Coexpression of granulocyte colony stimulating factor and its receptor in primary ovarian carcinomas

Savarese, Todd M.; Mitchell, Kathryn; McQuain, Cathy; Campbell, Cara L.; Guardiani, Rachel; Wuu, Joanne; Ollari, Christopher; Reale, Frank R.; Nelson, Beth E.; Chen, Annette; Quesenberry, Peter J.

doi:10.1016/s0304-3835(00)00623-6

Cited by 53 publications

(40 citation statements)

References 25 publications

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“…[19][20][21][22] Colorectal cancer, squamous cell carcinoma, melanoma, ovarian carcinoma, meningioma, and glioma cells have been shown to constitutively express either G-CSF or its receptor. [23][24][25][26][27][28] In the current study, we demonstrate for what we believe to be the first time that Ewing tumor cell lines and patient samples express high levels of both G-CSF and G-CSFR. Using the TC/7-1 nude mouse model, we also further demonstrate that the administration of G-CSF enhanced tumor growth.…”

supporting

confidence: 57%

Expression of granulocyte‐colony‐stimulating factor and its receptor in human Ewing sarcoma cells and patient tumor specimens

Morales-Arias

Meyers

Bolontrade

et al. 2007

Cancer

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BACKGROUND. Ewing sarcoma (ES) is a highly vascular malignancy. It has been demonstrated that both angiogenesis and vasculogenesis contribute to the growth of ES tumors. Granulocyte‐colony‐stimulating factor (G‐CSF), a cytokine known to stimulate bone marrow (BM) stem cell production and angiogenesis, is routinely administered to ES patients after chemotherapy. Whether ES cells and patient tumor samples express G‐CSF and its receptor (G‐CSFR) and whether treatment with this factor enhances tumor growth was examined. METHODS. Human ES cell lines were analyzed for expression of G‐CSF and G‐CSFR in vitro and in vivo. Sixty‐eight paraffin‐embedded and 15 frozen tumor specimens from patients with ES were also evaluated for the presence of G‐CSF and G‐CSFR. The in vivo effect of G‐CSF on angiogenesis and BM cell migration was determined. Using a TC/7‐1 human ES mouse model, the effect of G‐CSF administration on ES tumors was investigated. RESULTS. G‐CSF and G‐CSFR protein and RNA expression was identified in all ES cell lines and patient samples analyzed. In addition, G‐CSF was found to stimulate angiogenesis and BM cell migration in vivo. Tumor growth was found to be significantly increased in mice treated with G‐CSF. The average tumor volume for the group treated with G‐CSF was 1218 mm3 compared with 577 mm3 for the control group (P = .006). CONCLUSIONS. The findings that ES cells and patient tumors expressed both G‐CSF and its receptor in vitro and in vivo and that the administration of G‐CSF promoted tumor growth in vivo suggest that the potential consequences of G‐CSF administration should be investigated further. Cancer 2007. © 2007 American Cancer Society.

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supporting

confidence: 57%

Expression of granulocyte‐colony‐stimulating factor and its receptor in human Ewing sarcoma cells and patient tumor specimens

Morales-Arias

Meyers

Bolontrade

et al. 2007

Cancer

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“…Because G-CSF favors the in vitro differentiation of peripheral blood monocytes into TDCs through the release of IL-10 and IFN-g (21, 35), our experimental findings support the notion that G-CSF could be an important cytokine to inhibit antitumor immune activation by DCs in pancreatic cancer patients. Aberrant expression of G-CSF has been reported in many cancers (36)(37)(38); however, little is reported about G-CSFproducing pancreatic cancer (39)(40)(41). Furthermore, G-CSF treatment ameliorated autoimmune spontaneous type 1 diabetes in nonobese diabetic mice by activating TDCs and Treg cells (42).…”

Section: Discussionmentioning

confidence: 99%

Elevated Interleukin-6 and G-CSF in Human Pancreatic Cancer Cell Conditioned Medium Suppress Dendritic Cell Differentiation and Activation

Bharadwaj¹,

Li²,

Zhang³

et al. 2007

Cancer Research

133

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Although dendritic cell (DC) function is impaired in pancreatic cancer patients, the underlying mechanisms are unknown. This study analyzed the soluble factors released by pancreatic cancer cells responsible for inhibiting DC differentiation and activation. Medium conditioned by a highly metastatic human pancreatic cancer cell line BxPC-3 [BxPC-3 conditioned medium (BxCM)] was mainly used for the study. Both CD34 + hematopoietic progenitor cell-derived and CD14 + monocyte-derived immature DCs and mature DCs (mDCs) were inhibited by BxCM. Allostimulation of CD4 + and CD8 +

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“…The most common neutrophil chemoattractants produced by tumors include IL-8 (CXCL8/CXCL2), MIP-1α (CCL3), huGCP-2 (CXCL6) and KC (CXCL1) [167][168][169][170][171]. G-CSF is ectopically expressed in several human tumors such as leukemia [172], bladder [173], pancreatic [174], cervical [175], ovarian [176], head and neck [177], colorectal [178] and breast carcinoma [179]. Similarly, some human cancers show elevated GM-CSF expression levels [31,180,181].…”

Section: Regulation Of Neutrophil Mobilization Recruitment and Activmentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

342

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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Coexpression of granulocyte colony stimulating factor and its receptor in primary ovarian carcinomas

Cited by 53 publications

References 25 publications

Expression of granulocyte‐colony‐stimulating factor and its receptor in human Ewing sarcoma cells and patient tumor specimens

Expression of granulocyte‐colony‐stimulating factor and its receptor in human Ewing sarcoma cells and patient tumor specimens

Elevated Interleukin-6 and G-CSF in Human Pancreatic Cancer Cell Conditioned Medium Suppress Dendritic Cell Differentiation and Activation

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

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