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_:vb472092248 _:vb472092249 _:vb472092250 _:vb472092251 _:vb472092244 _:vb472092245 _:vb472092246 _:vb472092247 _:vb472092240 _:vb472092241 _:vb472092242 _:vb472092243 _:vb472092204 _:vb472092205 _:vb472092206 _:vb472092207 _:vb472092200 _:vb472092201 _:vb472092202 _:vb472092203 _:vb472092196 _:vb472092197 _:vb472092198 _:vb472092199 _:vb472092192 _:vb472092193 _:vb472092194 _:vb472092195 _:vb472092220 _:vb472092221 _:vb472092222 _:vb472092223 _:vb472092216 _:vb472092217 _:vb472092218 _:vb472092219 _:vb472092212 _:vb472092213 _:vb472092214 _:vb472092215 _:vb472092208 _:vb472092209 _:vb472092210 _:vb472092211 _:vb472092172 _:vb472092173 _:vb472092174 _:vb472092175 _:vb472092168 _:vb472092169 _:vb472092170 _:vb472092171 _:vb472092164 _:vb472092165 _:vb472092166 _:vb472092167 _:vb472092160 _:vb472092161 _:vb472092162 _:vb472092163 _:vb472092188 _:vb472092189 _:vb472092190 _:vb472092191 _:vb472092184 _:vb472092185 _:vb472092186 _:vb472092187 _:vb472092180 _:vb472092181 _:vb472092182 _:vb472092183 _:vb472092176 _:vb472092177 _:vb472092178 _:vb472092179
n3:pmcid: PMC0
bibo:doi: 10.1371%2Fjournal.pone.0023902
n5:contains: _:vb12444218 _:vb12444254 _:vb12444251 _:vb12444247

Subject Item: _:vb12444218
rdf:type: n5:Section
dc:title: introduction
n5:contains: _:vb12444220 _:vb12444221 _:vb12444222 _:vb12444223 _:vb12444219 _:vb12444236 _:vb12444237 _:vb12444238 _:vb12444239 _:vb12444232 _:vb12444233 _:vb12444234 _:vb12444235 _:vb12444228 _:vb12444229 _:vb12444230 _:vb12444231 _:vb12444224 _:vb12444225 _:vb12444226 _:vb12444227 _:vb12444244 _:vb12444245 _:vb12444246 _:vb12444240 _:vb12444241 _:vb12444242 _:vb12444243

Subject Item: _:vb12444219
rdf:type: n3:Context
rdf:value: Recent experimental and pre-clinical studies show an important role of tumor-infiltrating macrophages in tumor growth, metastasis and response to cancer treatments [>>1<<], [2]. Tumor-associated macrophages are attracted by tumor-released molecules which induce reprogramming/differentiation of macrophages into anti-inflammatory cells known as alternatively activated, in contrast to inflammatory M1-type
n3:mentions: n2:20144856

Subject Item: _:vb12444220
rdf:type: n3:Context
rdf:value: Recent experimental and pre-clinical studies show an important role of tumor-infiltrating macrophages in tumor growth, metastasis and response to cancer treatments [1], [>>2<<]. Tumor-associated macrophages are attracted by tumor-released molecules which induce reprogramming/differentiation of macrophages into anti-inflammatory cells known as alternatively activated, in contrast to inflammatory M1-type
n3:mentions: n2:20371344

Subject Item: _:vb12444221
rdf:type: n3:Context
rdf:value: M2-type macrophages from experimental tumors and various types of cancers express arginase-1 (Arg1), IL-10 and transforming growth factor beta 1 (TGF-β1), support tumor invasion, angiogenesis and matrix remodelling [>>2<<], [3], [4].
n3:mentions: n2:20371344

Subject Item: _:vb12444222
rdf:type: n3:Context
rdf:value: M2-type macrophages from experimental tumors and various types of cancers express arginase-1 (Arg1), IL-10 and transforming growth factor beta 1 (TGF-β1), support tumor invasion, angiogenesis and matrix remodelling [2], [>>3<<], [4]. The stromal signals influencing glioma progression are poorly known and are likely distinct from those implicated in non-nervous system cancers. Microglia are brain resident macrophages, which respond to pathogens or injury in the
n3:mentions: n2:12401408

