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

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

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

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

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

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

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

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

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

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

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

11 ecognizes tumor cells, tumor lymphatics, and tumor-associated macrophages.

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

13 n reduced tumor volumes and lower numbers of tumor-associated macrophages.

14 cells suggested that VEGF-C is derived from tumor-associated macrophages.

15 nitric oxide synthase (NOS) 2 expression in tumor-associated macrophages.

16 nd induced neuropilin 1 (NRP1) expression in tumor-associated macrophages.

17 s essential for VEGF-stimulated migration of tumor-associated macrophages.

18 radiation stimulated the generation of NO in tumor-associated macrophages.

19 occurs in both tumor epithelial cells and in tumor-associated macrophages.

20 also suggests expression of VEGFR-3 on some tumor-associated macrophages.

21 CSF-1R expression in areas of carcinoma- and tumor-associated macrophages.

22 accumulated predominantly in tumor cells and tumor-associated macrophages.

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

24 angiostatin directly or in cooperation with tumor-associated macrophages.

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

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

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

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

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

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

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

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

33 c production of tumor-promoting cytokines by tumor-associated macrophages and aggressive growth of lu

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

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

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

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

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

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

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

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

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

43 marily as an immune modulator that activates tumor-associated macrophages and induces a subsequent CD

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

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 Their study suggests how tumor-associated macrophages and neolymphatic vessels ma

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

50 filtration, in which an overall reduction in tumor-associated macrophages and neutrophils was evident

51 ge derived in this model, being expressed by tumor-associated macrophages and not by tumor or stromal

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

53 he HIFs in the regulation of angiogenesis by tumor-associated macrophages and suggests that administr

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

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

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

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

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

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

62 Efforts to test potent inhibitors of MDSC, tumor-associated macrophages, and Treg, particularly ear

63 Tumor-associated macrophages are a heterogeneous populat

64 Tumor-associated macrophages are a prominent component o

65 Recent findings indicate that tumor-associated macrophages are important drivers of tu

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

67 Tumor-associated macrophages are increasingly viewed as

68 Since tumor-associated macrophages are intimately associated w

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

70 regulating the infiltration and function of tumor-associated macrophages as, at the tumor site, CSF-

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

72 LF localized predominantly to the surface of tumor-associated macrophages, as well as to some endothe

73 or-1 (sVEGFR-1) and determined the effect on tumor-associated macrophage behavior and tumor growth.

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

75 These data show that activation of tumor-associated macrophages by DMXAA is an efficient wa

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

77 Tumor-associated macrophages can suppress tumor-infiltra

78 Tumor-associated macrophages constitute a major componen

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

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

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

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

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

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

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

86 In summary, tumor-associated macrophages express VEGFR2, and selecti

87 Our studies show that tumor-associated macrophages express VEGFR2.

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

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

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

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

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

93 Because tumor-associated macrophages have been shown to enhance

94 o our knowledge, this is the first time that tumor-associated macrophages have been shown to express

95 Tumor-associated macrophages have recently emerged as a

96 t and redirects their differentiation toward tumor-associated macrophages, hence providing a mechanis

97 quantified B7-H4 expression in the tumor and tumor-associated macrophages in 103 patients with ovaria

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

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

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

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

102 f inflammatory cytokines and chemokines from tumor-associated macrophages in the breast cancer model.

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

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

105 s associated with cancer, and the role of M2 tumor-associated macrophages in this phenomenon is well

106 gene expression profiles of cancer cells and tumor-associated macrophages in tumor biopsies before an

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

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

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

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

111 hed in MyD88- or TLR5-KD xenografts, whereas tumor-associated macrophage infiltration or angiogenesis

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

113 te infiltration, particularly a reduction of tumor-associated macrophage infiltration, in comparison

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

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

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

117 ed motility and invasiveness of cyclin D1-/- tumor-associated macrophages may contribute to the tumor

118 Tumor-associated macrophages may influence tumor progres

119 Tumor-associated macrophages mediate the link between in

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

121 ions, but immunosuppressive cells, including tumor-associated macrophages, myeloid-derived suppressor

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

123 sed form, as a new marker of tumor cells and tumor-associated macrophages/myeloid cells in hypoxic/me

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

125 Furthermore, tumor-associated macrophages of the corresponding tumors

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

127 3.5 million measured cells, we identified 17 tumor-associated macrophage phenotypes, 22 T cell phenot

