ライフサイエンスコーパス: TME

1 TME independently predicts the development of posttransp

2 TME was identified in 35 of 74 children.

3 Of 28 TME cytokines and growth factors tested, we identified O

4 gests that, following preoperative CMT and a TME-based resection, distal margins of 1 cm may provide

5 blood, thereby holding promise as not only a TME-derived anticancer target but also a novel biomarker

6 mAb-based targeting of PECAM-1 represents a TME-targeted therapeutic approach that suppresses the en

7 killing glioma cells in vitro, suggesting a TME-mediated resistance mechanism may be involved.

8 requiring preoperative CMT, and undergoing a TME-based resection.

9 hological implication of a therapy-activated TME, and provides the proof of principle of co-targeting

10 ; however, numerous species lack some or all TME components.

11 ial loss, independent regains of some or all TME structures were inferred within two minor clades and

12 In multivariate analysis TME and chemotherapy conditioning were independent risk

13 en by dynamic feedback between MCL cells and TME, leading to kinome adaptive reprogramming, bypassing

14 ation and Evaluation Before Chemotherapy and TME (PROSPECT), a randomized phase III trial to validate

15 n margin (CRM), distal resection margin, and TME completeness rates were determined.

16 opment of HCC and CCA in the hepatic PME and TME, focusing on myofibroblast- and extracellular matrix

17 e chemotherapy, all had tumor regression and TME without preoperative chemoradiotherapy.

18 essive disease were to have radiation before TME, whereas responders were to have immediate TME.

19 Increases in the interval between TME agent inoculations resulted in an extension of the i

20 Both TME strains were initially retrogradely transported in t

21 were susceptible to prion infection by both TME strains.

22 s stimulated the production of the CXCL13 by TME stromal cells, which in turn promoted ILC3-stromal i

23 of modified FOLFOX-6 (mFOLFOX-6) followed by TME 3 to 5 weeks later.

24 racil (5-FU)-based chemotherapy) followed by TME from 1988 to 2002.

25 hes more accurately recapitulate the complex TME, it is predicted that new opportunities for enhanced

26 tissues and Th1-TME CRCs but low in control-TME CRCs.

27 E CRCs) or worse clinical prognosis (control-TME CRCs).

28 Together, these findings demonstrate TME-dependent intertumoral TEC heterogeneity in CRC.

29 r EVs released in response to T-cell-derived TME signals, we performed microRNA (miRNA [miR]) profili

30 lioma can be primarily explained by distinct TME and signature genetic events, whereas both tumor typ

31 DY TME agent infectivity was not detected in spleen or lymp

32 smissible mink encephalopathy (TME) agent DY TME prior to superinfection of hamsters with the short-i

33 nal cord, interference between HY TME and DY TME did not occur.

34 For DY TME, hamsters were susceptible following intratongue but

35 d of HY TME corresponds with detection of DY TME PrP(Sc), the abnormal isoform of the prion protein,

36 us system corresponds with the ability of DY TME to block HY TME infection.

37 This suggests that DY TME agent replication interferes with HY TME agent repli

38 This suggests that DY TME agent-induced damage is not responsible for strain i

39 and replicates infectious agent and that DY TME can interfere, or completely block, the emergence of

40 The ability of the DY TME agent to extend the incubation period of HY TME corr

41 detection of HY PrP(Sc) in animals where DY TME had completely blocked HY TME from causing disease.

42 Most anurans possess a tympanic middle ear (TME) that transmits sound waves to the inner ear; howeve

43 g of solid was able to generate an efficient TME.

44 strain of transmissible mink encephalopathy (TME) (hamster) prions to a silty clay loam soil yielded

45 on-period transmissible mink encephalopathy (TME) agent DY TME prior to superinfection of hamsters wi

46 strain of transmissible mink encephalopathy (TME) agent had an incubation period that was not signifi

47 in of the transmissible mink encephalopathy (TME) agent prior to superinfection with the hyper (HY) s

48 ns of the transmissible mink encephalopathy (TME) agent.

49 in of the transmissible mink encephalopathy (TME) agent.

50 in of the transmissible mink encephalopathy (TME) agent.

