granulocyte colony-stimulating factor (G-CSF) acting via the G-CSF receptors. In this study, we show that mice lacking cyclin D3, a component of the core cell cycle machinery, are refractory to stimulation by the G-CSF. Consequently, cyclin D3-null mice display deficient maturation of granulocytes in the bone marrow and have reduced levels of neutrophil granulocytes in their peripheral blood. The mutant mice are unable to mount a normal response to bacterial challenge and succumb to microbial infections. In contrast, the expansion of hematopoietic stem cells and lineage-committed myeloid progenitors proceeds relatively normally in mice lacking cyclin D3, revealing that the requirement for cyclin D3 function operates at later stages of neutrophil development. Importantly, we verified that this requirement is specific to cyclin D3, as mice lacking other G1 cyclins (D1, D2, E1, or E2) display normal granulocyte counts. Our analyses revealed that in the bone marrow cells of wild-type mice, activation of the G-CSF receptor leads to upregulation of cyclin D3. Collectively, these results demonstrate that cyclin D3 is an essential cell cycle recipient of G-CSF signaling, and they provide a molecular link of how G-CSF-dependent signaling triggers cell proliferation.

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Gales, Barry J., and Mark A. Gales. "Granulocyte-Colony Stimulating Factor for Sulfasalazine-Induced Agranulocytosis." Annals of Pharmacotherapy 27, no. 9 (September 1993): 1052–54. http://dx.doi.org/10.1177/106002809302700907.

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OBJECTIVE: To report a case of sulfasalazine-induced agranulocytosis that was successfully treated with granulocyte-colony stimulating factor (G-CSF). CASE SUMMARY: An 82-year-old woman developed agranulocytosis within two months of initiating sulfasalazine therapy. She was hospitalized, empiric antibiotics and antifungal agents were prescribed, and sulfasalazine therapy was stopped. The patient received G-CSF 600 μg/d subcutaneously for six consecutive days, starting on hospital day 5. Agranulocytosis resolved on day 5 and leukopenia on day 6 of G-CSF therapy. No adverse reactions were attributed to administration of this agent and the patient was discharged on hospital day 13. DISCUSSION: Numerous agents, including sulfasalazine, have been associated with agranulocytosis. Agranulocytic patients frequently experience life-threatening bacterial and fungal infections. Administration of colony stimulating factors may reduce the duration of agranulocytosis and incidence of life-threatening infections. CONCLUSIONS: G-CSF administration appears to have decreased the duration of this elderly patient's agranulocytosis and hospitalization.

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Suzuki, A., T. Takahashi, K. Nakamura, R. Tsuyuoka, Y. Okuno, T. Enomoto, M. Fukumoto, and H. Imura. "Thrombocytosis in patients with tumors producing colony-stimulating factor." Blood 80, no. 8 (October 15, 1992): 2052–59. http://dx.doi.org/10.1182/blood.v80.8.2052.2052.

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Abstract We investigated the cause of thrombocytosis in 14 patients with tumors producing colony-stimulating factor (CSF). Of the 14 patients, 10 had tumors producing granulocyte-CSF (G-CSF) and 4 had tumors producing granulocyte-macrophage--CSF (GM-CSF). Thrombocytosis of greater than 400 x 10(9)/L was noted in 8 of 10 patients with G-CSF-producing tumors and all 4 patients with GM-CSF-producing tumors. Median peak platelet counts were, respectively, 511 x 10(9)/L (range, 384 to 694 x 10(9)/L) and 579 x 10(9)/L (range, 526 to 910 x 10(9)/L) in patients with tumors producing G-CSF and GM-CSF. In most patients, thrombocytosis declined towards the terminal stage. High interleukin-1 (IL-1) and IL-6 levels were found in addition to CSFs in the plasma or culture supernatants of tumor cells obtained from most patients. In patients with GM-CSF- producing tumors, these specimens had megakaryocyte-CSF (Meg-CSF) activity, which was abolished by anti-GM-CSF antibody. These specimens also had megakaryocyte potentiating (Meg-Pot) activity attributable to both GM-CSF and IL-6. In patients with G-CSF-producing tumors, only Meg- Pot activity due to IL-6 was detected. These results indicate that the thrombocytosis in GM-CSF-producing tumors was caused by both the Meg- CSF activity of GM-CSF and the Meg-Pot activity of IL-6 plus GM-CSF, while that in G-CSF-producing tumors was due to the Meg-Pot activity of IL-6.

