ライフサイエンスコーパス: tumoral

1 The pattern of tumoral (18)F-FDG uptake was rather homogeneous, whereas

2 This work demonstrates that imaging baseline tumoral (18)F-FES uptake and initial changes in (18)F-FF

3 Fourteen of 23 patients showed tumoral (18)F-FET uptake concurrent to and 4 of 23 befor

4 round ratio (TBRmax) and dynamic analysis of tumoral (18)F-FET uptake over time (increasing vs. decre

5 At first occurrence of tumoral (18)F-FET uptake, TBRmax was significantly highe

6 Increased tumoral (18)F-FLT uptake compared with muscle was observ

7 Conversely, YC-1 + GI increased intra-tumoral 8-OHdG and levels of apoptosis markers.

8 Tumoral accumulation of LCDIO was 0.11% +/- 0.06 of the

9 ed topically or intraperitoneally, increased tumoral accumulation of the PDT-activated ALA product pr

10 ic antibodies due to a possible reduction in tumoral accumulation that may be caused by bevacizumab c

11 peptide had a 24 minute blood half life and tumoral accumulation was 6.9% of injected dose/g, approx

12 protein Trx2 is a part of the microglial pro-tumoral activation pathway initiated by glioma cancer ce

13 -015 and chemotherapy have demonstrated anti-tumoral activity in patients with recurrent head and nec

14 preferentially in tumors, as compared to non-tumoral adjacent tissue.

15 rther investigated as a potential novel anti-tumoral agent.

16 ) SMCD-eos was distinctly diffuse with loose tumoral aggregates.

17 ance status is strongly associated with both tumoral and cirrhotic factors and accurately predicts lo

18 patients with localized PCa, which included tumoral and nontumoral adjacent regions (n = 45), fresh

19 unique among 263 profiles related to diverse tumoral and nontumoral liver samples.

20 linical sign in childhood, for both familial tumoral and nontumoral syndromes.

21 erexpression of RANK (FL-RANK) in a panel of tumoral and normal human mammary cells induces the expre

22 n 30 procedures (88%), gas was also found in tumoral and peritumoral tissues.

23 expression of mouse interleukin-12 elevated tumoral and serum levels of interferon-gamma and tumor n

24 utcomes through transcriptional induction of tumoral and stromal apolipoprotein-E (ApoE).

25 static lesions but distinct contributions of tumoral and stromal SPARC to tumorigenesis and progressi

26 Suboptimal suppression of tumoral androgen activity may lead to adaptive cellular

27 ent of novel inhibitors of adrenal and intra-tumoral androgen synthesis and novel androgen signaling

28 K2 downregulation is a relevant event in the tumoral angiogenic switch.

29 omote breast tumorigenesis or to trigger the tumoral angiogenic switch.

30 atment paradigms based on understanding true tumoral antibody delivery.

31 ver, the immunological consequences of intra-tumoral bacteria remain unclear.

32 some-mediated cellular communication and pro-tumoral baseline M2 macrophage polarization, the Panc-1

33 plexes containing 1 mol% grafted PAO reduced tumoral bcl-2 expression by up to 60%.

34 GHRH antagonists also significantly reduced tumoral bFGF, whereas VEGF levels were not suppressed.

35 trate that miRNAs can effectively be used as tumoral biomarkers with implications for diagnosis, prog

36 cDNA band, AP5-1, was present in normal and tumoral biopsy samples, but was absent in breast tissue

37 Tumoral blood flow was significantly greater than in nor

38 the phenotype of microvasculature, reducing tumoral blood pooling.

39 atterns, and flow voids; and angiograms, for tumoral blood supply.

40 nction expressed primarily in normal but not tumoral brain.

41 y of carcinoma cells but not in immortal non-tumoral breast epithelial cells, which provides a select

42 ducing the expression of miR-223 in the peri-tumoral breast tissue.

