ライフサイエンスコーパス: tumor-associated macrophage

1 o localized, biomaterial-based modulation of tumor-associated macrophage.

2 act on the crosstalk of tumor cells with the tumor associated macrophages.

3 and/or immune cells, the most critical being tumor-associated macrophages.

4 nd their presence correlated with that of M2 tumor-associated macrophages.

5 target genes in CD163(+) tissue-resident and tumor-associated macrophages.

6 ted on the surface of macrophages, including tumor-associated macrophages.

7 but not primary tumor growth, which involves tumor-associated macrophages.

8 as revealed the extensive presence of NLRC4+ tumor-associated macrophages.

9 by driving the recruitment of MMP9-positive tumor-associated macrophages.

10 as associated with both tumor cells and with tumor-associated macrophages.

11 toxic cells (P < .001), but no difference in tumor-associated macrophages.

12 tected in vivo in liver Kupffer cells and in tumor-associated macrophages.

13 on of factors that are recognized by SR-A on tumor-associated macrophages.

14 phages showed that ATM, but not MDM resemble tumor-associated macrophages.

15 ride-unresponsive phenotype close to that of tumor-associated macrophages.

16 reast cancers associated with high levels of tumor-associated macrophages.

17 to notable efforts to deplete or repolarize tumor-associated macrophages.

18 the frequency of CD163(+) anti-inflammatory tumor-associated macrophages.

19 M-CSF by increasing sVEGFR-1 production from tumor-associated macrophages.

20 obese versus lean women are more similar to tumor-associated macrophages.

21 ating macrophages from inflamed synovium and tumor-associated macrophages.

22 y "cold" tumors by recruiting and modulating tumor-associated macrophages.

23 etermine the role of Foxm1 in recruitment of tumor-associated macrophages, a mouse line with macropha

24 -infiltrating CD8(+) and CD4(+) T cells, and tumor-associated macrophage activation.

25 Our data demonstrates that tumor-associated macrophages also form them.

26 ecreased the suppressive lymphocytes such as tumor associated macrophages and myeloid derived suppres

27 Armored CAR T cells mediated depletion of tumor associated macrophages and resisted endogenous PD-

28 opulation increased while the populations of tumor-associated macrophage and regulatory T cell declin

29 pendent both on a paracrine interaction with tumor-associated macrophages and an autocrine regulation

30 Furthermore, we found increased tumor-associated macrophages and an enhanced effect of a

31 eflected by a decrease in the M2/M1 ratio of tumor-associated macrophages and an upregulation of CD3(

32 The depleted cells shared markers of tumor-associated macrophages and dendritic cells (M-DCs)

33 Cassetta and Pollard introduce tumor-associated macrophages and discuss their origin, d

34 umor-bearing mice also exerted morphology of tumor-associated macrophages and expressed high levels o

35 eveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute

36 poor prognosis, and enhanced recruitment of tumor-associated macrophages and fibroblasts, we propose

37 cells of the tumor microenvironment, such as tumor-associated macrophages and fibroblasts, which were

38 associated with an inflammatory phenotype of tumor-associated macrophages and fibroblasts, with conco

39 s and a correlation between B7-H4-expressing tumor-associated macrophages and FoxP3(+) regulatory T c

40 s, subsequently affecting the recruitment of tumor-associated macrophages and IL17A synthesis.

41 Tumor-associated macrophages and microglia (TAMs) have b

42 sociated immune infiltrates are dominated by tumor-associated macrophages and microglia (TAMs), which

43 ells in the glioma microenvironment, such as tumor-associated macrophages and microglia (TAMs).

44 Hence, modulation and reeducation of tumor-associated macrophages and microglia in GBM is con

45 Myeloid cells, including tumor-associated macrophages and myeloid-derived suppres

46 escape in the tumor microenvironment include tumor-associated macrophages and myeloid-derived suppres

47 CSF1 receptor on MSCs, drives recruitment of tumor-associated macrophages and myeloid-derived suppres

48 Recruitment of tumor-associated macrophages and neutrophils (TAM and TA

49 newal and induces the recruitment of M2-like tumor-associated macrophages and regulatory T cells, thu

50 eficient displayed an enhanced proportion of tumor-associated macrophages and regulatory T cells.

