ライフサイエンスコーパス: TME

1 TME also consists of physical factors, such as oxygen av

2 udies of function within the live, intact 3D TME.

3 mporal tumor-immune cross-talk within the 3D TME.

4 a set of 198 ICCs could be classified into 4 TME-based subtypes related to distinct immune escape mec

5 geneous tumor stroma composition and built a TME-based classification of ICC tumors that detects pote

6 provides a valuable approach to study how a TME affects the immune system.

7 this method on two different cell lines in a TME microfluidic model.

8 gy of these progenitor cell populations in a TME-like environment may advance our ability to target t

9 ified a subgroup of patients with an adverse TME associated with 17 fewer months of progression-free

10 composite evacuation scores 12 months after TME.

11 wth factor expression in tumor diversity and TME polarization.

12 c imaging-guided, photothermal-enhanced, and TME-specific sequential nanocatalytic tumor therapy.

13 al approaches aimed at disrupting Notch- and TME-mediated resistance that may aid in achieving in an

14 M1 mutations on IFNgamma-STAT1 signaling and TME, and can inform additional preclinical and clinical

15 e potential of a combined nanomedicine-based TME normalization and immunotherapeutic strategy designe

16 therefore comprehensively analyzed the brain TME landscape via flow cytometry, RNA sequencing, protei

17 -Me relieves immunosuppression in the breast TME and unleashes host adaptive anti-tumor immunity.

18 We show now that CDDO-Me remodels the breast TME, redirecting TAM activation and T cell tumor infiltr

19 tumor vasculature, and remodels the cellular TME, attenuating TNBC growth in mice.

20 ed to significant remodeling of the cellular TME, increasing pericyte numbers while decreasing cancer

21 stases arising over 8 years, to characterize TME interactions.

22 tools and gene sets and introduced Consensus(TME), a method that integrates gene sets from all the ot

23 nstrate that, with direct cell-cell contact, TME-derived endothelial cells provide the Notch ligand J

24 s with double markers (MADMs), we delineated TME evolution at single-cell resolution in sonic hedgeho

25 Furthermore, the image-derived TME features significantly correlated with the gene expr

26 In this Perspective, we describe TME normalization strategies that have the potential to

27 Given the interest in developing TME-targeted therapies for brain malignancies, this comp

28 tionally implemented for a three-dimensional TME, and a double hybrid continuous-discrete (DHCD) meth

29 lack of preclinical in vitro models of DLBCL TME hinders optimal therapeutic screening.

30 arly as 2 days after tumor initiation in ear TME.

31 ests for testing the total mediation effect (TME) and the component-wise mediation effects (CME), res

32 eg) cells to adapt to a lactic acid-enriched TME.

33 omplex and dynamic tumour micro-environment (TME).

34 testinal continuity reconstruction following TME is accompanied by postoperative defecation dysfuncti

35 onment Deconvolution (NITUMID) framework for TME profiling that addresses these limitations.

36 g the mechanisms by which EVs within the GBM TME are secreted and target recipient cells may offer an

37 ays and interactions within the heterogenous TME will be instrumental to advance this promising field

38 proach to converting the PDAC TME into a hot TME, thereby empowering immunotherapeutic strategies suc

39 rs such as failure to recapitulate the human TME in animal models and issues with NP targeting effica

40 1 loss is associated with a less immunogenic TME and upregulated angiogenesis.

41 nocytes correlates with an immunosuppressive TME in multiple human tumors.

42 GES levels at baseline; an immunosuppressive TME may also preclude CR.

43 art in the formation of an immunosuppressive TME.

44 GEM treatment promoting immunosuppression in TME via upregulation of GM-CSF and efferocytosis as well

45 potential in targeting certain cell types in TME.

46 noparticle delivery strategies to individual TME components, including cancer-associated blood and ly

47 human cancers revealed distinct inflammatory TME phenotypes resembling those associated with cancer i

48 en gene body enhancers and expression of key TME genes in both entities.