Subject Item: _:vb12444223
rdf:type: n3:Context
rdf:value: M2-type macrophages from experimental tumors and various types of cancers express arginase-1 (Arg1), IL-10 and transforming growth factor beta 1 (TGF-β1), support tumor invasion, angiogenesis and matrix remodelling [2], [3], [>>4<<]. The stromal signals influencing glioma progression are poorly known and are likely distinct from those implicated in non-nervous system cancers.
n3:mentions: n2:18467655

Subject Item: _:vb12444224
rdf:type: n3:Context
rdf:value: gamma - IFNγ) they are characterized by increased chemotaxis, production of inflammation mediators and cytokines, activation of the respiratory burst, and they become immune effector cells mediating both innate and adaptive responses [>>5<<], [6]. Histopathologic and flow cytometry studies of human glioma tissue have shown high intratumoral microglia density which correlates with the grade of malignancy [7], [8], [9].
n3:mentions: n2:17965659

Subject Item: _:vb12444225
rdf:type: n3:Context
rdf:value: - IFNγ) they are characterized by increased chemotaxis, production of inflammation mediators and cytokines, activation of the respiratory burst, and they become immune effector cells mediating both innate and adaptive responses [5], [>>6<<]. Histopathologic and flow cytometry studies of human glioma tissue have shown high intratumoral microglia density which correlates with the grade of malignancy [7], [8], [9].
n3:mentions: n2:20012873

Subject Item: _:vb12444226
rdf:type: n3:Context
rdf:value: Histopathologic and flow cytometry studies of human glioma tissue have shown high intratumoral microglia density which correlates with the grade of malignancy [>>7<<], [8], [9].
n3:mentions: n2:7889340

Subject Item: _:vb12444227
rdf:type: n3:Context
rdf:value: Histopathologic and flow cytometry studies of human glioma tissue have shown high intratumoral microglia density which correlates with the grade of malignancy [7], [>>8<<], [9]. Microglial cells in tumors do not secrete cytokines critical in developing effective innate immune responses and an anti-tumor immune response is suppressed in glioma patients [9], [10], [11]. The presence of cells positively
n3:mentions: n2:10764271

Subject Item: _:vb12444228
rdf:type: n3:Context
rdf:value: Histopathologic and flow cytometry studies of human glioma tissue have shown high intratumoral microglia density which correlates with the grade of malignancy [7], [8], [>>9<<]. Microglial cells in tumors do not secrete cytokines critical in developing effective innate immune responses and an anti-tumor immune response is suppressed in glioma patients [9], [10], [11]. The presence of cells positively stained for
n3:mentions: n2:16573834

Subject Item: _:vb12444229
rdf:type: n3:Context
rdf:value: Microglial cells in tumors do not secrete cytokines critical in developing effective innate immune responses and an anti-tumor immune response is suppressed in glioma patients [>>9<<], [10], [11].
n3:mentions: n2:16573834

Subject Item: _:vb12444230
rdf:type: n3:Context
rdf:value: Microglial cells in tumors do not secrete cytokines critical in developing effective innate immune responses and an anti-tumor immune response is suppressed in glioma patients [9], [>>10<<], [11]. The presence of cells positively stained for CD163 and CD204, putative markers for “M2” macrophages [12], as well as myeloid-derived suppressor cell-like cells have been detected in glioma patients [13]. Several glioma-secreted
n3:mentions: n2:16775224

Subject Item: _:vb12444231
rdf:type: n3:Context
rdf:value: Microglial cells in tumors do not secrete cytokines critical in developing effective innate immune responses and an anti-tumor immune response is suppressed in glioma patients [9], [10], [>>11<<]. The presence of cells positively stained for CD163 and CD204, putative markers for “M2” macrophages [12], as well as myeloid-derived suppressor cell-like cells have been detected in glioma patients [13]. Several glioma-secreted factors
n3:mentions: n2:17697783

Subject Item: _:vb12444232
rdf:type: n3:Context
rdf:value: The presence of cells positively stained for CD163 and CD204, putative markers for “M2” macrophages [>>12<<], as well as myeloid-derived suppressor cell-like cells have been detected in glioma patients [13].
n3:mentions: n2:18553315