51 ns of the transmissible mink encephalopathy (TME) agent.

52 strain of transmissible mink encephalopathy (TME).

53 Transplacental maternal engraftment (TME), the presence of maternal T cells in peripheral blo

54 followed by at least 10 losses of the entire TME.

55 (SG) 1 underwent total mesorectal excision (TME) 6 weeks later.

56 kely to receive a total mesorectal excision (TME) [odds ratio (OR) = 3.89; 95% confidence interval (C

57 ed with transanal total mesorectal excision (TME) and laparoscopic surgery.

58 tcomes of robotic total mesorectal excision (TME) at an NCI designated cancer center.

59 anastomosis after total mesorectal excision (TME) is associated with significant morbidity.

60 e CRT followed by total mesorectal excision (TME) is the standard of care for locally advanced rectal

61 nts who underwent total mesorectal excision (TME) without neoadjuvant radiotherapy in a multicenter c

62 onjunction with a total mesorectal excision (TME)-based resection, in terms of resection margins usin

63 or resection with total mesorectal excision (TME).

64 rectal cancers is total mesorectal excision (TME).

65 mTOR axis leads to release of MCL cells from TME, reversal of drug resistance and enhanced anti-MCL a

66 ctivity whether these cells are derived from TME or TFME.

67 One hundred eighty-six patients had TME quality assessed, and only 1 patient (0.5%) had an i

68 ing cyclic amplification (PMCA) of DY and HY TME maintains the strain-specific properties of PrP(Sc)

69 e animals contained a mixture of 139H and HY TME PrP(Sc) This finding expands the definition of strai

70 ly in scrapie-infected wild-type mice and HY TME-infected hamsters.

71 along the same neuroanatomical tracks as HY TME, adding to the growing body of evidence indicating t

72 lumbar spinal cord, interference between HY TME and DY TME did not occur.

73 r (HY) strain of TME can completely block HY TME from causing disease.

74 ponds with the ability of DY TME to block HY TME infection.

75 Under conditions where 139H blocked HY TME from causing disease, the strain-specific properties

76 imals where DY TME had completely blocked HY TME from causing disease.

77 d hypertransmissible mink encephalopathy (HY TME) PrP(Sc) is highly infectious and has a titer that i

78 tribution was consistent with a spread of HY TME agent along both somatosensory and gustatory cranial

79 agent to extend the incubation period of HY TME corresponds with detection of DY TME PrP(Sc), the ab

80 gent is required for complete blockage of HY TME in PMCA compared to several previous in vivo studies

81 The emergence of HY TME in PMCA was controlled by the initial ratio of the T

82 an extension of the incubation period of HY TME or a complete block of the ability of the HY TME age

83 The increased incubation period of HY TME or the inability of the HY TME agent to cause diseas

84 onds with a reduction in the abundance of HY TME PrP(Sc) in the lumbar spinal cord.

85 re, or completely block, the emergence of HY TME.

86 hamsters with the short-incubation-period HY TME agent.

87 previous in vivo studies, suggesting that HY TME persists in animals coinfected with the two strains.

88 Therefore, the HY TME agent did not enter the central nervous system via t

89 ain tissue from animals infected with the HY TME agent that are in the terminal stage of disease.

90 period of HY TME or the inability of the HY TME agent to cause disease in the coinfected animals cor

91 or a complete block of the ability of the HY TME agent to cause disease.

92 er os inoculation of the same dose of the HY TME agent.

93 A higher ratio of DY to HY TME agent is required for complete blockage of HY TME in

94 DY TME agent replication interferes with HY TME agent replication when the two strains infect a comm

95 eport, we found that 139H interferes with HY TME infection, which is likely due to both strains targe

96 reased fibronectin deposition in the hypoxic TME.

97 Here, we performed a screen to identify TME cytokines and growth factors that promote epithelial

98 E, whereas responders were to have immediate TME.

99 these NPs resulted in priming of the immune TME, characterized by increased IFN-gamma, p-STAT-1, GM-

100 ulator of the fibrotic and immunosuppressive TME.