43 Normophosphatemic familial tumoral calcinosis (NFTC) is caused by mutations in the

44 Familial tumoral calcinosis is characterized by ectopic calcifica

45 a 13-year-old girl who presented with severe tumoral calcinosis with dural and carotid artery calcifi

46 nnective tissues, as exemplified by familial tumoral calcinosis, pseudoxanthoma elasticum, generalize

47 enesis imperfecta), mineralization (familial tumoral calcinosis/hyperostosis hyperphosphatemia syndro

48 We discover that intra-tumoral CD8(+) T cells increase following combination tr

49 Negative tumoral CEACAM6 expression was associated with absence o

50 Tumoral CEACAM6 expression was detected in 82 (92%) panc

51 Tumoral CEACAM6 expression was dichotomized into negativ

52 erative or antiproliferative effect in human tumoral cell lines.

53 a surprising finding given that other intra-tumoral cell types are known to secrete fibulin-2.

54 ain actors of this dynamic interplay between tumoral cells and their microenvironment are the nano-si

55 t the classical paradigm that NB arises from tumoral cells capable of development along multiple line

56 ient down-regulation of the VEGF produced by tumoral cells using antisense strategies has an antitumo

57 moral properties, which are inhibited in non-tumoral cells.

58 ntibody responses to microbial pathogens and tumoral cells.

59 e and therapeutic immunity against viral and tumoral challenges as well as against transplanted tumor

60 Because no clinical, laboratory, or tumoral characteristic distinguishes patients with LN pr

61 Somatic mutations and other molecular tumoral characteristics offer opportunities for treatmen

62 antibodies correlating morphological (peri-)tumoral characteristics to levels of antibody delivery,

63 rd ratio of death, adjusted for clinical and tumoral characteristics, including KRAS, BRAF, PIK3CA, b

64 its the accumulation of high levels of intra-tumoral chemotherapy and a robust therapeutic response.

65 very and histological localization in (peri-)tumoral compartments of antibody-based therapeutics in h

66 yte-like location in melanoma, forming angio-tumoral complexes.

67 Tumoral concentration of IGF-I and its mRNA expression w

68 loid populations arising in inflammatory and tumoral conditions and multipotent cells, mobilized by h

69 els are starting to be reported in different tumoral contexts and shown to promote breast tumorigenes

70 Delayed tumoral contrast enhancement is a typical feature of int

71 microspheres and contrast material, retained tumoral contrast remained qualitatively visible with all

72 ially tumor dependent involving induction of tumoral CYP3A4 metabolism, with host pretreatment alone

73 Importantly, high intra-tumoral cytolytic T cell inflammation prior to MAPKi the

74 26A1, correlated with reduced frequencies of tumoral cytotoxic CD8(+) T cells and with worse disease

75 use of granzyme B, a downstream effector of tumoral cytotoxic T cells, as an early biomarker for tum

76 CpG activation of tumoral DCs alone was not sufficient to induce tumor reg

77 -3alpha) chemokine to increase the number of tumoral DCs and intratumoral injections of CG-rich motif

78 These results indicate that the number of tumoral DCs as well as the tumor milieu determines the a

79 ated inhibition of DC activation and enabled tumoral DCs to cross-present tumor antigens to naive CD8

80 ber of circulating DCs but not the number of tumoral DCs.

81 Tumoral deposition of calcium pyrophosphate dihydrate cr

82 nta flava from surgical specimens but not as tumoral depositions.

83 atory microenvironment that has an impact on tumoral development.

84 In the enucleation group, median tumoral diameter was 40 mm (18-65 mm), without any mucos

85 In the esophagectomy group, the median tumoral diameter was 85 mm (55-250 mm), with mucosal ulc

86 Tumoral dihydropyrimidine dehydrogenase expression is a

87 analyzes 450,000 CpG sites was used to study tumoral DNA obtained from 444 patients with NSCLC that i

88 nCRT resulted in tumoral downstaging (pT0, 40.7% vs 1.1%, P < 0.001), LN

89 peutic efficacy of carfilzomib by increasing tumoral drug accumulation while decreasing systemic toxi

90 l energy into tissues, which increases intra-tumoral drug perfusion and blood-flow.

91 ce of PARP3 confers hypersensitivity to anti-tumoral drugs generating DSB.