Subject Item: _:vb12444233
rdf:type: n3:Context
rdf:value: The presence of cells positively stained for CD163 and CD204, putative markers for “M2” macrophages [12], as well as myeloid-derived suppressor cell-like cells have been detected in glioma patients [>>13<<]. Several glioma-secreted factors have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [12], [14], granulocyte/macrophage colony-stimulating factor [15], hepatocyte growth factor [16] and
n3:mentions: n2:20308313

Subject Item: _:vb12444234
rdf:type: n3:Context
rdf:value: Several glioma-secreted factors have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [>>12<<], [14], granulocyte/macrophage colony-stimulating factor [15], hepatocyte growth factor [16] and monocyte chemotactic protein 3 [17].
n3:mentions: n2:18553315

Subject Item: _:vb12444235
rdf:type: n3:Context
rdf:value: Several glioma-secreted factors have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [12], [>>14<<], granulocyte/macrophage colony-stimulating factor [15], hepatocyte growth factor [16] and monocyte chemotactic protein 3 [17].
n3:mentions: n2:8086034

Subject Item: _:vb12444236
rdf:type: n3:Context
rdf:value: Several glioma-secreted factors have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [12], [14], granulocyte/macrophage colony-stimulating factor [>>15<<], hepatocyte growth factor [16] and monocyte chemotactic protein 3 [17].
n3:mentions: n2:1377084

Subject Item: _:vb12444237
rdf:type: n3:Context
rdf:value: Several glioma-secreted factors have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [12], [14], granulocyte/macrophage colony-stimulating factor [15], hepatocyte growth factor [>>16<<] and monocyte chemotactic protein 3 [17].
n3:mentions: n2:9393765

Subject Item: _:vb12444238
rdf:type: n3:Context
rdf:value: have been characterized as promoting microglial chemotaxis: macrophage colony-stimulating factor 1 [12], [14], granulocyte/macrophage colony-stimulating factor [15], hepatocyte growth factor [16] and monocyte chemotactic protein 3 [>>17<<]. Immunosuppressive properties of glioma cancer stem cells, producing CSF-1, TGF-β1 and macrophage inhibitory cytokine, and inducing polarisation of recruited macrophages/microglia have been demonstrated [18], [19], [20].
n3:mentions: n2:19424580

Subject Item: _:vb12444239
rdf:type: n3:Context
rdf:value: Immunosuppressive properties of glioma cancer stem cells, producing CSF-1, TGF-β1 and macrophage inhibitory cytokine, and inducing polarisation of recruited macrophages/microglia have been demonstrated [>>18<<], [19], [20].
n3:mentions: n2:20068105

Subject Item: _:vb12444240
rdf:type: n3:Context
rdf:value: Immunosuppressive properties of glioma cancer stem cells, producing CSF-1, TGF-β1 and macrophage inhibitory cytokine, and inducing polarisation of recruited macrophages/microglia have been demonstrated [18], [>>19<<], [20].
n3:mentions: n2:20667896

Subject Item: _:vb12444241
rdf:type: n3:Context
rdf:value: Immunosuppressive properties of glioma cancer stem cells, producing CSF-1, TGF-β1 and macrophage inhibitory cytokine, and inducing polarisation of recruited macrophages/microglia have been demonstrated [18], [19], [>>20<<].
n3:mentions: n2:21056915

Subject Item: _:vb12444242
rdf:type: n3:Context
rdf:value: Experimental studies using brain organotypic slices depleted of microglia, genetic models of microglia ablation and microglia-glioma co-cultures pinpoint a pro-invasive role of glioma-infiltrating microglia [>>21<<], [22]. Glioma-exposed microglia release metalloproteinase MT1-MMP which activates a latent metalloproteinase 2 (pro-MMP-2) produced by glioma cells that promotes tumor invasion, as was shown using brain slices from MT1-MMP-deficient mice
n3:mentions: n2:16141784

Subject Item: _:vb12444243
rdf:type: n3:Context
rdf:value: Experimental studies using brain organotypic slices depleted of microglia, genetic models of microglia ablation and microglia-glioma co-cultures pinpoint a pro-invasive role of glioma-infiltrating microglia [21], [>>22<<]. Glioma-exposed microglia release metalloproteinase MT1-MMP which activates a latent metalloproteinase 2 (pro-MMP-2) produced by glioma cells that promotes tumor invasion, as was shown using brain slices from MT1-MMP-deficient mice and in
n3:mentions: n2:17107968