51 ctivity suppresses alternative activation of tumor-associated macrophages and the growth of colon can

52 rowth, but instead increased the presence of tumor-associated macrophages and the metastatic spread o

53 We further demonstrate that coculture of tumor-associated macrophages and tumor cells induces sec

54 mary tumors in proximity to CD206(+)CD163(+) tumor-associated macrophages and vessels.

55 cal for cytokine and chemokine production in tumor-associated macrophages and was necessary for the g

56 nt increases in MHCII and IL12 expression in tumor-associated macrophages and with >90% reductions in

57 d molecular similarities between obesity and tumor-associated macrophages, and assessed the regulator

58 production of IFNalpha by activated MHCII(+) tumor-associated macrophages, and enables tumor regressi

59 ctivated receptorgamma, is also expressed in tumor-associated macrophages, and its inhibition blocks

60 mune modulators, such as regulatory T cells, tumor-associated macrophages, and myeloid-derived suppre

61 is mediated by its effect on tumor cells and tumor-associated macrophages, and not directly over T ce

62 PD-L1 is expressed on tumor cells, tumor-associated macrophages, and other cells in the tum

63 First, systemic methods for targeting tumor-associated macrophage are summarized and limitatio

64 for Ki-67 and the macrophage marker CD68, as tumor-associated macrophages are important for PNET deve

65 Tumor-associated macrophages are increasingly viewed as

66 Although increased numbers of tumor-associated macrophages are linked to poor prognosi

67 Tumor-associated macrophages are major contributors to m

68 ied CtsZ, which is predominantly supplied by tumor-associated macrophages, as the compensatory protea

69 4-deficient mice contained higher numbers of tumor-associated macrophages, as well as more lymphatic

70 tion in type 1 regulatory T cells and PD-L1+ tumor-associated macrophages at this early time point of

71 induces not only an expected deprivation of tumor-associated macrophages, but also an accumulation o

72 Other immune cells such as tumor-associated macrophages can have other pro-tumorige

73 Tumor-associated macrophages constitute a major componen

74 ler tumors, prolonged survival and a reduced tumor-associated macrophage content.

75 Tumor-associated macrophages contribute to tumor progres

76 n E-R72 mice also had an increased influx of tumor-associated macrophages, contributing to angiogenes

77 expression in epithelial cells is induced by tumor-associated macrophages, contributing to the recipr

78 T cell IFN-gamma and GM-CSF activated local, tumor-associated macrophages, decreased expression of re

79 d with >90% reductions in IL10 expression in tumor-associated macrophages, dendritic cells (DC), and

80 Here, we report that caspase-1 promotes tumor-associated macrophage differentiation by cleaving

81 endogenous regulatory mechanisms underlying tumor-associated macrophage differentiation remain large

82 accumulation of lipid droplets and promoting tumor-associated macrophage differentiation.

83 In high-grade tumors, both tumor cells and tumor-associated macrophages exhibited high expression l

84 xpression by T cells is necessary for proper tumor-associated macrophage expression of IFNgamma-induc

85 poA1 in the tumor microenvironment, altering tumor-associated macrophages from a pro-tumor M2 to an a

86 secrete stimulating factors, which polarize tumor-associated macrophages from an antitumor M1 phenot

87 are superior to the high doses in polarizing tumor-associated macrophages from an immune inhibitory M

88 -derived xenograft resulted in a shift among tumor-associated macrophages from the immunosuppressive

89 bility to redirect the polarization state of tumor-associated macrophages (from M1/immunogenic/proinf

90 Tumor-associated macrophages have been shown to promote

91 Tumor-associated macrophages have recently emerged as a

92 e of Immunity, Zhu et al. (2017) report that tumor-associated macrophages in a mouse model of pancrea

93 cretion of proinflammatory cytokine IL6 from tumor-associated macrophages in a TLR7/8-dependent manne

94 and to reduce monocyte differentiation into tumor-associated macrophages in an MCA-203 fibrosarcoma

95 We confirmed increased tumor-associated macrophages in bevacizumab-resistant gl

96 large-scale single-cell RNA-seq analysis of tumor-associated macrophages in gliomas has unveiled a n

97 ters PRMT1 expression in blood monocytes and tumor-associated macrophages in human HCC.