101 bined approach reverts the immunosuppressive TME and recruits CD8 T cells with an increased number an

102 This augmented immunotolerant TME in p53(null) mice was associated with a marked expan

103 mechanisms of protons and Pi accumulation in TME.

104 lin-3a, we show that local p53 activation in TME comprising overt tumor-infiltrating leukocytes (TILe

105 only limited tumor necrosis and no change in TME cytokines or TAM phenotype and highlighting the impo

106 amined the effects of TGF-beta1 crosstalk in TME and its role in mediating tumor formation and progre

107 whereas IND-treated MDSCs differentiated in TME aggravated clinical symptoms and delayed resolution

108 pecies production in MDSCs differentiated in TME but not in TFME.

109 or immunity and tumor regression, but not in TME with scarce TILeus, such as B16 melanoma.

110 Hence, targeting the p53 pathway in TME can be exploited to reverse immunosuppression and au

111 ophage over microglia expression programs in TME.

112 e existence of hypoxic and acidic regions in TME, the most dramatic differences, about 2-fold higher

113 and only 1 patient (0.5%) had an incomplete TME.

114 Intact TME specimens were achieved in 85%, with minor defects i

115 ical characteristics treated by laparoscopic TME in the immediate chronological period.

116 The effectiveness of laparoscopic TME could not be established, but the robotic-assisted a

117 ted to attenuation of BCR-dependent lymphoma-TME interactions.

118 3, we show that these pathways regulate many TME functions associated with sporadic colonic tumorigen

119 are the local tumor immune microenvironment (TME) in anal SCCs from HIV-positive and HIV-negative pat

120 th the sample, a transient microenvironment (TME), which can shield analytes from direct ionization,

121 ) in the progressive tumor microenvironment (TME) acquire OX40 expression and bind fluorescently labe

122 targeting p53 in the tumor microenvironment (TME) also represents an immunologically desirable strate

123 ng attributes of the tumor microenvironment (TME) and bias immunity toward type 2, away from the type

124 also present in the tumor microenvironment (TME) and contributes to therapeutic resistance.

125 onstrains within the tumor microenvironment (TME) and to what degree this affects their ability to co

126 phages (TAMs) in the tumor microenvironment (TME) are crucial in promoting tumor cell invasion and pr

127 ell types within the tumor microenvironment (TME) are genetically stable and thus represent an attrac

128 essive nature of the tumor microenvironment (TME) can be relieved.

129 The tumor microenvironment (TME) consists of cells, soluble factors, signaling molec

130 e B-cell/plasma cell tumor microenvironment (TME) contributes significantly to malignant transformati

131 it is clear that the tumor microenvironment (TME) contributes to cancer cell plasticity, the specific

132 The tumor microenvironment (TME) exerts critical pro-tumorigenic effects through cyt

133 3 dysfunction in the tumor microenvironment (TME) favors tumor establishment and progression.

134 heterogeneity of the tumor microenvironment (TME) hampers the long-term efficacy of first-line therap

135 he immunosuppressive tumor microenvironment (TME) has provided many therapeutic strategies to battle

136 , the tumor, and the tumor microenvironment (TME) in different cancer settings.

137 The tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDA) is charac

138 The tumor microenvironment (TME) is a complex heterogeneous assembly composed of a v

139 The tumor microenvironment (TME) is a major barrier to clinical success by compromis

140 l exclusion from the tumor microenvironment (TME) is a major barrier to overcoming immune escape.

141 Tumor microenvironment (TME) is commonly implicated in regulating the growth of

142 roduction within the tumor microenvironment (TME) is increased up to 5-fold as compared with naive su

143 che factors, and the tumor microenvironment (TME) may similarly influence tumor cell clonogenic growt

144 The tumor microenvironment (TME) mediates immunosuppression resulting in tumor cell

145 Hypoxia in the tumor microenvironment (TME) mediates resistance to radiotherapy and contributes

146 PD-1(+) cells in the tumor microenvironment (TME) of cHL.

147 sessment of chemical tumor microenvironment (TME) parameters such as oxygen (pO2), extracellular acid