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Suzuki, A., T. Takahashi, K. Nakamura, R. Tsuyuoka, Y. Okuno, T. Enomoto, M. Fukumoto, and H. Imura. "Thrombocytosis in patients with tumors producing colony-stimulating factor." Blood 80, no. 8 (October 15, 1992): 2052–59. http://dx.doi.org/10.1182/blood.v80.8.2052.bloodjournal8082052.

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We investigated the cause of thrombocytosis in 14 patients with tumors producing colony-stimulating factor (CSF). Of the 14 patients, 10 had tumors producing granulocyte-CSF (G-CSF) and 4 had tumors producing granulocyte-macrophage--CSF (GM-CSF). Thrombocytosis of greater than 400 x 10(9)/L was noted in 8 of 10 patients with G-CSF-producing tumors and all 4 patients with GM-CSF-producing tumors. Median peak platelet counts were, respectively, 511 x 10(9)/L (range, 384 to 694 x 10(9)/L) and 579 x 10(9)/L (range, 526 to 910 x 10(9)/L) in patients with tumors producing G-CSF and GM-CSF. In most patients, thrombocytosis declined towards the terminal stage. High interleukin-1 (IL-1) and IL-6 levels were found in addition to CSFs in the plasma or culture supernatants of tumor cells obtained from most patients. In patients with GM-CSF- producing tumors, these specimens had megakaryocyte-CSF (Meg-CSF) activity, which was abolished by anti-GM-CSF antibody. These specimens also had megakaryocyte potentiating (Meg-Pot) activity attributable to both GM-CSF and IL-6. In patients with G-CSF-producing tumors, only Meg- Pot activity due to IL-6 was detected. These results indicate that the thrombocytosis in GM-CSF-producing tumors was caused by both the Meg- CSF activity of GM-CSF and the Meg-Pot activity of IL-6 plus GM-CSF, while that in G-CSF-producing tumors was due to the Meg-Pot activity of IL-6.

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42

Walker, Francesca, Hui-Hua Zhang, Vance Matthews, Janet Weinstock, Edouard C. Nice, Matthias Ernst, Stefan Rose-John, and Antony W. Burgess. "IL6/sIL6R complex contributes to emergency granulopoietic responses in G-CSF– and GM-CSF–deficient mice." Blood 111, no. 8 (April 15, 2008): 3978–85. http://dx.doi.org/10.1182/blood-2007-10-119636.

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AbstractMice defective in both granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have severely impaired neutrophil production and function, yet these mice respond to acute pathogen challenge with a significant neutrophil response. We have recently reported the development of an in vitro system to detect granulopoietic cytokines secreted from cells isolated from G-CSF, GM-CSF double knockout mice. The conditioned media produced by these cells after stimulation with lipopolysaccharide or Candida albicans supports the production and differentiation of granulocytes (ie, the conditioned media contains neutrophil promoting activity [NPA]). We now show that the NPA in the G-CSF−/−/GM-CSF−/− conditioned media requires interleukin-6 (IL6), is abolished by soluble gp130, and can be specifically immunodepleted by an anti-IL6R antibody. NPA effects on bone marrow cells are also mimicked by Hyper-IL6, and the soluble IL6R is present in NPA. These results show that the IL6/sIL6R complex is the major effector of NPA. NPA production by mice defective for both G-CSF and GM-CSF uncovers an alternative pathway to granulocyte production, which is activated after exposure to pathogens.

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43

Mok, Tsz Ching, Lok Ping Ng, Eva Tsz Fung Chui, and Ho Yin Chung. "Potentiation of Lupus Activity by Granulocyte Colony-Stimulating Factor." Journal of Clinical Rheumatology and Immunology 21, no. 01 (February 4, 2021): 37–41. http://dx.doi.org/10.1142/s2661341721720019.

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Recombinant human granulocyte colony-stimulating factor (G-CSF) is commonly used to accelerate recovery of neutropenia in patients with marrow suppression. We hereby report a patient with systemic lupus erythematosus (SLE) who developed diffuse lupus nephritis and impending cytokine storm after G-CSF therapy. The exact mechanisms by which G-CSF leads to lupus flares remains enigmatic. Increased neutrophil apoptosis and release of cytokines have been postulated. The use of G-CSF in patients with autoimmune disease should be cautious.