92 licated in tumor angiogenesis through direct tumoral effects and through reduction of proangiogenic c

93 ectly target tumor cells, exert minimal anti-tumoral effects in vivo, despite killing glioma cells in

94 In addition, this flavonoid shows anti-tumoral effects on colon cancer cells (SW480, DLD-1, and

95 CD103(+) DCs were required to promote anti-tumoral effects upon blockade of the checkpoint ligand P

96 ive, anti-inflammatory, anti-viral, and anti-tumoral effects.

97 daptive immune response constrain viral anti-tumoral efficacy.

98 Among patients who were studied for tumoral EGFR expression, 90% were positive, with no trea

99 for which the role and the importance in the tumoral environment remain to be completely elucidated.

100 d effects on the different components of the tumoral environment.

101 Further analysis of tumoral epigenetic alterations in hematopoietic CDRs poi

102 ent immunosuppressive enzyme, contributes to tumoral escape, immune tolerance, and protection against

103 ior of colorectal carcinoma, we compared the tumoral expression by immunohistochemical analysis of mo

104 h NIRF optical imaging, while differences in tumoral expression may correlate with tumor aggressivene

105 These analyses suggested a possible role of tumoral expression of IL-6R in ovarian cancer.

106 also demonstrate that irinotecan reduced the tumoral expression of monocarboxylate transporter 4, whi

107 rectal cancer patients revealed that reduced tumoral expression of PHD3 correlated with increased fre

108 In conclusion, tumoral expression of the CX3CL1-CX3CR1 chemokine axis f

109 N Among nonobese patients with colon cancer, tumoral FASN overexpression is associated with improved

110 Changes in tumoral FDG uptake, expressed as standardized uptake val

111 sted for patient characteristics and related tumoral features, including KRAS, BRAF, p53, microsatell

112 ; P = 0.0007) that adjusted for clinical and tumoral features, including microsatellite instability,

113 Clinical and tumoral features, TtD, and outcome associations were stu

114 hetic was associated with greater amounts of tumoral gas (P < .008) and PVG (P < .03).

115 The role of N(2)O anesthetic in PVG and tumoral gas formation during ablation also was studied.

116 Also, when tumoral gas was seen on CT scans, the largest cross-sect

117 a common yet benign cause of transient PVG, tumoral gas, and peritumoral gas.

118 Tumoral gas, peritumoral gas, and PVG dissipated within

119 hods were compared for quantities of PVG and tumoral gas.

120 ld promise as prodrug activation systems for tumoral gene therapy.

121 Intra-tumoral genetic and functional heterogeneity correlates

122 Intra-tumoral genetic heterogeneity has been characterized acr

123 ional and advanced imaging features of three tumoral genotypes with prognostic and therapeutic conseq

124 ld be partly direct and mediated by SV(1) of tumoral GH-RH receptors.

125 cause the antiserum developed recognizes the tumoral GHRH receptor protein encoded by SV1, it should

126 dent prostate cancer, by suppressing diverse tumoral growth factors, especially GHRH itself, which ac

127 uding prostate cancer by suppressing various tumoral growth factors.

128 ANG, resulted in the diminution of xenograft tumoral growth through the inhibition of angiogenesis.

129 medicine platform combining up-regulation of tumoral H2O2 level and self-sufficing H2O2-responsive dr

130 1/2) skin rash and two patients had positive tumoral HER1/EGFR expression.

131 Intra-tumoral heterogeneity and dramatic improvement in spatia

132 The underlying mechanism for this intra-tumoral heterogeneity can be explained by the clonal evo

133 However, the mechanisms by which intra-tumoral heterogeneity impacts therapeutic outcome remain

134 eports have stressed the importance of intra-tumoral heterogeneity in the development of a metastatic

135 mmarize recent efforts to characterize intra-tumoral heterogeneity of melanoma and delineate key ques

136 ur volume and textural features, relating to tumoral heterogeneity, has recently emerged from several

137 ic gene activation or repression, normal and tumoral human breast tissues obtained before and during

138 for further evaluation of the role of intra-tumoral IL-6 expression and of which cancers might benef

139 l, our findings uncover a novel mechanism of tumoral immune escape and suggest that a soluble multiva

140 es (TAM), but its potential contributions to tumoral immune escape and therapeutic targeting have bee

141 el mechanism by which hypoxia contributes to tumoral immune escape from cytotoxic T lymphocytes (CTL)

142 ic benefits of B-cell depletion in combating tumoral immune escape have been debated.