49 The protective effect of DVF during L-TME on pelvic autonomic nerves and postoperative urogeni

50 DVF preservation during L-TME revealed protective effects on postoperative urogeni

51 ns were enrolled, and randomly assigned to L-TME with DVF preservation (Exp-group, n = 123) or resect

52 surgical approach for rectal cancer is LAR + TME.

53 racterize the tumor immune microenvironment (TME).

54 l determinant of a tumor's microenvironment (TME), and profoundly affect drug delivery, therapeutic e

55 Immunosuppressive tumor microenvironment (TME) and ascites-derived spheroids in ovarian cancer (OC

56 ubpopulations in the tumor microenvironment (TME) and cooperatively promoted intratumoral T cell exha

57 he immunosuppressive tumor microenvironment (TME) and enhancing response rates to immune checkpoint i

58 etabolism change the tumor microenvironment (TME) and impact anti-tumor immunity is not understood.

59 heterogeneity of the tumor microenvironment (TME) and its molecular underpinnings remain largely unst

60 understanding of the tumor microenvironment (TME) and its role in tumor progression.

61 he immunosuppressive tumor microenvironment (TME) and limited immune cell access due to the surroundi

62 major components of tumor microenvironment (TME) and play crucial roles in tumor development and met

63 he immunosuppressive tumor microenvironment (TME) and whether platelet inhibition can be leveraged to

64 nd remodeling of the tumor microenvironment (TME) by sustaining the calcium transients and neurotrans

65 aints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progressi

66 l factors within the tumor microenvironment (TME) can have a profound impact on the metabolic activit

67 o combat tumors, the tumor microenvironment (TME) contains ROS, which suppress NK cell antitumor acti

68 how signals from the tumor microenvironment (TME) contribute to aberrant Zeb1 expression.

69 crophages within the tumor microenvironment (TME) exhibit a spectrum of protumor and antitumor functi

70 ies (ROS) within the tumor microenvironment (TME) for codelivery of anti-PD1 antibody (aPD1) and Zebu

71 an immunosuppressive tumor microenvironment (TME) for the support of tumor growth.

72 recently to profile tumor microenvironment (TME) from bulk RNA data, and they have proved useful for

73 gh immunosuppressive tumor microenvironment (TME) GES levels at baseline; an immunosuppressive TME ma

74 iltration within the tumor microenvironment (TME) has been extensively investigated via histological

75 ells (T(reg)) to the tumor microenvironment (TME) has the potential to weaken the antitumor response

76 esearch to study the tumor microenvironment (TME) in metastasis.

77 apeutic value of the tumor microenvironment (TME) in various cancer types is of major interest.

78 ell types within the tumor microenvironment (TME) in which myeloid cells and T cells were the most ab

79 The tumor microenvironment (TME) is a complex neighborhood that consists of immune c

80 The tumor microenvironment (TME) is a highly complex environment that surrounds tumo

81 he immunosuppressive tumor microenvironment (TME) is a major barrier to immunotherapy.

82 -L1) molecule in the tumor microenvironment (TME) is a major immune evasion mechanism in some patient

83 The tumor microenvironment (TME) is a potential target.

84 A non-immunogenic tumor microenvironment (TME) is a significant barrier to immune checkpoint block

85 sive features of the tumor microenvironment (TME) is an attractive strategy for cancer treatment; how

86 The tumor microenvironment (TME) is an essential contributor to the development and

87 The cHL tumor microenvironment (TME) is compartmentalized into "niches" rich in programm

88 The tumor microenvironment (TME) is critical for tumor progression.

89 The tumor microenvironment (TME) is increasingly appreciated as an important determi

90 breast tumor and its tumor microenvironment (TME) is linked to poor clinical outcomes in treatment of

91 nnate sensing inside tumor microenvironment (TME) limits T cell-targeted immunotherapy.

92 tly decreased in the tumor microenvironment (TME) of GEM-treated mice.

93 pDC) enriched in the tumor microenvironment (TME) of head and neck squamous cell carcinoma.