148 TING activity in the tumor microenvironment (TME) promoted the growth of Lewis lung carcinoma (LLC).

149 within the lymphoma tumor microenvironment (TME) provide sanctuary for subpopulations of tumor cells

150 immune cells in the tumor microenvironment (TME) regulates tumorigenesis and provides emerging targe

151 The tumor microenvironment (TME) serves as a multidrug resistant center for tumors u

152 Contributions of the tumor microenvironment (TME) to progression in thyroid cancer are largely unexpl

153 ssive effects in the tumor microenvironment (TME) via induction of regulatory T cell recruitment and

154 ely expressed in the tumor microenvironment (TME), have emerged as key players in immune evasion prog

155 dynamics between the tumor microenvironment (TME), nontumor microenvironment (NTME), and the systemic

156 side in the lymphoid tumor microenvironment (TME), promoting the reprogramming of these cells into ca

157 he immunosuppressive tumor microenvironment (TME), the efficacy of adoptive cell transfer (ACT) is mu

158 in the human breast tumor microenvironment (TME), the presence of increased numbers of RORgammat(+)

159 r cells but also the tumor microenvironment (TME), which contains diverse cell populations, signaling

160 nisms in addition to tumor microenvironment (TME)-mediated extrinsic resistance.

161 ing component in the tumor microenvironment (TME).

162 cancer cells and the tumor microenvironment (TME).

163 f T cells within the tumor microenvironment (TME).

164 eractions within the tumor microenvironment (TME).

165 s pattern and unique tumor microenvironment (TME).

166 mor cells within the tumor microenvironment (TME).

167 stromal cells in the tumor microenvironment (TME).

168 hanisms based in the tumor microenvironment (TME).

169 accumulation in the tumor microenvironment (TME).

170 rate observed in the tumor microenvironment (TME).

171 ls as well as by the tumor microenvironment (TME).

172 tumor cells and the tumor microenvironment (TME).

173 e composition of the tumor microenvironment (TME).

174 n immune-suppressive tumor microenvironment (TME).

175 two hallmarks of the tumor microenvironment (TME).

176 ine functions in the tumor microenvironment (TME).

177 and fibrosis in its tumor microenvironment (TME).

178 ly immunosuppressive tumor microenvironment (TME).

179 ctional role of the tumour microenvironment (TME) in ibrutinib activity and acquired ibrutinib resist

180 e importance of the tumour microenvironment (TME) to innate resistance, to molecularly targeted thera

181 y were derived from tumor microenvironments (TME) or from tumor-free microenvironments (TFME).

182 es interstitial inorganic phosphate as a new TME marker for tumor progression.

183 pathways in cancer cells and stroma cells of TME leading to a decrease in cancer cell survival.

184 ses of quantitative MINT methylation data of TME trial patients demonstrated two prognostic subclasse

185 n of intrinsic and extrinsic determinants of TME-mediated lymphoma survival and drug resistance.

186 have learned so far from the development of TME-targeting agents.

187 iated drug resistance to delineate a form of TME-mediated drug resistance that protects hematopoietic

188 ns have converged the singlet-triplet gap of TME as a function of methodology and basis set.

189 The impact of TME-dependent heterogeneity of tumor endothelial cells (

190 activation to alter the immune landscape of TME and subsequently amplify immune response to systemic

191 echanisms that underlie the morphogenesis of TME structures.

192 Although the presence of TME is associated with a decreased risk of rejecting a m

193 The presence of TME should be considered when assessing the risk of aGVH

194 The role of TME in modulating tumor drug sensitivity is increasingly

195 In this study, we investigate the role of TME in resistance to cixutumumab, an anti-IGF-1R monoclo

196 demonstrate that the lowest singlet state of TME is energetically lower than the lowest triplet state

197 superinfection with the hyper (HY) strain of TME can completely block HY TME from causing disease.

198 nd surgeon volume for the outcomes of use of TME (P < 0.01) and local recurrence (P = 0.01).

199 ming the fibrotic and immunosuppressive PDAC TME and renders tumors responsive to immunotherapy.