143 Here, we report mechanistic evidence of tumoral immune escape in an exemplary clinical case: a p

144 to arrest an important cellular mechanism of tumoral immune escape mediated by MDSCs and TAM in cance

145 stem plays a role in tumor progression, with tumoral immune escape now well recognized as a crucial h

146 e a novel subset of CCR2(+) Treg involved in tumoral immune escape, and they offer evidence that this

147 of immunosuppressive mechanisms that promote tumoral immune escape.

148 omal LDH-A as an effective strategy to blunt tumoral immune escape.

149 overlap with those that support evolution of tumoral immune escape.

150 peutic target owing to its role in promoting tumoral immune escape.

151 deficiency resulted in an alteration of the tumoral immune microenvironment, reflected by a decrease

152 Our results describe a mechanism of tumoral immune resistance based on TDO expression and es

153 peripheral immune tolerance contributing to tumoral immune resistance, and IDO1 inhibition is an act

154 ise recently been shown to be a mechanism of tumoral immune resistance.

155 umor growth by blocking T-cell-mediated anti-tumoral immune response through depletion of arginine th

156 nd Treg may provide a new strategy to ablate tumoral immune suppression and thereby heighten response

157 t using molecular targeted agents to reverse tumoral immune suppression may offer a powerful method t

158 lications for understanding the evolution of tumoral immune tolerance and for interpreting preclinica

159 Agents that interfere with tumoral immune tolerance may be useful to prevent or tre

160 n treatment, such as targeting mechanisms of tumoral immune tolerance.

161 SOCS2 limits adaptive anti-tumoral immunity and DC-based priming of T cells in vivo

162 mune homeostasis to key determinants of anti-tumoral immunity and escape, revealing co-opting of tiss

163 mmune system and are thought to mediate anti-tumoral immunity.

164 points that participate in key steps of anti-tumoral immunity.

165 on-genomic alterations and co-evolving intra-tumoral immunity.

166 may be accompanied by co-evolution of intra-tumoral immunity.

167 evidence that retroviral genes contribute to tumoral immunosurveillance in a process that can be gene

168 -L1 expression in HCC, and facilitated intra-tumoral infiltration of cytotoxic CD8+ T cells.

169 oncurrent with this was a reduction in intra-tumoral infiltration of innate and adaptive immune cells

170 mphoma effect is impaired because of delayed tumoral infiltration of PB T cells and a relative bias t

171 for diffusion MR imaging in the detection of tumoral infiltration that is not visible on conventional

172 me in extracellular matrix remodeling during tumoral, inflammatory, and angiogenic processes.

173 Although intra-tumoral injection of dl1520 shows promising responses in

174 genesis in tumor models lacking constitutive tumoral integrin alphavbeta3 expression but may be less

175 increasingly recognized as being critical to tumoral invasion, metastasis, and development of resista

176 Conversely, greater tumoral Ki-67 staining was observed in female mice (71%

177 Tumoral LCDIO accumulation was not negligible and helped

178 ients with the GA or GG genotype have higher tumoral levels of EGF, irrespective of EGFR status, that

179 lculated with the PMCD, D(mean) delivered to tumoral liver (TL) ranged from 19.5 to 118 Gy for D(mean

180 ty of Anesthesiologists scores, supracarinal tumoral location, and cervical anastomosis, but not NCRT

181 simultaneously, we demonstrate the distinct tumoral locations of probes in multiple channels in vivo

182 one (0/20) of normal and 8.0% (2/25) of peri-tumoral lung tissues (P<0.01).

183 SOX30 was expressed in normal and peri-tumoral lung tissues in which SOX30 was unmethylated, bu

184 wer metastatic rates correlated with reduced tumoral lymphatic vessel density and diameter and with i

185 astasis occurred via the cancer cell-bearing tumoral lymphatic vessels.