94 of the desmoplastic tumor microenvironment (TME) of ICC has been stressed but was insufficiently tak

95 The tumor microenvironment (TME) plays a significant role in cancer progression and

96 The tumor microenvironment (TME) plays critical roles in tumor growth and progressio

97 The tumor microenvironment (TME) promotes tumor development via complex intercellula

98 immunity within the tumor microenvironment (TME) remain largely undefined.

99 tanding of the brain tumor microenvironment (TME) remains limited, and it is unknown whether it is sc

100 signaling creates a tumor microenvironment (TME) reminiscent of poorly prognostic human CRC subtypes

101 s now clear that the tumor microenvironment (TME) restrains immunity.

102 interactions in the tumor microenvironment (TME) significantly govern cancer progression and drug re

103 er 20,000 cancer and tumor microenvironment (TME) single-cell profiles exposed a rich and dynamic tum

104 ctive targeting, and tumor microenvironment (TME) targeting are summarized here.

105 an immunosuppressive tumor microenvironment (TME) that prevents infiltrating immune cells from perfor

106 jor component of the tumor microenvironment (TME) that promotes tumor growth and immune evasion.

107 fying signals in the tumor microenvironment (TME) that shape CD8(+) T cell phenotype can inform novel

108 be recruited to the tumor microenvironment (TME) through the C-C chemokines CCL17 and CCL22.

109 ental feature of the tumor microenvironment (TME), and tackling spatial heterogeneity in neoplastic m

110 of NK cells into the tumor microenvironment (TME), blockade of inhibitory receptors that limit NK cel

111 oncentrations in the tumor microenvironment (TME), suppresses immune function via inhibition of T cel

112 nt components of the tumor microenvironment (TME), the immune cells, and the fibroblasts.

113 rgeting Mertk in the tumor microenvironment (TME), we observed distinct functions of TAM as oncogenic

114 asts, comprising the tumor microenvironment (TME), which may represent anywhere from 15% to 85% of th

115 mark of the abnormal tumor microenvironment (TME)-that causes immunosuppression.

116 ntext of the complex tumor microenvironment (TME).

117 une landscape of the tumor microenvironment (TME).

118 ly immunosuppressive tumor microenvironment (TME).

119 an immunosuppressive tumor microenvironment (TME).

120 be secreted from the tumor microenvironment (TME).

121 nerating TAMs in the tumor microenvironment (TME).

122 erpetuating a unique tumor microenvironment (TME).

123 d their dysregulated tumor microenvironment (TME).

124 plexity of the solid-tumor microenvironment (TME).

125 ll exhaustion in the tumor microenvironment (TME).

126 accumulation in the tumor microenvironment (TME).

127 moting a suppressive tumor microenvironment (TME).

128 tumor cells and the tumor microenvironment (TME).

129 up-regulated in the tumor microenvironment (TME).

130 r cells aided by the tumor microenvironment (TME).

131 when present in the tumor microenvironment (TME).

132 dynamic immunogenic tumor microenvironment (TME).

133 ulate the volumetric tumor microenvironment (TME).

134 cer cells within the tumor microenvironment (TME).

135 es that regulate the tumor microenvironment (TME).

136 nformation about the tumor microenvironment (TME).

137 cific T cells in the tumor microenvironment (TME).

138 vation and a hostile tumor microenvironment (TME).

139 ity by reshaping the tumor microenvironment (TME).

140 se the ICB-resistant tumor microenvironment (TME).

141 antitumor one in the tumor microenvironment (TME).

142 ive cells within the tumor microenvironment (TME).

143 e immunosuppressive tumour microenvironment (TME) and thus limited reinvigoration of antitumour immun

144 orts to exploit the tumour microenvironment (TME) for therapy, but strategies aimed at deconstructing

145 The tumour microenvironment (TME) forms a major obstacle in effective cancer treatmen

146 The tumour microenvironment (TME) has recently drawn much attention due to its profou

147 The tumour microenvironment (TME) is a major cause of the failure of both nanomedicin

148 t components in the tumour microenvironment (TME), where they can perform several protumourigenic fun

149 e the immunological tumour microenvironment (TME).