98 This study points to a new role for tumor-associated macrophages in the induction of a const

99 (FLIM) as a means to non-invasively identify tumor-associated macrophages in the intact mammary tumor

100 promotes the protumoral M2-like phenotype of tumor-associated macrophages in the tumor microenvironme

101 Since B7-H4 is expressed on tumor cells and tumor-associated macrophages in various cancer types, th

102 ver, we detected CD163, a reliable marker of tumor-associated macrophages, in the tumor microenvironm

103 p110alpha interaction altered the nature of tumor-associated macrophages, inducing expression of mar

104 rized by enhanced angiogenesis and augmented tumor-associated macrophage infiltration and M2 polariza

105 Nuclear density, tumor-associated macrophage infiltration, and nuclear mo

106 tumor microenvironment, whereby Ron loss in tumor-associated macrophages inhibits prostate cancer ce

107 ombination with cisplatin; and reprogramming tumor-associated macrophages into a proinflammatory stat

108 -L1 expression on both tumor cells and CD68+ tumor-associated macrophages is geographically localized

109 arizes M0-macrophages into Gas6-secreting M2-tumor-associated macrophages (M2-TAMs).

110 egulatory networks of mesenchymal-associated tumor-associated macrophages (MA-TAMs), which drive the

111 CD163 positive tumor-associated macrophages, many of which coexpress CD

112 lular matrix (ECM) in response to injury and tumor-associated macrophage microenvironmental cues faci

113 We present evidence that tumor-associated macrophages/microglia (TAMs) can promot

114 NF1 deficiency resulted in increased tumor-associated macrophages/microglia infiltration.

115 and murine models correlates with increased tumor-associated macrophages/monocytes/microglia.

116 In contrast to tumor-associated macrophages, myeloid-derived suppressor

117 In contrast, there was a paucity of NLRC4+ tumor-associated macrophages observed in human metastati

118 Furthermore, tumor-associated macrophages of the corresponding tumors

119 mune checkpoints other than PD-1; modulating tumor-associated macrophage phenotype from tumor-promoti

120 3.5 million measured cells, we identified 17 tumor-associated macrophage phenotypes, 22 T cell phenot

121 Interactions between tumor cells and tumor-associated macrophages play critical roles in the

122 tumor-induced macrophages represent a major tumor-associated macrophage population, which can furthe

123 sized that a tumor-extrinsic factor, notably tumor-associated macrophages, promotes and contributes t

124 for OC progression principally by promoting tumor-associated macrophage recruitment and activation v

125 ion of mast cells suppresses accumulation of tumor-associated macrophages, reduces tumor cell prolife

126 pression of fibroblast-activating factors in tumor-associated macrophages resulting in decreased abun

127 ced acquisition of procancerous phenotype by tumor-associated macrophages, resulting in activation of

128 rison with gene expression profiles of human tumor-associated macrophages showed that ATM, but not MD

129 myeloid-derived suppressor cells (MDSC) and tumor-associated macrophage (TAM) also inhibit antitumor

130 eolin protein family, increases M1-polarized tumor-associated macrophage (TAM) and CD8 T cell infiltr

131 t and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived su

132 cer Cell, Casazza and colleagues report that tumor-associated macrophage (TAM) entry into avascular t

133 h reflected high vascularization and greater tumor-associated macrophage (TAM) levels.

134 restingly, HOXB7 overexpression also induced tumor-associated macrophage (TAM) recruitment and acquis

135 Tumor-associated macrophage (TAM) significantly contribu

136 prised of discrete MHC-II(hi) and MHC-II(lo) tumor-associated macrophage (TAM) subpopulations that or

137 er, MUC1-ST induced macrophages to display a tumor-associated macrophage (TAM)-like phenotype, with i

138 cells restored activation of proinflammatory tumor-associated macrophages (TAM) and intratumoral immu

139 Tumor-associated macrophages (TAM) and myofibroblasts ar

140 d therapy-induced tumor regression; however, tumor-associated macrophages (TAM) and their products ma

141 Tumor-associated macrophages (TAM) are an important comp

142 Tumor-associated macrophages (TAM) are exposed to multip

143 Tumor-associated macrophages (TAM) are highly expressed

144 Tumor-associated macrophages (TAM) are important compone

145 Tumor-associated macrophages (TAM) are important tumor-p

146 Tumor-associated macrophages (TAM) are known to limit th

147 Tumor-associated macrophages (TAM) contribute to all asp

148 Accumulation of tumor-associated macrophages (TAM) correlates with malig

149 myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) in tumor tissue has b