186 The congestion of these tumoral lymphatics with cancer cells may have restricted

187 ose-dependent way (0-10mg/mL) but not in non-tumoral lymphocytes.

188 iated macrophages (TAMs) shift towards a pro-tumoral M2 phenotype.

189 V infections as well as other infectious and tumoral manifestations.

190 ved elements constitute less than 10% of the tumoral mass.

191 3)C]-arginine could therefore serve to image tumoral MDSC function and more broadly M2-like macrophag

192 A related increase is found in intra-tumoral MHC-I, Th1 and T-effector markers, and chemokine

193 These features may be determined by the tumoral microenvironment.

194 t MR imaging, were presumed to be related to tumoral microvascularity.

195 rial shows promise as a marker for increased tumoral microvascularity.

196 s a diagnostic marker in PDAC, whereas intra-tumoral miR-10b promotes PCC proliferation and invasion

197 ic potential and tumor growth in vivo and in tumoral MMP-9 activity.

198 es, adjusted for patient characteristics and tumoral molecular features, including the CpG island met

199 its tumor specificity, increasing its intra-tumoral motility should improve its therapeutic effectiv

200 ted with a family history was independent of tumoral MSI or MMR status.

201 ll survival compared with patients with high tumoral MYO1A (logrank test P = 0.004 and P = 0.009, res

202 can be substantially reduced, and the intra-tumoral nanoparticle transport is restricted due to the

203 The tumoral NIR fluorescence intensity was more than 30-fold

204 Dose-related increases in tumoral nitroreductase expression measured by immunohist

205 reased polyamine content and increased intra-tumoral NK cells expressing perforin plus IFN-gamma comp

206 specimens established an association between tumoral NRP-1 levels and clinical outcome.

207 in irradiated wild-type mice, underlying the tumoral origin of the disease.

208 on-PCR analysis of 17 colon tumors indicated tumoral overexpression of OATP1B3 by approximately 100-f

209 c characteristics were compared according to tumoral parameters (size, pathologic type, grade, hormon

210 umoral tissue, but not their surrounding non-tumoral parenchyma, had nuclear beta-Cat and Axin2 overe

211 essed genes showed distinct inter- and intra-tumoral patterns in and between conventional squamous ca

212 document that the in vivo modulation of the tumoral pharmacokinetics of 5-FU can be measured noninva

213 with no other unusually severe infectious or tumoral phenotype who died from disseminated KS at two y

214 of this study was to characterize the intra-tumoral phenotypic heterogeneity between two iso-clonal

215 olecular oncology manifests the hallmarks of tumoral physiology with deteriorating propensity in elim

216 in vitro effects of BIM-23A760 in normal and tumoral pituitaries remains incomplete.

217 In tumoral pituitaries, BIM-23A760 also inhibited Ca(2+) co

218 d tumor necrosis factor-alpha, increased the tumoral populations of T lymphocyte and natural killer c

219 stages of initiation and progression of this tumoral process.

220 dependent functions of p38alpha signaling in tumoral processes is of obvious importance for the use o

221 vasculogenesis in human MM may develop from tumoral production of PTN, which orchestrates the transd

222 n contrast, rapamycin exerted less effect on tumoral production of VEGF.

223 ge and were strongly correlated with mammary tumoral progression.

224 apoptotic and cytostatic activities, and pro-tumoral promoting growth and metastasis.

225 thesized that the BAI family might have anti-tumoral properties and studied the expression of BAI1 pr

226 unctions as a second messenger that enhances tumoral properties, which are inhibited in non-tumoral c

227 ctivatable near-infrared probes sensitive to tumoral protease activity.

228 ly, activation of the near-infrared probe by tumoral proteases could be detected in peritoneal tumor

229 ncer and different imaging probes to measure tumoral proteases, macrophage content and integrin expre

230 Our findings suggest that the tumoral protein encoded by SV 1 (SV1) is a likely functi

231 Microvascularity identified as a tumoral pseudoblush at ultrahigh-field-strength high-res

232 low signal intensity within the tumor bed ("tumoral pseudoblush") at MR imaging, were presumed to be

233 y no clinically relevant method to visualize tumoral PTK7 expression noninvasively such as PET or SPE

234 on, meaning that this treatment enhanced the tumoral radioresponse.

