Production of granulocyte colony-stimulating factor by head and neck carcinomas

Tsukuda, Mamoru; Nagahara, Taro; Yago, Tadayuki; Matsuda, Hideki; Yanoma, Shunsuke

doi:10.1007/bf01878079

Cited by 15 publications

(10 citation statements)

References 23 publications

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“…This therapeutic use relies on data showing no adverse effect of both factors (55). However, our data as well as that of other studies demonstrate the association of G-CSF and/or GM-CSF expression with an enhanced invasive and metastatic potential (5,19) and thus warrant a careful reevaluation of the role of G-CSF and GM-CSF in the growth of solid tumors in vivo and the consequences of their use in cancer therapy protocols.…”

Section: Discussionsupporting

confidence: 72%

“…2 This clearly supports the need for an additive or synergistic contribution of both factors to the establishment of an enhanced malignant tumor phenotype. Comparably, de novo expression of both growth factors has been reported in highgrade malignant gliomas, meningiomas, head and neck tumors, and SCCs of the skin (5,8,16,17,19,20).…”

Section: Effect Of G-csf and Gm-csf For Tumor Growth And Progressionmentioning

confidence: 90%

“…G-CSF has been described to be newly expressed in squamous cell carcinomas (SCCs) of the esophagus (16) and tongue (17), carcinosarcomas (18), and head and neck carcinomas (19). Constitutive expression of G-CSF and GM-CSF together has been found in SCCs (11,12,20), osteosarcoma (21), gliomas (5), meningiomas, and pulmonary adenocarcinoma (22).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cooperative Autocrine and Paracrine Functions of Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor in the Progression of Skin Carcinoma Cells

et al. 2004

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Section: Discussionsupporting

confidence: 72%

Section: Effect Of G-csf and Gm-csf For Tumor Growth And Progressionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cooperative Autocrine and Paracrine Functions of Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor in the Progression of Skin Carcinoma Cells

et al. 2004

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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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“…However, G-CSF exposure paradoxically can also elicit adverse effects, and inhibit innate and adaptive immunity [24], [25]; yet, the precise mechanisms by which G-CSF does so remain incompletely understood. Moreover, the idea that G-CSF may not always be beneficial to the host is supported by the findings that G-CSF is aberrantly expressed by diverse human tumors, including head and neck, cervical, ovarian, pancreatic, bladder and leukemia [26], [27], [28], [29], [30], [31].…”

Section: Introductionmentioning

confidence: 99%

Tumor-Derived G-CSF Facilitates Neoplastic Growth through a Granulocytic Myeloid-Derived Suppressor Cell-Dependent Mechanism

et al. 2011

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Myeloid-derived suppressor cells (MDSC) are induced under diverse pathologic conditions, including neoplasia, and suppress innate and adaptive immunity. While the mechanisms by which MDSC mediate immunosuppression are well-characterized, details on how they develop remain less understood. This is complicated further by the fact that MDSC comprise multiple myeloid cell types, namely monocytes and granulocytes, reflecting diverse stages of differentiation and the proportion of these subpopulations vary among different neoplastic models. Thus, it is thought that the type and quantities of inflammatory mediators generated during neoplasia dictate the composition of the resultant MDSC response. Although much interest has been devoted to monocytic MDSC biology, a fundamental gap remains in our understanding of the derivation of granulocytic MDSC. In settings of heightened granulocytic MDSC responses, we hypothesized that inappropriate production of G-CSF is a key initiator of granulocytic MDSC accumulation. We observed abundant amounts of G-CSF in vivo, which correlated with robust granulocytic MDSC responses in multiple tumor models. Using G-CSF loss- and gain-of-function approaches, we demonstrated for the first time that: 1) abrogating G-CSF production significantly diminished granulocytic MDSC accumulation and tumor growth; 2) ectopically over-expressing G-CSF in G-CSF-negative tumors significantly augmented granulocytic MDSC accumulation and tumor growth; and 3) treatment of naïve healthy mice with recombinant G-CSF protein elicited granulocytic-like MDSC remarkably similar to those induced under tumor-bearing conditions. Collectively, we demonstrated that tumor-derived G-CSF enhances tumor growth through granulocytic MDSC-dependent mechanisms. These findings provide us with novel insights into MDSC subset development and potentially new biomarkers or targets for cancer therapy.

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Production of granulocyte colony-stimulating factor by head and neck carcinomas

Cited by 15 publications

References 23 publications

Cooperative Autocrine and Paracrine Functions of Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor in the Progression of Skin Carcinoma Cells

Cooperative Autocrine and Paracrine Functions of Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor in the Progression of Skin Carcinoma Cells

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Tumor-Derived G-CSF Facilitates Neoplastic Growth through a Granulocytic Myeloid-Derived Suppressor Cell-Dependent Mechanism

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