Subject Item: _:vb12444244
rdf:type: n3:Context
rdf:value: metalloproteinase MT1-MMP which activates a latent metalloproteinase 2 (pro-MMP-2) produced by glioma cells that promotes tumor invasion, as was shown using brain slices from MT1-MMP-deficient mice and in a microglia depletion model [>>23<<]. Furthermore, microglial cells secrete active TGF-β1, which stimulates glioblastoma invasion [24].
n3:mentions: n2:19617536

Subject Item: _:vb12444245
rdf:type: n3:Context
rdf:value: Furthermore, microglial cells secrete active TGF-β1, which stimulates glioblastoma invasion [>>24<<].
n3:mentions: n2:17684491

Subject Item: _:vb12444246
rdf:type: n3:Context
rdf:value: To interfere with glioma-microglia interactions, we used cyclosporine A (CsA) which has been shown to reduce microglia activation and invasion of glioma cells in vitro and in organotypic brain slices [>>22<<]. Systemically-applied CsA inhibits microglia/macrophage infiltration, induces cell death of infiltrating cells and blocks expression/activity of enzymes and cytokines, important for the establishment of a pro-invasive phenotype of
n3:mentions: n2:17107968

Subject Item: _:vb12444247
rdf:type: n5:Section
dc:title: materials and methods
n5:contains: _:vb12444248 _:vb12444249 _:vb12444250

Subject Item: _:vb12444248
rdf:type: n3:Context
rdf:value: GL261-glioma cells stably expressing pEGFP-N1 [>>21<<] obtained from Prof.
n3:mentions: n2:16141784

Subject Item: _:vb12444249
rdf:type: n3:Context
rdf:value: Primary cultures of astrocytes were prepared from cerebral cortex of 2-day-old C57BL/6 newborn mice as described previously [>>25<<]. Astrocytes were cultured in DMEM with high glucose (GlutaMAX™, Gibco) supplemented with 10% FBS, 100 U/ml penicillin and 100 µg/ml streptomycin.
n3:mentions: n2:15758174

Subject Item: _:vb12444250
rdf:type: n3:Context
rdf:value: Arginase activity was determined in brain tissue extracts using a colorimetric method based on the conversion of L-arginine to L-ornithine as described [>>26<<]. Optical density of ornithine-ninhydrin complexes formed in the samples was measured using a microplate reader at 515 nm.
n3:mentions: n2:3707749

Subject Item: _:vb12444251
rdf:type: n5:Section
dc:title: results
n5:contains: _:vb12444252 _:vb12444253

Subject Item: _:vb12444252
rdf:type: n3:Context
rdf:value: Differences in the surface expression of CD11b and CD45 antigens on microglia (CD11b+/CD45low) and blood-derived macrophages (CD11b+/CD45high) isolated from tumor tissue permitted distinction of the two populations by flow cytometry [>>27<<]. We determined the relative contribution of resident and blood-derived cells to the Iba1-positive population within the tumor.
n3:mentions: n2:1651506

Subject Item: _:vb12444253
rdf:type: n3:Context
rdf:value: CsA effectively impairs the pro-invasive activity of microglia in vitro and in organotypic brain slices [>>22<<]. As kinetic studies indicated different phases of microglia and macrophage accumulation, CsA was injected starting from the 2nd or 8th day after tumor implantation.
n3:mentions: n2:17107968

Subject Item: _:vb12444254
rdf:type: n5:Section
dc:title: discussion
n5:contains: _:vb12444255 _:vb12444284 _:vb12444285 _:vb12444286 _:vb12444287 _:vb12444280 _:vb12444281 _:vb12444282 _:vb12444283 _:vb12444276 _:vb12444277 _:vb12444278 _:vb12444279 _:vb12444272 _:vb12444273 _:vb12444274 _:vb12444275 _:vb12444268 _:vb12444269 _:vb12444270 _:vb12444271 _:vb12444264 _:vb12444265 _:vb12444266 _:vb12444267 _:vb12444260 _:vb12444261 _:vb12444262 _:vb12444263 _:vb12444256 _:vb12444257 _:vb12444258 _:vb12444259

Subject Item: _:vb12444255
rdf:type: n3:Context
rdf:value: The concept that macrophages play instructive roles in tumor growth by regulating cell motility, invasion, angiogenesis and immunomodulation has gained great attention over last years. [>>2<<], [28], [29]. Tumor-derived cytokines such as IL-4, IL-10, TGF-β, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype [30], [31].
n3:mentions: n2:20371344