235 trongly suggesting that ZAK induces such pro-tumoral reaction cascades in human cancers.

236 d HT lymphomas by direct effects mediated by tumoral receptors for GHRH.

237 he production of molecules required for anti-tumoral responses.

238 are rarely utilized in the field of in vivo tumoral ROS-responsive applications due to the fact that

239 ection of double-agent chemotherapy based on tumoral RRM1 and ERCC1 expression would be feasible and

240 performance status (PS) of 2 and assessed if tumoral RRM1 and ERCC1 protein levels are predictive of

241 The results strongly suggest that tumoral RRM1 expression is a major predictor of disease

242 val for patients with low as opposed to high tumoral RRM1 expression when treated with gemcitabine-co

243 emically administered RRM2 siRNA to suppress tumoral RRM2 expression in an orthotopic xenograft model

244 The mechanisms underlying tumoral secretion of signaling molecules into the microe

245 a breast cancer sample represents intrinsic tumoral sensitivity to adjuvant endocrine therapy.

246 sy specimens of lung cancers identify unique tumoral signatures that provide information about tissue

247 n=3) with corresponding RDEB and non-EB peri-tumoral skin, with microarray analysis using DermArray m

248 tal procedural volume, cervical anastomosis, tumoral stage III/IV, and pulmonary and cardiovascular c

249 assessed static parameters (maximal and mean tumoral standardized uptake value corrected for mean bac

250 Inhibition of CXCR4-regulated tumoral, stem cell, and immune mechanisms by adjunctive

251 only in the negative area, suggesting intra-tumoral sub-clonal genomic evolution.

252 y men, which may be beneficial for viral and tumoral surveillance.

253 njection; however, (18)F-FETrp showed higher tumoral SUV than (11)C-AMT in all 3 tumor types tested.

254 The biodistribution and tumoral SUVs for both tracers were compared.

255 cell activity while anti-VEGF augments intra-tumoral T-cell infiltration, potentially through vascula

256 Following dissection of the tumoral (T) and nontumoral (NT) tissue on formalin-fixed

257 AhR-null tumoral tissue, but not their surrounding non-tumoral pa

258 mutation in the GNA11 gene was identified in tumoral tissue.

259 heir differential distribution in normal and tumoral tissues are described with emphasis on breast, p

260 L is often overexpressed in human colorectal tumoral tissues.

261 ession in every metastasis, whereas no extra-tumoral transgene induction was observed.

262 ut accumulates in gliomas, mainly because of tumoral transport and metabolism via the immunomodulator

263 ammaR) IIb at the tumor site prevented intra-tumoral Treg cell depletion, which may underlie the lack

264 endent molecular program is evident in intra-tumoral Treg cells.

265 o systems when dosed by optical density, the tumoral uptake and biodistribution profiles for each of

266 some solid tumors that textural features of tumoral uptake in (18)F-FDG PET images are associated wi

267 firmed that ccRCC tumors exhibited increased tumoral uptake of (18)F-(2S,4R)4-fluoroglutamine compare

268 umors to paclitaxel therapy, we examined the tumoral uptake of (18)F-fluoropaclitaxel ((18)F-FPAC) in

269 th tumors that progressed demonstrated lower tumoral uptake of (18)F-FPAC than mice with tumors that

270 (18)F-FETrp tumoral uptake, biodistribution, and radiation dosimetry

271 Measurements of tumoral VVF at high-resolution MR imaging with long-circ

272 Mean tumoral VVF differed significantly among the different t

273 Tumoral VVFs were measured at submillimeter voxel resolu

274 from 11 patients with CTCL, both normal and tumoral, were target-enriched and sequenced by massive p

275 d)-E-cad), as well as other well known human tumoral xenografts exhibiting no (MCF-7, T47D), low (MDA

276 High tumoral ZNF304 expression is associated with poor overal