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Kawaida, Keisuke, Jun Kadono, Hideaki Kanda, Masahiko Osako, Naoki Ishizaki, Ken Shimizu, Junichiro Sameshima, Yutaka Imoto, and Mineo Tabata. "A Case of Granulocyte-colony Stimulating Factor Producing Colon Cancer." Japanese Journal of Gastroenterological Surgery 45, no. 5 (2012): 537–43. http://dx.doi.org/10.5833/jjgs.45.537.

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45

Iwasaki, Hiromi, Kazuya Shimoda, Seiichi Okamura, Teruhisa Otsuka, Koji Nagafuji, Naoki Harada, Yuju Ohno, et al. "Production of Soluble Granulocyte Colony-Stimulating Factor Receptors from Myelomonocytic Cells." Journal of Immunology 163, no. 12 (December 15, 1999): 6907–11. http://dx.doi.org/10.4049/jimmunol.163.12.6907.

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Abstract It has been speculated that a soluble form of G-CSFR might be physiologically present in humans, since G-CSFR mRNA that lacks a transmembrane domain has been identified from a human myelomonocytic cell line. Here, we demonstrate human soluble G-CSFR (sG-CSFR) of two different molecular sizes (80 and 85 kDa) on an immunoblot analysis using Abs generated against the amino-terminal, extracellular domain of the full-length G-CSFR. Both isoforms of sG-CSFR were able to bind recombinant human G-CSF (rhG-CSF). RT-PCR analysis with primers targeted outside of the transmenbrane region revealed that membrane-anchored G-CSFR is expressed at all maturation stages of purified myeloid cells, including CD34+CD13+ cells (blasts), CD11b−CD15+ cells (promyelocytes or myelocytes), CD11b+CD15+ cells (metamyelocytes and mature neutrophils), and CD14+ cells (monocytes). On the other hand, sG-CSFR mRNA was detectable in CD11b−CD15+, CD11b+CD15+, and CD14+ cells, but not in the CD34+CD13+ blast population. The serum concentration of both isoforms of sG-CSFR appeared to be correlated with the numbers of neutrophils/monocytes before and after rhG-CSF treatment in normal individuals. Thus, two isoforms of sG-CSFR are physiologically secreted from relatively mature myeloid cells and might play an important role in myelopoiesis through their binding to serum G-CSF.

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46

Ren, Zhihua, Wenhong Jiang, Zhenwang Jie, Xiaoxiao Liu, Fei Xia, Jie Fan, Keyong Shi, Xinxin Ding, Wei Dai, and Yongping Jiang. "Pre-Clinical Studies of a Novel Recombinant Human Granulocyte Colony-Stimulating Factor." Blood 124, no. 21 (December 6, 2014): 2920. http://dx.doi.org/10.1182/blood.v124.21.2920.2920.

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Abstract The human granulocyte colony-stimulating factor (G-CSF), a glycoprotein consisting of 174 amino acids, enhances the survival, proliferation, and differentiation of neutrophil precursors. G-CSF also induces the mobilization of hematopoietic stem cells and progenitors, which further stimulates recovery from neutropenia. Further studies indicates that Glu19 in the A helix of G-CSF molecule electrostatically inter-reacts with Arg288 of G-CSF-R. A recent study on the crystal structure of G-CSF, complexed with the cytokine homologous region of G-CSF-R, reveals that residues in the amino-terminus of G-CSF may act as additional contact sites with G-CSF-R. In this investigation, we designed and purified a novel recombinant human granulocyte colony-stimulating factor analog (rhG-CSFa), which has three extra amino acid residues (arginine, glycine, and serine) added at the amino-terminus. The structural modification resulted in more positive charge in the amino-terminus of G-CSFa, and was expected to further enhance the binding between the cytokine and its receptor. We optimized the purification procedure, achieving further improvements in refolding rate and overall yield. In preclinical studies, we evaluated the pharmacodynamics, pharmacokinetics, acute, subacute, and chronic toxicity of rhG-CSFa. Pharmacodynamics study in non-human primates demonstrated that intravenous rhG-CSFa induces typical peripheral neutrophil responses (with two peaks from treatment day 8 to day 20) and dramatic increases in the recovery rate in the animal model. More importantly, rhG-CSFa induced a higher peak of neutrophil recovery on day 7 than wild G-CSF did in monkeys, a result indicating that rhG-CSFa would provide greater benefit for patients receiving myeloid-suppressive therapies. In addition, rhG-CSFa maintained higher neutrophil counts than wild-type G-CSF did after cessation of G-CSF administration in monkeys; its effects persisted over 20 days post-treatment, which should be more helpful to patients for combating deleterious infections and preparing for the next round of treatment in clinic. In pharmacokinetics studies, the novel rhG-CSFa displayed a lower plasma clearance rate, 0.28 ml/min/kg (vs 0.5-0.7 ml/min/kg for wild-type G-CSF). This result suggests that rhG-CSFa may dissociate from its receptor at a slower rate than does wild-type G-CSF, which is possibly due to a tighter binding to its cognate receptor, and would result in a much extended plasma functional half-life. In further preclinical safety evaluation, no obvious toxicity or immunogenicity was observed, neither was any adverse drug reaction. In conclusion, we have generated a novel rhG-CSFa protein, with much higher yield, enhanced circulation half-life, improved thermal stability and greater bioactivity (without changing the overall conformation), compared with wild type G-CSF. Our preclinical studies strongly suggest that rhG-CSFa can be further explored for clinical trials for eventual applications in the clinic. Disclosures Ren: Biopharmagen corp: Employment. Jiang:Biopharmagen.corp: Employment. Shi:Biopharmagen corp: Employment. Jiang:Biopharmagen.corp: Employment.

