Expression of granulocyte colony stimulating factor and granulocyte-macrophage colony stimulating factor genes in human astrocytoma cell lines and in glioma specimens

Nitta, Taizo; Satô, Kiyoshi; Allegretta, Mark; Brocke, Stefan; Lim, Mae; Mitchell, Dennis J.; Steinman, Lawrence

doi:10.1016/0006-8993(92)90505-4

Cited by 52 publications

(39 citation statements)

References 29 publications

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“…The propensity for tumor cells to respond to growth factors is readily observed in several types of cancer [9][10][11][12][13]. This documented response to growth factors, coupled with the observation that neuronal progenitor cells utilize GCSF as a growth and development factor in normal development [15] suggest that these cells either never lose GCSF receptor expression, or reclaim expression as part of functional changes during mutagenesis or oncogenesis [16].…”

Section: Discussionmentioning

confidence: 99%

Granulocyte colony stimulating factor alters the phenotype of neuroblastoma cells: implications for disease-free survival of high-risk patients

Gay

Chang

Rutland

et al. 2008

Journal of Pediatric Surgery

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Corresponding Author: (Same for reprint requests), Oluyinka Olutoye, MB, ChB, PhD, Division of Pediatric Surgery, Baylor College of Medicine, 6621 Fannin St, CC650.00, Houston, TX 77030-2399, Tel: (832) Fax: (832) 825-3141, oolutoye@bcm.tmc.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Presented at the 39 th Annual Meeting of the Canadian Association of Pediatric Surgeons. Winner of the best basic science paper presentation (ANG). NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptIntroduction-GCSF is commonly employed for the treatment of chemotherapy-induced neutropenia. Despite high-dose intensive chemotherapy for advanced stage neuroblastoma, the survival rate remains poor. GCSF therapy is quite common in these children, thus we questioned its effect on neuroblastoma cells. We hypothesized that exogenous GCSF stimulates the proliferation and invasive character of neuroblastoma cells.

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Section: Discussionmentioning

confidence: 99%

Granulocyte colony stimulating factor alters the phenotype of neuroblastoma cells: implications for disease-free survival of high-risk patients

Gay

Chang

Rutland

et al. 2008

Journal of Pediatric Surgery

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“…In vivo expression of G-CSF has been reported in neoplastic astrocytes (36 -38), but was lost at higher degrees of dedifferentiation. Inflammatory and viral stimuli enhance M-CSF expression and promote G-CSF production by human and murine astrocytes (25,26). We report here that the constitutive, high level expression of M-CSF in spinal cords increases in mice with EAE, but returns to basal levels in mice given G-CSF, whereas G-CSF itself was not significantly induced by either EAE disease or G-CSF treatment.…”

Section: Discussionmentioning

confidence: 99%

“…M-CSF is constitutively expressed by human and murine astrocytes, and GM-CSF and G-CSF can be produced by these cells after inflammatory or viral stimulation (25)(26)(27)(28). We therefore investigated whether expression and/or regulation of these factors might be implicated in the EAE disease process.…”

Section: Rpa Analysis Of Mrna Production Of Cytokines Chemokines Anmentioning

confidence: 99%

G-CSF Therapy of Ongoing Experimental Allergic Encephalomyelitis Via Chemokine- and Cytokine-Based Immune Deviation

Zavala

Abad

Ezine

et al. 2002

The Journal of Immunology

108

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Converging evidence that G-CSF, the hemopoietic growth factor of the myeloid lineage, also exerts anti-inflammatory and pro-Th2 effects, prompted us to evaluate its direct therapeutic potential in autoimmune diseases. Here we report a novel activity of G-CSF in experimental allergic encephalomyelitis, a murine model for multiple sclerosis, driven by Th1-oriented autoaggressive cells. A short 7-day treatment with G-CSF, initiated at the onset of clinical signs, provided durable protection from experimental autoimmune encephalomyelitis. G-CSF-treated mice displayed limited demyelination, reduced recruitment of T cells to the CNS, and very discrete autoimmune inflammation, as well as barely detectable CNS mRNA levels of cytokines and chemokines. In the periphery, G-CSF treatment triggered an imbalance in the production by macrophages as well as autoreactive splenocytes of macrophage inflammatory protein-1α and monocyte chemoattractant protein-1, the prototypical pro-Th1 and pro-Th2 CC chemokines, respectively. This chemokine imbalance was associated with an immune deviation of the autoreactive response, with reduced IFN-γ and increased IL-4 and TGF-β1 levels. Moreover, G-CSF limited the production of TNF-α, a cytokine also associated with early CNS infiltration and neurological deficit. These findings support the potential application of G-CSF in the treatment of human autoimmune diseases such as multiple sclerosis, taking advantage of the wide clinical favorable experience with this molecule.

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“…30,31 The use of G-CSF and GM-CSF in patients with malignant tumors relies on data showing no influence of either growth factor on tumor growth. [32][33][34] Recently there has been an increasing number of reports describing the expression of G-CSF and/or GM-CSF by nonhematopoietic human tumor cells, [35][36][37][38] suggesting a potential role of these factors in tumor growth and invasion. 36,39,40 Previous studies on the expression of either G-CSF or GM-CSF alone in gliomas provided rather contradictory results, claiming that the factors were either expressed exclusively in vitro but not in vivo 41,42 or were expressed in vivo without showing an autocrine stimulatory function in vitro.…”

mentioning

confidence: 99%

Autocrine Growth Regulation by Granulocyte Colony-Stimulating Factor and Granulocyte Macrophage Colony-Stimulating Factor in Human Gliomas with Tumor Progression

Mueller¹,

Herold‐Mende²,

Riede³

et al. 1999

The American Journal of Pathology

117

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Granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSFGliomas are the most common primary malignant brain tumors in adults. Their most malignant form, the glioblastoma multiforme, forms highly vascularized, uniformly fatal neoplasms. Glioma cells, like all tumor cells, are characterized by their uncontrolled growth and increasing escape from regulatory mechanisms of the environment. Current research on brain tumor biology focuses on the mechanisms underlying the stimulation of tumor proliferation and/or angiogenesis. In the past several years a number of growth factors have been identified that stimulate glioma cell growth and glioma-induced angiogenesis through autocrine or paracrine mechanisms (ref 1 and references therein, and refs 2-4). These new insights into the biology of gliomas offer promising therapeutic concepts that are currently under investigation. [5][6][7][8] To date the prognosis of patients with malignant glioma remains poor, offering a median survival time of only 1 year, despite aggressive treatments, including surgical resection and radio-and chemotherapy.9,10 The latter two treatments are limited by two major complications, neutropenia and sepsis. The hematopoietic growth factors granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) were shown to be of therapeutic value in different conditions of primary and secondary bone marrow dysfunction.11 Consequently they now find widespread clinical application in reducing the duration and severity of neutropenic periods in routine cancer therapy. [12][13][14][15]

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Expression of granulocyte colony stimulating factor and granulocyte-macrophage colony stimulating factor genes in human astrocytoma cell lines and in glioma specimens

Cited by 52 publications

References 29 publications

Granulocyte colony stimulating factor alters the phenotype of neuroblastoma cells: implications for disease-free survival of high-risk patients

Granulocyte colony stimulating factor alters the phenotype of neuroblastoma cells: implications for disease-free survival of high-risk patients

G-CSF Therapy of Ongoing Experimental Allergic Encephalomyelitis Via Chemokine- and Cytokine-Based Immune Deviation

Autocrine Growth Regulation by Granulocyte Colony-Stimulating Factor and Granulocyte Macrophage Colony-Stimulating Factor in Human Gliomas with Tumor Progression

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