150 ctly by shaping the tumour microenvironment (TME).

151 ms shaping the immune tumor microenvironment(TME), focusing on pancreatic adenocarcinoma because it i

152 y, and deleterious tumor microenvironmental (TME) crosstalk.

153 Complex tumor microenvironmental (TME) features influence the outcome of cancer immunother

154 logic landscape and tumor microenvironments (TME) vary between different organs which discretely shap

155 individual macrophages within 3D microscale TME models.

156 bserve that granulocyte signatures in the MM TME contribute to a more accurate prognosis.

157 impairs CD8(+) T cell function in the murine TME, accelerating tumor growth.

158 -like functions of UBR5 in regulating the OC-TME crosstalk and suggests that UBR5 is a potential ther

159 The molecular pathways involved in the OC-TME interactions, how the crosstalk impinges on OC aggre

160 Analysis of TME cell composition, DNA copy number, mutations and gen

161 Currently, isolation of TME stroma from patients is complicated by issues such a

162 We proposed that normalization of TME using antiangiogenic drugs and/or mechanotherapeutic

163 ew focuses on recent advances on the role of TME in drug resistance, with a particular focus on the o

164 conventional 2D co-cultures for the study of TME-imprinting mechanisms.

165 clinical studies, their combined effects on TME are not fully understood.

166 The impact of Polybromo-1 (PBRM1) on TME and response to ICB in renal cell carcinoma (RCC) re

167 T3 as a critical regulator in the pancreatic TME.

168 describe an approach to converting the PDAC TME into a hot TME, thereby empowering immunotherapeutic

169 this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particular

170 clinicians treating patients should quantify TME components, in particular monocytes and granulocytes

171 melanoma cells, we generate a reconstructed TME that closely resembles tumour growth as observed in

172 sets from all the other methods for relative TME cell estimation of 18 cell types.

173 w activated NK cells survive in the ROS-rich TME and suggests that smokers with lung cancer may benef

174 Coincidentally, the same TME features that impair nanomedicine delivery can also

175 ible strategies to overcome tumor-supporting TME properties and instead harness the TME to fight canc

176 facile platform to modulate the suppressive TME, and enable in situ personalized cancer vaccination.

177 Second, we identified that TME-derived IGF1 promotes tumor progression.

178 The TME already shows a reduction in type 1 regulatory T cel

179 The TME is composed of all non-cellular and cellular compone

180 The TME, however, can be metabolically hostile due to insuff

181 their ER to in vivo stress and to adjust the TME to facilitate malignant growth.

182 ex interactions between cancer cells and the TME may reduce treatment efficacy and ultimately lead to

183 development, and reemerge in tumors and the TME, where they are implicated in invasion, metastasis,

184 ation-related features that characterize the TME.

185 ing clinical trials aiming at disrupting the TME- and the extracellular matrix-mediated protection ag

186 study supports a new regulatory role for the TME in mitochondrial heterogeneity and metastatic potent

187 immunotherapy and excludes T cells from the TME.

188 and EP4 receptors on NK cells, hampered the TME switch, and enabled immune evasion.

189 rting TME properties and instead harness the TME to fight cancer.

190 rent stages of their development and how the TME imposes barriers to the metabolism and activity of t

191 titumor functions, yet it is unclear how the TME regulates this macrophage heterogeneity.

192 nges in tumor cell metabolism can impact the TME to limit immune responses and present barriers to ca

193 role of extracellular macromolecules in the TME affecting endothelial cells we exposed normal and ca

194 tes a major pathway of ADO production in the TME and can reverse ADO-mediated immune suppression.

195 metabolism to pro-inflammatory states in the TME and highlight a need to better replicate physiologic

196 otential to identify novel components in the TME and improve our understanding of their local interac

197 glec-15 amplifies anti-tumor immunity in the TME and inhibits tumor growth in some mouse models.