200 e whether the presence of pretransplantation TME is associated with posttransplantation GVHD in patie

201 The primary endpoint was "good-quality TME surgery." Secondary endpoints were short-term advers

202 hese findings demonstrate an immune-reactive TME in anal SCCs from HIV-positive patients and support

203 tors released by a therapeutically remodeled TME remains largely unexplored.

204 ll lead to development of novel and specific TME-targeting therapeutic strategies, which offer consid

205 utes to cancer cell plasticity, the specific TME factors most actively controlling plasticity remain

206 actors for poor specimen outcome (suboptimal TME specimen, perforation, and/or R1 resection) on multi

207 As such, TME represents an important target and should be conside

208 ot be generated due to an immune suppressive TME.

209 ity is increasingly recognized and targeting TME has been the focus of novel therapeutic approaches.

210 nts that function like tetramethyleneethane (TME), allowing for back-to-back [4 + 2] cycloadditions,

211 ic ground state of the tetramethyleneethane (TME) diradical has proven to be a challenge for both exp

212 rbene (3,5-DN-PhCCl) to tetramethylethylene (TME), cyclohexene, and 1-hexene.

213 ssed in ECs in healthy colon tissues and Th1-TME CRCs but low in control-TME CRCs.

214 hat exhibited TMEs with either improved (Th1-TME CRCs) or worse clinical prognosis (control-TME CRCs)

215 SPARCL1 was most strongly upregulated in Th1-TME TECs.

216 the favorable prognoses associated with Th1-TME CRCs.

217 m, it has been increasingly appreciated that TME also contributes to tumor initiation and progression

218 Within this review, we propose that TME and the tumor co-evolve as a consequence of bidirect

219 of an immunosuppressive gradient across the TME, NTME, and peripheral blood in primary HCC that mani

220 f of principle of co-targeting tumor and the TME to prevent acquired resistance, with the aim of impr

221 ics to their specific targeted cells and the TME.

222 diated interactions between lymphoma and the TME.

223 ocytic MDSCs in both the bone marrow and the TME.

224 nic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and

225 we investigated the relationship between the TME and thyroid cancer progression in a mouse model wher

226 nown regarding 5-LO products produced by the TME.

227 he interaction among mature tumor cells, the TME, and TICs, and strategies targeting GDF15 may affect

228 erestingly, Tregs and TRMs isolated from the TME expressed multiple markers for T-cell exhaustion, in

229 tumor cells in response to TGF-beta from the TME.

230 unosuppression and T-cell exclusion from the TME.Significance: These findings define a myeloid-based

231 uisition of drug resistant phenotypes in the TME after repeated cisplatin NP treatment was examined.

232 g chemokine CCL2 (C-C motif ligand 2) in the TME along with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granu

233 imetic targets immunosuppressive MDSC in the TME and enhances the quantity and quality of both effect

234 cesses: reversal of immunosuppression in the TME and induction of tumor immunogenic cell death, leadi

235 endothelial cells (VEC) were observed in the TME early after treatment with OX40L-Fc.

236 Although PGs in the TME have been well studied, less is known regarding 5-LO

237 rstand the impact of p53 inactivation in the TME in tumor progression, we compared the growth of subc

238 We find that the majority of PD-L1 in the TME is expressed by the abundant PD-L1(+) TAMs, which ph

239 inactive, the proinflammatory changes in the TME later resulted in the loss of accumulating M2 and in

240 TNF-alpha, and inducible NO synthase in the TME merely 4 d postinfection, before significant virus s

241 derscoring how innate immune pathways in the TME modify tumorigenesis in distinct tumor settings, wit

242 ng revealed comparable levels of IFNG in the TME of both HIV-positive and HIV-negative patients.

243 Oxidative stress in the TME promotes immunosuppression by tumor-infiltrating mye

244 ded different oxygen generation rates in the TME relevant to different clinical settings.

245 novel pathway for the capacity of DCs in the TME to regulate genomic integrity.