128 Taken together, this study shows that tumor-associated macrophages play a key role in promotin

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

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

131 tion of angiostatin has been correlated with tumor-associated macrophage production of elastolytic me

132 Tumor-associated macrophage production of specific lymph

133 Tumor-associated macrophages promote Th17 cells through

134 Tumor-associated macrophages promote tumor growth by sti

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

136 metastatic lymph nodes suggests that CD68(+) tumor-associated macrophages represent the major source

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

138 Our previous work showed that tumor-associated macrophages spontaneously produced chem

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

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

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

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

143 Tumor-associated macrophage (TAM) significantly contribu

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

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

146 We further show that tumor-associated macrophage (TAM)-supplied cathepsins B

147 The distinct microenvironments where tumor-associated macrophages (TAM) act include areas of

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

149 As NF-kappaB inhibitors block both tumor-associated macrophages (TAM) and MEC NF-kappaB, th

150 Tumor-associated macrophages (TAM) and myofibroblasts ar

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

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

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

154 Tumor-associated macrophages (TAM) are implicated in bre

155 Tumor-associated macrophages (TAM) are important compone

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

157 Tumor-associated macrophages (TAM) can either promote or

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

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

160 Because increasing numbers of tumor-associated macrophages (TAM) in the HBTM negativel

161 from immunosuppressive M2-oriented F4/80(+) tumor-associated macrophages (TAM) into M1-oriented CD11

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

163 Tumor-associated macrophages (TAM) may have tumor-promot

164 litative change in the expression pattern of tumor-associated macrophages (TAM) observed in lung tumo

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

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

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

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

169 idney cancer, is frequently infiltrated with tumor-associated macrophages (TAM) that can promote mali

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 spleens of tumor-bearing mice become F4/80+ tumor-associated macrophages (TAM).

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

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

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

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

189 tant for the recruitment of CD11b(+)F4/80(+) tumor-associated macrophages (TAMs) and contributes to m

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

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

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

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

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

195 Tumor-associated macrophages (TAMs) are associated with

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

197 Tumor-associated macrophages (TAMs) are essential compon

198 Tumor-associated macrophages (TAMs) are highly active im

199 Tumor-associated macrophages (TAMs) are increasingly inv

200 Tumor-associated macrophages (TAMs) are known regulators

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

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

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

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

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

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

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

208 Tumor-associated macrophages (TAMs) can influence ovaria

209 Tumor-associated macrophages (TAMs) constitute a major c

210 Tumor-associated macrophages (TAMs) derived from primary

211 Tumor-associated macrophages (TAMs) encourage and coordi

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

213 Tumor-associated macrophages (TAMs) expressing the multi

214 Tumor-associated macrophages (TAMs) facilitate disease p

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

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

217 In vivo, Arg1 expression in tumor-associated macrophages (TAMs) from Ron(-/-) mice w

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

219 Tumor-associated macrophages (TAMs) have essential roles

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

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

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

223 at interactions between neoplastic cells and tumor-associated macrophages (TAMs) in the tumor microen

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

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

226 -2alpha, and overexpression of HIF-2alpha in tumor-associated macrophages (TAMs) is specifically corr

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

228 Tumor-associated macrophages (TAMs) may have an importan

229 Tumor-associated macrophages (TAMs) play a major role in

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

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

232 cal and experimental evidence indicates that tumor-associated macrophages (TAMs) promote malignant pr

233 Tumor-associated macrophages (TAMs) promote tumor develo

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

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

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

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

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

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

240 hemotaxis is dependent on the comigration of tumor-associated macrophages (TAMs) with obligate recipr

241 ly recruited into tumors, differentiate into tumor-associated macrophages (TAMs), and then accumulate

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

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

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

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

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

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

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

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

250 r subverted during lengthy interactions with tumor-associated macrophages (TAMs).

251 intaining the immunosuppressive phenotype of tumor-associated macrophages (TAMs).

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

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

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

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

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

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

258 Here, we report that depletion of tumor-associated macrophages (TAMvarphi) by systemic or

259 mouse model of breast cancer, we found that tumor-associated macrophages that are recruited to the t

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

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

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

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

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

265 Various myeloid cell types, including tumor-associated macrophages, Tie2-expressing monocytes

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

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

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

269 We show that DMXAA efficiently activated tumor-associated macrophages to release a variety of imm

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

271 ronment created by the tumor and enforced by tumor-associated macrophages, treatment of tumor-bearing

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

273 In advanced carcinomas, tumor-associated macrophages were reduced in TF(DeltaCT)

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

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

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