198 veals the dynamic regulation of IL-15 in the TME and its importance in antitumor immunity.

199 itumor effects through modifying TAMs in the TME and removing T-cell inhibitory signals, thereby prov

200 eloid-derived suppressor cells (MDSC) in the TME are a major source of Wnt5A and are reliant upon Wnt

201 We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) popu

202 s and activation of the STING pathway in the TME as assessed by western blot analysis and gene expres

203 Further, inhibitory receptors present in the TME can inhibit T cell metabolism and alter T cell signa

204 f activated effector T cells (T(eff)) in the TME can potentiate antitumor immune responses.

205 t that reducing the T(reg) population in the TME can potentiate the antitumor immune response of chec

206 the physical properties and the cells in the TME change significantly, impacting the efficacy of the

207 -15 reporter mice, most myeloid cells in the TME express IL-15 with CD11b(+)Ly6C(hi) cells being the

208 T(reg) accumulation in the TME has been shown to dampen the antitumor immune respon

209 o derived from cell type-specific EVs in the TME is essential.

210 xl expressed on tumor cells and Mertk in the TME is predicted to have a combinatorial benefit to enha

211 austed CD8(+) T cells and macrophages in the TME of C-MPNSTs.

212 ver key regulators of gene expression in the TME of cutaneous malignant peripheral nerve sheath tumor

213 ession of genes related to mast cells in the TME of SCMs, and a predominance of exhausted CD8(+) T ce

214 es that induce Trp and Arg catabolism in the TME remain incompletely defined.

215 s cells and cells/non-cell components in the TME support tumor initiation, development, and metastasi

216 , we present evidence of a pDC subset in the TME that favors antitumor immunity.

217 applied to regulate other components in the TME to realize synergistic or additive anti-tumor activi

218 These early changes in the TME were distinct from alterations found in a separate s

219 ized that inhibiting CS-GAG signaling in the TME would stem GBM invasion.

220 solution atlas of cellular metabolism in the TME, detailing how it changes with diet-induced obesity.

221 In the TME, monocyte-macrophage lineage cells produced glucocor

222 e major proliferative cell components in the TME, the crosstalk between macrophages and Tregs contrib

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

224 e cells (PSCs), the two major players in the TME, we can effectively manipulate the physiological bar

225 ne cells meet their metabolic demands in the TME, which can be leveraged for therapeutic benefit.

226 efficacy, even when agents accumulate in the TME.

227 nt role in modulating T cell function in the TME.

228 erogenic dendritic cells are dominant in the TME.

229 of these diverse metabolic phenotypes in the TME.

230 stromal cells and immune infiltrates in the TME.

231 analysis of hemodynamic heterogeneity in the TME.

232 is directly related to their activity in the TME.

233 tiation and function of protumor TAMs in the TME.

234 between T cells and other components in the TME.

235 o access novel therapeutic biomarkers in the TME.

236 in response to nutrient availability in the TME.

237 tors that impact local immune balance in the TME.

238 ectional inter-cellular communication in the TME.

239 psies, ignoring spatial heterogeneity in the TME.

240 nd limiting immunosuppressive factors in the TME.

241 function as the major source of Wnt5A in the TME.

242 with decreased accumulation of M-MDSC in the TME.

243 edicines and reduce immunosuppression in the TME.

244 ibutes to potential immunosuppression in the TME.

245 t inhibit the recruitment of T(reg) into the TME and elicit antitumor responses as a single agent or

246 ic target in OC treatment for modulating the TME and cancer stemness.

247 isolate or control individual factors of the TME and in vitro models often do not include all the con

248 ntified 14 gene expression signatures of the TME and those of 3 functional indicators (liver activity

249 ntified 14 gene-expression signatures of the TME and those of 3 functional indicators (liver activity

250 ) cells induced a profound remodeling of the TME and unleashed cytotoxic T cell (CTL)-mediated tumor

251 the complexity of exploring features of the TME as isolated targets.

252 s so that the immunomodulatory effect of the TME can affect systemic immunity.