Subject Item: _:vb12444256
rdf:type: n3:Context
rdf:value: The concept that macrophages play instructive roles in tumor growth by regulating cell motility, invasion, angiogenesis and immunomodulation has gained great attention over last years. [2], [>>28<<], [29]. Tumor-derived cytokines such as IL-4, IL-10, TGF-β, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype [30], [31].
n3:mentions: n2:16439202

Subject Item: _:vb12444257
rdf:type: n3:Context
rdf:value: [2], [28], [>>29<<]. Tumor-derived cytokines such as IL-4, IL-10, TGF-β, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype [30], [31].
n3:mentions: n2:17114237

Subject Item: _:vb12444258
rdf:type: n3:Context
rdf:value: Tumor-derived cytokines such as IL-4, IL-10, TGF-β, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype [>>30<<], [31]. Mechanisms of accumulation and a role of microglia/macrophages in glioma pathobiology are still poorly understood and controversial. Several experimental studies demonstrated that microglia contribute to glioma progression by
n3:mentions: n2:16520032

Subject Item: _:vb12444259
rdf:type: n3:Context
rdf:value: Tumor-derived cytokines such as IL-4, IL-10, TGF-β, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype [30], [>>31<<]. Mechanisms of accumulation and a role of microglia/macrophages in glioma pathobiology are still poorly understood and controversial. Several experimental studies demonstrated that microglia contribute to glioma progression by secreting
n3:mentions: n2:19741157

Subject Item: _:vb12444260
rdf:type: n3:Context
rdf:value: Several experimental studies demonstrated that microglia contribute to glioma progression by secreting growth factors, angiogenic molecules, extracellular matrix–degrading enzymes, and immunosuppressive factors [>>21<<], [22], [23], [24].
n3:mentions: n2:16141784

Subject Item: _:vb12444261
rdf:type: n3:Context
rdf:value: Several experimental studies demonstrated that microglia contribute to glioma progression by secreting growth factors, angiogenic molecules, extracellular matrix–degrading enzymes, and immunosuppressive factors [21], [>>22<<], [23], [24].
n3:mentions: n2:17107968

Subject Item: _:vb12444262
rdf:type: n3:Context
rdf:value: Several experimental studies demonstrated that microglia contribute to glioma progression by secreting growth factors, angiogenic molecules, extracellular matrix–degrading enzymes, and immunosuppressive factors [21], [22], [>>23<<], [24]. However, Galarneau et al. showed that ablation of CD11b cells (ganciclovir-treated B6 mice expressing a mutant form of HSV-1 TKmt-30 under CD11b promoter) increases glioma growth [32], a recent study demonstrated that ablation of
n3:mentions: n2:19617536

Subject Item: _:vb12444263
rdf:type: n3:Context
rdf:value: Several experimental studies demonstrated that microglia contribute to glioma progression by secreting growth factors, angiogenic molecules, extracellular matrix–degrading enzymes, and immunosuppressive factors [21], [22], [23], [>>24<<]. However, Galarneau et al. showed that ablation of CD11b cells (ganciclovir-treated B6 mice expressing a mutant form of HSV-1 TKmt-30 under CD11b promoter) increases glioma growth [32], a recent study demonstrated that ablation of CD11b
n3:mentions: n2:17684491

Subject Item: _:vb12444264
rdf:type: n3:Context
rdf:value: However, Galarneau et al. showed that ablation of CD11b cells (ganciclovir-treated B6 mice expressing a mutant form of HSV-1 TKmt-30 under CD11b promoter) increases glioma growth [>>32<<], a recent study demonstrated that ablation of CD11b in vivo (ganciclovir-treated CD11b-HSVTK mice) decreases tumor size and improves survival [33].
n3:mentions: n2:17875729

Subject Item: _:vb12444265
rdf:type: n3:Context
rdf:value: expressing a mutant form of HSV-1 TKmt-30 under CD11b promoter) increases glioma growth [32], a recent study demonstrated that ablation of CD11b in vivo (ganciclovir-treated CD11b-HSVTK mice) decreases tumor size and improves survival [>>33<<].
n3:mentions: n2:21264953