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47

Channon, Jacqueline Y., Kristin A. Miselis, Laurie A. Minns, Chaitali Dutta, and Lloyd H. Kasper. "Toxoplasma gondii Induces Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor Secretion by Human Fibroblasts: Implications for Neutrophil Apoptosis." Infection and Immunity 70, no. 11 (November 2002): 6048–57. http://dx.doi.org/10.1128/iai.70.11.6048-6057.2002.

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ABSTRACT Human neutrophils are rescued from apoptosis following incubation with once-washed, fibroblast-derived Toxoplasma gondii tachyzoites. Both infected and uninfected neutrophils are rescued, implicating a soluble mediator. In this study we investigated the origin and identity of this soluble mediator. Neutrophils were incubated either with purified tachyzoites or with conditioned medium derived from T. gondii-infected human fibroblasts. Conditioned medium was found to be a potent stimulus that delayed neutrophil apoptosis up to 72 h, whereas purified and extensively washed tachyzoites had no effect. Delayed apoptosis correlated with up-regulation of the neutrophil antiapoptotic protein, Mcl-1, and the neutrophil interleukin 3 receptor α subunit (IL-3Rα), suggesting a role for granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF and granulocyte colony-stimulating factor (G-CSF) were measurable in conditioned medium by enzyme-linked immunosorbent assay. Neutralizing antibodies to GM-CSF and G-CSF were additive in abrogating delayed neutrophil apoptosis induced by conditioned medium. Inhibitors of Src family tyrosine kinases, Gi proteins, phosphatidylinositol 3-kinase, p44 erk1 and p42 erk2 mitogen-activated protein kinases, and Jak2 kinases partially attenuated the effect of conditioned medium, consistent with a role for G-CSF and/or GM-CSF. Hence, delayed neutrophil apoptosis is mediated by GM-CSF and G-CSF secreted by T. gondii-infected human fibroblasts. This enhanced neutrophil survival may contribute to the robust proinflammatory response elicited in the T. gondii-infected host.

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48

Hess, David A., Krysta D. Levac, Francis N. Karanu, Michael Rosu-Myles, Martin J. White, Lisa Gallacher, Barbara Murdoch, et al. "Functional analysis of human hematopoietic repopulating cells mobilized with granulocyte colony-stimulating factor alone versus granulocyte colony-stimulating factor in combination with stem cell factor." Blood 100, no. 3 (August 1, 2002): 869–78. http://dx.doi.org/10.1182/blood.v100.3.869.