150 r (NSCLC), accumulation of anti-inflammatory tumor-associated macrophages (TAM) is associated with wo

151 Monocyte-derived Mvarphi or tumor-associated macrophages (TAM) isolated from HCC tis

152 among them being of monocytic origin such as tumor-associated macrophages (TAM) or myeloid-derived su

153 In the tumor stroma, E-FABP-expressing tumor-associated macrophages (TAM) produce high levels o

154 Growing evidence suggests that tumor-associated macrophages (TAM) promote cancer progre

155 Tumor-associated macrophages (TAM) promote triple-negati

156 In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to one h

157 ting, including from tumor stromal cells and tumor-associated macrophages (TAM) that contribute struc

158 myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) that inhibit T cells

159 mic reticulum chaperone gp96 is essential in tumor-associated macrophages (TAM) to license their cont

160 ntitumoral and protumoral roles of M1 and M2 tumor-associated macrophages (TAM) typify the complexity

161 with tumor-associated neutrophils (TAN) and tumor-associated macrophages (TAM) versus females, and t

162 Tumor-associated macrophages (TAM) were more numerous in

163 IM), including CD11b (ITGAM)(+)F4/80 (EMR1)+ tumor-associated macrophages (TAM), and CD11b(+)Gr-1 (LY

164 B7-H4 is expressed by tumor cells and tumor-associated macrophages (TAM), but its potential co

165 s and tumor-derived myeloid cells, including tumor-associated macrophages (TAM), dendritic cells, and

166 vels of CCL3 were detected in LRP1-deficient tumor-associated macrophages (TAM), isolated from PanO2

167 as critical for the interaction of CSCs with tumor-associated macrophages (TAM), leading to enhanced

168 nt creates an immunosuppressive signature on tumor-associated macrophages (TAM), which favors express

169 d markedly in primary melanomas and CD163(+) tumor-associated macrophages (TAM).

170 ber and metastatic potential of infiltrating tumor-associated macrophages (TAM).

171 nd constitutive TTP expression in late-stage tumor-associated macrophages (TAM).

172 cells of the tumor stroma, in particular in tumor-associated macrophages (TAM).

173 erleukin (IL)-10-mediated M2 polarization of tumor-associated macrophages (TAM).

174 etastatic gene expression and recruitment of tumor-associated macrophages (TAM).

175 eg-attracting chemokine Ccl17 by MHCII(high) tumor-associated macrophages (TAM).

176 reased numbers of lymphatic vessels (LV) and tumor-associated macrophages (TAM).

177 decreased the immunosuppressive function of tumor-associated macrophages (TAM).

178 approaches that rely on immune modulation of tumor associated macrophages (TAMs) from a pro-tumorigen

179 Within the TME, tumor associated macrophages (TAMs) mediate angiogenesis

180 Tumor associated macrophages (TAMs) play a critical role

181 peutic approach to prevent tumor progression.Tumor associated macrophages (TAMs) promote cancer progr

182 s to IH accelerated tumor progression with a tumor associated macrophages (TAMs) shift towards a pro-

183 ration, NHWD-870 blocks the proliferation of tumor associated macrophages (TAMs) through multiple mec

184 that elicits recruitment and polarization of tumor associated macrophages (TAMs).

185 Absence of miR-21 expression in tumor- associated macrophages (TAMs), caused a global re

186 Furthermore, it is likely that TANs and tumor-associated macrophages (TAMs) act in tandem within

187 The roles of tumor-associated macrophages (TAMs) and circulating mono

188 h contributes to differentiation of MDSCs to tumor-associated macrophages (TAMs) and DCs.

189 Tumor-associated macrophages (TAMs) and tumor-associated

190 Tumor-associated macrophages (TAMs) are a complex and he

191 Tumor-associated macrophages (TAMs) are a major componen

192 Tumor-associated macrophages (TAMs) are abundant in glio

193 In tumors, a polarized M2 phenotype called tumor-associated macrophages (TAMs) are associated with

194 CD11b(+)Gr1(+) suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) are considered a maj

195 Tumor-associated macrophages (TAMs) are essential compon

196 Tumor-associated macrophages (TAMs) are increasingly inv

197 nant disease progression, both apoptosis and tumor-associated macrophages (TAMs) are often associated