Subject Item: _:vb12444266
rdf:type: n3:Context
rdf:value: The relevance of this finding for human pathology is unclear, because although human astrocytoma and glioblastoma cell lines produce GM-CSF, no evidence of its production by glioblastoma cells was found in vivo [>>34<<]. Our findings suggest that GM-CSF and IL-10 could be important cytokines for establishment of a pro-invasive phenotype of glioma-infiltrating microglia/macrophages.
n3:mentions: n2:1315829

Subject Item: _:vb12444267
rdf:type: n3:Context
rdf:value: The macrophagic expression of Arg-1 is tightly regulated by exogenous stimuli such as IL-4 and IL-13 [>>35<<]. L-arginine depletion due to extensive myeloid arginase activity may suppress T cell immune responses [36]. Expression of iNos and Arg-1 define classically and alternatively activated macrophages in the context of Th2-polarised immune
n3:mentions: n2:9605134

Subject Item: _:vb12444268
rdf:type: n3:Context
rdf:value: L-arginine depletion due to extensive myeloid arginase activity may suppress T cell immune responses [>>36<<]. Expression of iNos and Arg-1 define classically and alternatively activated macrophages in the context of Th2-polarised immune responses [37], [38]. Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma
n3:mentions: n2:19764983

Subject Item: _:vb12444269
rdf:type: n3:Context
rdf:value: Expression of iNos and Arg-1 define classically and alternatively activated macrophages in the context of Th2-polarised immune responses [>>37<<], [38]. Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma [39], in the human papillomavirus E6/E7-expressing murine tumors [40] and in CD11b+/CD14− myeloid cells from renal carcinoma patients [41].
n3:mentions: n2:20483789

Subject Item: _:vb12444270
rdf:type: n3:Context
rdf:value: Expression of iNos and Arg-1 define classically and alternatively activated macrophages in the context of Th2-polarised immune responses [37], [>>38<<]. Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma [39], in the human papillomavirus E6/E7-expressing murine tumors [40] and in CD11b+/CD14− myeloid cells from renal carcinoma patients [41].
n3:mentions: n2:19360123

Subject Item: _:vb12444271
rdf:type: n3:Context
rdf:value: Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma [>>39<<], in the human papillomavirus E6/E7-expressing murine tumors [40] and in CD11b+/CD14− myeloid cells from renal carcinoma patients [41].
n3:mentions: n2:15313928

Subject Item: _:vb12444272
rdf:type: n3:Context
rdf:value: Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma [39], in the human papillomavirus E6/E7-expressing murine tumors [>>40<<] and in CD11b+/CD14− myeloid cells from renal carcinoma patients [41].
n3:mentions: n2:19549768

Subject Item: _:vb12444273
rdf:type: n3:Context
rdf:value: Enhanced expression of Arg-1 associated with TAMs was found in 3LL murine lung carcinoma [39], in the human papillomavirus E6/E7-expressing murine tumors [40] and in CD11b+/CD14− myeloid cells from renal carcinoma patients [>>41<<]. Cyclooxygenase-2 (COX-2) expression and prostaglandins (PGE) have been implicated in the development of many cancers [42] serving as pro-inflammatory mediators under some conditions, but having anti-inflammatory and immunosuppressive
n3:mentions: n2:17255300

Subject Item: _:vb12444274
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rdf:value: Cyclooxygenase-2 (COX-2) expression and prostaglandins (PGE) have been implicated in the development of many cancers [>>42<<] serving as pro-inflammatory mediators under some conditions, but having anti-inflammatory and immunosuppressive properties under other conditions [43].
n3:mentions: n2:19136477

Subject Item: _:vb12444275
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rdf:value: and prostaglandins (PGE) have been implicated in the development of many cancers [42] serving as pro-inflammatory mediators under some conditions, but having anti-inflammatory and immunosuppressive properties under other conditions [>>43<<]. Stimulation of PGE2 signalling in dendritic cells facilitates their migration and maturation, while in T cells potently suppresses activation and proliferation [44].
n3:mentions: n2:15563582

Subject Item: _:vb12444276
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rdf:value: Stimulation of PGE2 signalling in dendritic cells facilitates their migration and maturation, while in T cells potently suppresses activation and proliferation [>>44<<]. The observed up-regulation of cox2 mRNA in CD11b+ cells corroborates with a study showing the macrophagic expression of COX-2 and enhanced production of PGE1 by glioma-derived factors [45]. A chemokine CXCL14 was identified as a
n3:mentions: n2:14607267