246 In the TME trial, patients with rectal cancer (n = 1,530) were

247 We examined the role of 5-LO in the TME using a model in which Lewis lung carcinoma cells ar

248 ber and percentage of MDSCs and Tregs in the TME, but also induced a shift in cytokine expression fro

249 tion of cytotoxic T lymphocytes (CTL) in the TME, consistent with a relief of MDSC-mediated immunosup

250 Factors present in the TME, including tumor growth factor-beta (TGF-beta), allo

251 ancers diagnosed in patients included in the TME, PORTEC-1, and PORTEC-2 trials were analyzed.

252 and their CCL2-mediated accumulation in the TME, there were defects in these processes in glioma-bea

253 n with an increase in CXCL10 and CTLs in the TME, underscoring a critical role for MDSCs in glioma de

254 the most abundantly secreted cytokine in the TME, where it imparts various aggressive characteristics

255 pment of MDSCs and their accumulation in the TME, where they limit CTL infiltration.

256 t mode of intercellular communication in the TME.

257 dy was to examine the role of cPLA(2) in the TME.

258 ocal chemokine milieu of cancer cells in the TME.

259 cell infiltration and IL10 production in the TME.

260 A was controlled by the initial ratio of the TME agents.

261 a complex interplay between elements of the TME and advanced tumor metastases directs end-stage meta

262 ckade altered the suppressive feature of the TME by decreasing the presence of monocytic myeloid-deri

263 Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and met

264 The many losses and gains of the TME in anurans is unparalleled among tetrapods.

265 stions on how to include the analysis of the TME in personalized cancer diagnosis and treatment.

266 racellular matrix as pivotal features of the TME in promoting thyroid cancer progression, illuminatin

267 The reappearance of the TME in the latter clade was followed by at least 10 loss

268 The inferred evolutionary history of the TME is exceptionally complex in true toads (Bufonidae),

269 merging concepts in our understanding of the TME: its dynamic evolution, how it is educated by tumor

270 ouse breast tumor cells and TAMs remodel the TME, leading to the upregulation of Fra-1, a member of t

271 g biocompatible materials to reoxygenate the TME by reacting with endogenous H2O2 MDNP containing hyd

272 erent therapeutic strategies that target the TME, focusing on agents that are at the most advanced st

273 Our analysis indicates that the TME was completely lost at least 38 independent times in

274 -of-flight mass cytometry, we found that the TME was enriched in regulatory T cells (Tregs), tissue r

275 Here we show that the TME, functioning in part through platelet endothelial ce

276 found that fibroblasts were recruited to the TME of Braf(V600E)/Pten(-/-)/TPO-Cre thyroid tumors.

277 ivery of a synthetic STAT-3 inhibitor to the TME, combined with an HER-2 DNA vaccine can improve immu

278 payload capable of specific delivery to the TME, which showed an effective therapeutic inhibition of

279 empts to re-educate stromal cells within the TME to have anti-tumorigenic effects.

280 CD4(+) T-cell:tumor interactions within the TME.

281 unction of tumor-reactive T cells within the TME.

282 of tumor-reactive CD8(+) T cells within the TME.

283 e autophagy at the cellular level within the TME.

284 g of innate and adaptive immunity within the TME.

285 Further study of how these TME components relate to the different stages of tumor p

286 e for in vivo concurrent assessment of these TME parameters in various mouse models of cancer.

287 Maneuvers that recruit leukocytes to TME, such as TLR3 ligand in B16 tumors, greatly enhanced

288 Transanal TME appears as an alternative in the treatment of rectal

289 prospective cohort and treated by transanal TME assisted by laparoscopy.

290 rt-term outcomes demonstrated that transanal TME is a feasible and safe technique associated with a s

291 specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse

292 atic nerve route of inoculation gave the two TME strains access to the same population of neurons, al

293 reasing complications in patients undergoing TME for locally advanced rectal cancer.

294 Approximately one fourth underwent TME.

295 This study unifies TME-mediated de novo and acquired drug resistance mechan

296 ting a maternal graft, it is unknown whether TME plays a role in development of GVHD after HSCT.

297 Given the morbidity associated with TME, local excision (LE) for early-stage rectal cancer h

298 ed retrospectively 483 consecutive LARs with TME and CAA carried out in a single center between 1996

299 dence of 57.1% versus 17.9% in those without TME (P < .001).

300 mpared in patients with versus those without TME.