198 In cancer, tumor-associated macrophages (TAMs) are recruited to the

199 Increased tumor-associated macrophages (TAMs) are reported to be a

200 e stromal cell types common to solid tumors, tumor-associated macrophages (TAMs) are significant for

201 Tumor-associated macrophages (TAMs) are the major compon

202 pressor cells (MDSCs) and differentiation of tumor-associated macrophages (TAMs) are the major factor

203 Tumor-associated macrophages (TAMs) are the most abundan

204 Tumor-associated macrophages (TAMs) are the most promine

205 Herein, we identify tumor-associated macrophages (TAMs) as the primary sourc

206 Accumulation of tumor-associated macrophages (TAMs) associates with mali

207 Tumor-associated macrophages (TAMs) can exist in pro- an

208 Tumor-associated macrophages (TAMs) can have protumor pr

209 Tumor-associated macrophages (TAMs) can influence ovaria

210 M2 polarization of tumor-associated macrophages (TAMs) correlates with poor

211 Tumor-associated macrophages (TAMs) derived from primary

212 Tumor-associated macrophages (TAMs) exhibit an M2 macrop

213 However, tumor-associated macrophages (TAMs) express cytokines an

214 Tumor-associated macrophages (TAMs) expressing the multi

215 Tumor-associated macrophages (TAMs) facilitate disease p

216 myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) form an important co

217 llmarks of malignancy is the polarization of tumor-associated macrophages (TAMs) from a pro-immune (M

218 Tumor-associated macrophages (TAMs) have a significant p

219 Tumor-associated macrophages (TAMs) have been shown to p

220 Tumor-associated macrophages (TAMs) have essential roles

221 Of the cell types in the TME, tumor-associated macrophages (TAMs) have gained attentio

222 The role of tumor-associated macrophages (TAMs) in cancer is often c

223 ut to test the hypothesis that morphology of tumor-associated macrophages (TAMs) in colorectal liver

224 iptolide conjugate that specifically targets tumor-associated macrophages (TAMs) in glioblastoma from

225 Tumor-associated macrophages (TAMs) in localized and met

226 The presence of tumor-associated macrophages (TAMs) in patients with HCC

227 Recent studies of the role of tumor-associated macrophages (TAMs) in the progression o

228 ensive reports have defined the dual role of tumor-associated macrophages (TAMs) in tumor development

229 myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) into tumor microenvi

230 Tumor-associated macrophages (TAMs) isolated from Camkk2

231 Both peripheral and tumor-associated macrophages (TAMs) isolated from melano

232 Tumor-associated macrophages (TAMs) play an essential ro

233 Tumor-associated macrophages (TAMs) play an important ro

234 become a prominent therapeutic target, with tumor-associated macrophages (TAMs) playing a critical r

235 In particular, tumor-associated macrophages (TAMs) produce many cytokin

236 Tumor-associated macrophages (TAMs) promote tumor develo

237 ile anti-inflammatory M2 macrophages such as tumor-associated macrophages (TAMs) promote tumor growth

238 y between glioblastoma stem cells (GSCs) and tumor-associated macrophages (TAMs) promotes progression

239 ntially differentiate into immunosuppressive tumor-associated macrophages (TAMs) rather than immunost

240 Tumor-associated macrophages (TAMs) recruited from blood

241 In this context, tumor-associated macrophages (TAMs) represent key regula

242 Tumor-associated macrophages (TAMs) represent the most a

243 an increase in CD1C(+) dendritic cells, the tumor-associated macrophages (TAMs) showed pro-tumoral f

244 Tumor-associated macrophages (TAMs) support tumor growth

245 Among tumor-infiltrating immune cells, tumor-associated macrophages (TAMs) take a center stage

246 sion of which correlates with the numbers of tumor-associated macrophages (TAMs) that are found in th

247 ary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypica

248 e (MSS) phenotypes and had a high density of tumor-associated macrophages (TAMs) that expressed CD274

249 mor microenvironment, where they mature into tumor-associated macrophages (TAMs) that promote disease

250 ccine activates the NF-kappaB pathway in the tumor-associated macrophages (TAMs) through the TLR2 and

251 factors, secreted by cancer cells, polarize tumor-associated macrophages (TAMs) to a tumorigenic M2

252 of cancers is known to favor polarization of tumor-associated macrophages (TAMs) to alternatively act