Subject Item: _:vb12444277
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rdf:value: The observed up-regulation of cox2 mRNA in CD11b+ cells corroborates with a study showing the macrophagic expression of COX-2 and enhanced production of PGE1 by glioma-derived factors [>>45<<]. A chemokine CXCL14 was identified as a chemoattractant for monocytes [46], and can induce dendritic cell migration and maturation [47], [48]. The enhanced expression of cxcl14 in glioma-infiltrating CD11b+ cells could be involved in
n3:mentions: n2:18240928

Subject Item: _:vb12444278
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rdf:value: A chemokine CXCL14 was identified as a chemoattractant for monocytes [>>46<<], and can induce dendritic cell migration and maturation [47], [48].
n3:mentions: n2:11561000

Subject Item: _:vb12444279
rdf:type: n3:Context
rdf:value: A chemokine CXCL14 was identified as a chemoattractant for monocytes [46], and can induce dendritic cell migration and maturation [>>47<<], [48]. The enhanced expression of cxcl14 in glioma-infiltrating CD11b+ cells could be involved in macrophage infiltration or their differentiation. Down-regulation of cxcl14 expression in CsA-treated mice correlates with reduced CD11b+
n3:mentions: n2:15548693

Subject Item: _:vb12444280
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rdf:value: A chemokine CXCL14 was identified as a chemoattractant for monocytes [46], and can induce dendritic cell migration and maturation [47], [>>48<<]. The enhanced expression of cxcl14 in glioma-infiltrating CD11b+ cells could be involved in macrophage infiltration or their differentiation. Down-regulation of cxcl14 expression in CsA-treated mice correlates with reduced CD11b+ cell
n3:mentions: n2:15843547

Subject Item: _:vb12444281
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rdf:value: Depleting macrophages in tumors in CSF-1 null mice (Csf1op) delayed the angiogenic switch and malignant transition, whereas restoration of macrophages rescued the vessel phenotype in these tumors [>>29<<]. High-grade gliomas demonstrate the highest levels of tumor angiogenesis when compared to non-neural solid cancers. Numbers of infiltrating macrophages have been found to correlate with small vessel density and tumor grade [49]. We
n3:mentions: n2:17114237

Subject Item: _:vb12444282
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rdf:value: Numbers of infiltrating macrophages have been found to correlate with small vessel density and tumor grade [>>49<<]. We observed an increase in microglia/macrophage infiltration and the development of a dense vessel network in implanted gliomas (not shown). Furthermore, early treatment with CsA inhibited vessel network development in tumor-bearing mice.
n3:mentions: n2:10353745

Subject Item: _:vb12444283
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rdf:value: Evaluation of implanted GL261 mouse gliomas by MR microimaging indicated blood-brain barrier disruption already in early-stage of tumors (1–2 week) [>>50<<]. Thus intraperitoneally administered CsA can easily penetrate brain parenchyma.
n3:mentions: n2:12704767

Subject Item: _:vb12444284
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rdf:value: Previous studies showed an important role of microglia-derived MT1-MMP in regulation of MMP-2 activity [>>21<<], [23].
n3:mentions: n2:16141784

Subject Item: _:vb12444285
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rdf:value: Previous studies showed an important role of microglia-derived MT1-MMP in regulation of MMP-2 activity [21], [>>23<<].
n3:mentions: n2:19617536

Subject Item: _:vb12444286
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rdf:value: Despite of developments of new therapeutics, glioblastomas are difficult to treat due to frequent dysfunctions of tumor suppressors and oncogenes; the mean survival of patients with glioblastomas ranges between 1–2 years [>>51<<], [52]. Counteracting of brain macrophage accumulation and activation should be taken into account when considering the development of more effective therapy against malignant gliomas.
n3:mentions: n2:19723323

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rdf:value: Despite of developments of new therapeutics, glioblastomas are difficult to treat due to frequent dysfunctions of tumor suppressors and oncogenes; the mean survival of patients with glioblastomas ranges between 1–2 years [51], [>>52<<]. Counteracting of brain macrophage accumulation and activation should be taken into account when considering the development of more effective therapy against malignant gliomas.
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