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Abstract Using in vitro progenitor assays, serum-free in vitro cultures, and the nonobese diabetic/severe combined immune-deficient (NOD/SCID) ecotropic murine virus knockout xenotransplantation model to detect human SCID repopulating cells (SRCs) with multilineage reconstituting function, we have characterized and compared purified subpopulations harvested from the peripheral blood (PB) of patients receiving granulocyte colony-stimulating factor (G-CSF) alone or in combination with stem cell factor (SCF). Mobilized G-CSF plus SCF PB showed a 2-fold increase in total mononuclear cell content and a 5-fold increase in CD34-expressing cells depleted for lineage-marker expression (CD34+Lin−) as compared with patients treated with G-CSF alone. Functionally, G-CSF plus SCF–mobilized CD34+CD38−Lin−cells contained a 2-fold enhancement in progenitor frequency as compared with G-CSF–mobilized subsets. Despite enhanced cellularity and progenitor capacity, G-CSF plus SCF mobilization did not increase the frequency of SRCs as determined by limiting dilution analysis by means of unfractionated PB cells. Purification of SRCs from these sources demonstrated that as few as 1000 CD34+CD38−Lin− cells from G-CSF–mobilized PB contained SRC capacity while G-CSF plus SCF–mobilized CD34+CD38−Lin−cells failed to repopulate at doses up to 500 000 cells. In addition, primitive CD34−CD38−AC133+Lin−cells derived from G-CSF plus SCF–mobilized PB were capable of differentiation into CD34-expressing cells, while the identical subfractions from G-CSF PB were unable to produce CD34+cells in serum-free cultures. Our study defines qualitative and quantitative distinctions among subsets of primitive cells mobilized by means of G-CSF plus SCF versus G-CSF alone, and therefore has implications for the utility of purified repopulating cells from these sources.

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Fibbe, WE, J. van Damme, A. Billiau, HM Goselink, PJ Voogt, G. van Eeden, P. Ralph, BW Altrock, and JH Falkenburg. "Interleukin 1 induces human marrow stromal cells in long-term culture to produce granulocyte colony-stimulating factor and macrophage colony- stimulating factor." Blood 71, no. 2 (February 1, 1988): 430–35. http://dx.doi.org/10.1182/blood.v71.2.430.430.

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Abstract Pure interleukin 1 (IL 1) was found to stimulate established human bone marrow stromal layers in long-term culture to produce colony- stimulating activity (CSA). Maximal concentrations in the culture medium were reached 24 hours after a single IL 1 pulse. The effect could be neutralized by a specific rabbit anti-IL 1 antiserum. Stromal layers, once stimulated by IL 1, continued to release CSA into the culture medium in the absence of exogenous IL 1. A second IL 1 pulse induced CSA release in an identical manner, as did the primary stimulation, indicating that the CSA released was actively produced. Using specific immunologic assays, both granulocyte colony-stimulating factor (G-CSF) and macrophage CSF (M-CSF) could be identified in the culture supernatants, and production of both factors was inducible by IL 1. Shortly after initiation of the long-term marrow cultures “spontaneous” G-CSF and M-CSF release occurred. The release of G-CSF diminished following addition of the anti-IL 1 antiserum, indicating that endogenous production of IL 1 by stromal cells had contributed to this effect. These results further support the role of IL 1 as an important modulator of CSF production by cells of the hematopoietic microenvironment.

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50

Fibbe, WE, J. van Damme, A. Billiau, HM Goselink, PJ Voogt, G. van Eeden, P. Ralph, BW Altrock, and JH Falkenburg. "Interleukin 1 induces human marrow stromal cells in long-term culture to produce granulocyte colony-stimulating factor and macrophage colony- stimulating factor." Blood 71, no. 2 (February 1, 1988): 430–35. http://dx.doi.org/10.1182/blood.v71.2.430.bloodjournal712430.

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Pure interleukin 1 (IL 1) was found to stimulate established human bone marrow stromal layers in long-term culture to produce colony- stimulating activity (CSA). Maximal concentrations in the culture medium were reached 24 hours after a single IL 1 pulse. The effect could be neutralized by a specific rabbit anti-IL 1 antiserum. Stromal layers, once stimulated by IL 1, continued to release CSA into the culture medium in the absence of exogenous IL 1. A second IL 1 pulse induced CSA release in an identical manner, as did the primary stimulation, indicating that the CSA released was actively produced. Using specific immunologic assays, both granulocyte colony-stimulating factor (G-CSF) and macrophage CSF (M-CSF) could be identified in the culture supernatants, and production of both factors was inducible by IL 1. Shortly after initiation of the long-term marrow cultures “spontaneous” G-CSF and M-CSF release occurred. The release of G-CSF diminished following addition of the anti-IL 1 antiserum, indicating that endogenous production of IL 1 by stromal cells had contributed to this effect. These results further support the role of IL 1 as an important modulator of CSF production by cells of the hematopoietic microenvironment.

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Journal articles on the topic 'Granulocyte colony stimulating factor (G-CSF)'

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