253 ted within the tumor microenvironment induce tumor-associated macrophages (TAMs) to differentiate int

254 ling pathway responsible for polarization of tumor-associated macrophages (TAMs) to immunosuppressive

255 Tumor-associated macrophages (TAMs) usually display an a

256 Tumor-associated macrophages (TAMs) usually express an M

257 We found that the number of tumor-associated macrophages (TAMs) was not affected by

258 t exhibited distinct transcriptional states, tumor-associated macrophages (TAMs) were associated with

259 ions between exhausted T cells and SLAMF7(+) tumor-associated macrophages (TAMs), and a unique subset

260 PD-L1 is also expressed by nonmalignant tumor-associated macrophages (TAMs), but the relationshi

261 The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs), either of periphera

262 ion of colony-stimulating factor-1 while the tumor-associated macrophages (TAMs), in turn, aid in tum

263 mor spatial structure is the localization of tumor-associated macrophages (TAMs), one of the most com

264 Recent data indicated that tumor-associated macrophages (TAMs), which are abundant

265 eath-1 ligand (PD-L1)-positive HRS cells and tumor-associated macrophages (TAMs), which associate wit

266 ionable, given the well-known limitations of tumor-associated macrophages (TAMs).

267 ), resident natural killer cells (NKRs), and tumor-associated macrophages (TAMs).

268 ocytes that appear in the circulation and as tumor-associated macrophages (TAMs).

269 , we analyzed its expression and function in tumor-associated macrophages (TAMs).

270 Dual therapy also led to changes in tumor-associated macrophages (TAMs).

271 t M1-type macrophages, and the occurrence of tumor-associated macrophages (TAMs).

272 eath, leading to an increase in inflammatory tumor-associated macrophages (TAMs).

273 undly influence or depend on the function of tumor-associated macrophages (TAMs).

274 or growth by impairing classic activation of tumor-associated macrophages (TAMs).

275 NKT cells inhibit tumor growth by targeting tumor-associated macrophages (TAMs).

276 mmunosuppressive microenvironment created by tumor-associated macrophages (TAMs).

277 eritoneally (i.p.) selectively accumulate in tumor-associated macrophages (TAMs).

278 t by promoting the survival of both GSCs and tumor-associated macrophages (TAMs).

279 finity for cognate Fc receptors expressed by tumor-associated macrophages (TAMs).

280 cid synthesis in immunosuppressive (M2-like) tumor-associated macrophages (TAMs).

281 Iron deposits are a phenotypic trait of tumor-associated macrophages (TAMs).

282 d use of these inhibitors as tools to ablate tumor-associated macrophages that enable malignant progr

283 melanoma, PHD3 expression marked a subset of tumor-associated macrophages that exhibit a weak (e.g.,

284 We also defined a population of tumor-associated macrophages that increase dramatically

285 Compared to tissue-resident tumor-associated macrophages, these newly differentiated

286 data show that MCMV infection and sensing in tumor-associated macrophages through STING signaling is

287 owed the extramedullary tissue to supply new tumor-associated macrophages throughout cancer progressi

288 immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one, w

289 cinoma cells secrete VEGFA, which stimulates tumor-associated macrophages to produce CXCL1 in the pri

290 ary malignant cell-secreted VEGFA stimulates tumor-associated macrophages to produce CXCL1, which rec

291 of cancer immunotherapies aiming to polarize tumor-associated macrophages toward an antitumor phenoty

292 mic tumor-specific CD8 + T cells, repolarize tumor-associated macrophages towards an inflammatory M1-

293 cell types in glioblastoma tumors, including tumor-associated macrophages, tumor-infiltrating dendrit

294 osis in tumor cells, as well as depletion of tumor-associated macrophages, vascular ectasia, and hemo

295 CD163 and Arg1, markers for tumor-associated macrophages, were also detected and inc

296 on HIF-2alpha-driven sVEGFR-1 production by tumor-associated macrophages, whereas HIF-1alpha specifi

297 on depends on an interplay between Tregs and tumor-associated macrophages, which can be reversed by A

298 s promotes a macrophage phenotype similar to tumor-associated macrophages, which may contribute to th

299 age activation and polarization into M2 type tumor-associated macrophages, which promote tumor growth

300 Such adaptive response is mediated by tumor associated macrophages, whose blockage improves th