253 g to the relatively stable properties of the TME compared to tumor cells, which exhibit frequent gene

254 be crucial to understanding the role of the TME in cancer progression.

255 on rescue the immunosuppressive state of the TME induced by chemotherapy.

256 wever, the establishment and function of the TME remain obscure because of its complex cellular compo

257 olism that includes important aspects of the TME spanning subcellular-, cellular- and tissue-level sc

258 functions, and therapeutic modulation of the TME to enhance antitumor NK cell function.

259 y modulate different cell populations of the TME, such as targeting pericytes and endothelial cells f

260 notherapy via metabolic reprogramming of the TME.

261 models fail to include essential cues of the TME.

262 ters and gene bodies and their effect on the TME composition of C-MPNSTs and SCMs.

263 the impact of intratumoral Treg cells on the TME.

264 apeutic targeting of LM-MDSC could prime the TME in a favorable manner.

265 lysis of a CyTOF dataset, which profiled the TME in 73 ccRCC patients, revealed cell-type-specific SL

266 ntegrated targets - which aim to remodel the TME against PDAC.

267 Microfluidics can be used to reproduce the TME in vitro and hence provide valuable insight on tumou

268 s, i.v. administered STING-NPs reprogram the TME towards a more immunogenic antitumor milieu, charact

269 targeting this pathway for reprogramming the TME.

270 ges also reveal opportunities to reshape the TME by targeting metabolic pathways to favor immunity.

271 ep learning-based analysis tool to study the TME in pathology images and demonstrate that the cell sp

272 hanges, therapeutic strategies targeting the TME using multifunctional nanomedicines hold great poten

273 ment of several new treatments targeting the TME.

274 These findings support that the TME composition of C-MPNSTs and SCMs is at least partial

275 It has become clear that the TME has diminished innate sensing that is critical to ac

276 iple murine sarcoma models, we find that the TME induces tumor cells to produce retinoic acid (RA), w

277 s the mechanisms of eosinophil homing to the TME and examine their diverse pro-tumorigenic and antitu

278 e to the preferential homing of AnxA5 to the TME enriched with PS+ tumor cells, we demonstrate in viv

279 eg) express CCR4 and can be recruited to the TME through the CC chemokine ligands CCL17 and CCL22.

280 a) within the TME and its restriction to the TME.

281 n vivo delivery barriers associated with the TME and their potential for clinical translation.

282 First, we found that astrocytes within the TME (TuAstrocytes) were trans-differentiated from tumor

283 of folate receptor beta (FRbeta) within the TME and its restriction to the TME.

284 Cells within the TME are highly plastic, continuously changing their phen

285 ression of CD8(+) T cell function within the TME but not in the draining lymph nodes.

286 lear decrease in Wnt5A expression within the TME in vivo as well as a decrease in intratumoral MDSC a

287 at a cognate Fas-FasL interaction within the TME might limit both T cell persistence and antitumor ef

288 produces a multi-lateral network within the TME of medulloblastoma: a fraction of tumor cells trans-

289 n of tumor ablation, interference within the TME, and immunotherapy in one potential modality.

290 metabolic dynamics of macrophages within the TME, mouse macrophages or human monocytes (RAW264.7 or T

291 Within the TME, tumor associated macrophages (TAMs) mediate angioge

292 eflect the phenotype of the cells within the TME.

293 innate and adaptive immune cells within the TME.

294 terize the anomalous hemodynamics within the TME.

295 pts the ER in TNBC cells and modulates their TME, and whether IRE1alpha inhibition can enhance antian

296 n't eat me" signal on tumor growth and tumor-TME interactions.

297 Based on the unique TME for achieving tumor-specific therapy, here a novel c

298 We performed an unsupervised TME-based classification of 198 ICCs (training set) and

299 NQO1 potently triggers innate sensing within TME that synergizes with immunotherapy to overcome adapt

300 rmacologic inhibition of RA signaling within TME increases stimulatory monocyte-derived cells, enhanc