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 Biodistribution studies showed a specific tumoral accumulation of daratumumab.

9 Biodistribution studies showed a specific tumoral accumulation of Daratumumab.

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

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

12 ed tumors exhibit increased numbers of intra-tumoral activated T cells and decreased expression of Cc

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

14 accompanied by concomitant increases in the tumoral activity concentrations of the glycoengineered r

15 We found that anti-tumoral activity of gemcitabine and the Wee1 kinase inhi

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

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

18 (IFN) are being rediscovered as potent anti-tumoral agents.

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

20 dominating the phenotypic plasticity of both tumoral and microenvironmental components.

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

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

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

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

25 uptake and to quantify tracer uptake in the tumoral and peritumoral areas.

26 apparent diffusion coefficient (ADC) of the tumoral and peritumoural regions was made.

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

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

29 derstanding of the complex interplay between tumoral and systemic immune response has been provided t

30 tus of (18)F-FDG PET/CT in the monitoring of tumoral and systemic immune response.

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

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

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

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

35 atment paradigms based on understanding true tumoral antibody delivery.

36 omal area of the tumor and are excluded from tumoral area compared with melanoma, where the immune in

37 une infiltrates are primarily present in the tumoral area.

38 ("SCHMOWDER") uses an attention mechanism on tumoral areas annotated by a pathologist whereas the sec

39 Pathological review showed that the tumoral areas most predictive of poor survival were char

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

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

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

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

44 the phenotype of microvasculature, reducing tumoral blood pooling.

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

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

47 loci associated with altered methylation in tumoral but not nonmalignant tissue.

48 s an integrin alpha11-positive subset of pro-tumoral CAFs that exploits PDGFRbeta/JNK signalling axis

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

50 n can lead to severe hyperphosphatemia as in tumoral calcinosis and chronic kidney disease (CKD).

51 Familial tumoral calcinosis is characterized by ectopic calcifica

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

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

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

55 CRPC model despite an increase in the intra-tumoral CD4 T cells, which are polarized to T(h)17 rathe

56 cking antibody in association with increased tumoral CD8(+) T cells and established immune memory.

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

58 ne-cold" microenvironment with an absence of tumoral CD8+ T cells was defined by elevated expression

59 erative or antiproliferative effect in human tumoral cell lines.

60 50% cell growth inhibition in four selected tumoral cell lines.

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

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

63 pment of compounds selectively targeting the tumoral cells.

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

65 ntibody responses to microbial pathogens and tumoral cells.

66 ylation (p-STAT3) in EGFRT790M and EGFRC797S tumoral cells.

67 athogens, cellular debris, and apoptotic and tumoral cells.

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

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

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

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

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

73 nsification and tangential alignment of peri-tumoral collagen.

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

75 ltaneously and dynamically mapping the intra-tumoral concentration of two MRI contrast agents (Gd-BOP

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

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

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

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

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

81 26A1, correlated with reduced frequencies of tumoral cytotoxic CD8(+) T cells and with worse disease

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

83 immunosuppressive environment that promotes tumoral development.

84 atory microenvironment that has an impact on tumoral development.

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

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

87 Tumoral dihydropyrimidine dehydrogenase expression is a

88 In chronic lymphocytic leukemia (CLL), intra-tumoral DNA methylation (DNAme) heterogeneity empowers e

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

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

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

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

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

94 uring avascular tumor growth within the peri-tumoral ECM remain poorly understood.

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

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

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

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

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

100 daptive immune response constrain viral anti-tumoral efficacy.

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

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

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

104 Further analysis of tumoral epigenetic alterations in hematopoietic CDRs poi

105 g histone modifications, suggestive of intra-tumoral epigenetic diversity.

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

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

108 Combining circulating and intra-tumoral expression levels of PD-L1 or Galectin-9 further

109 vels of PD-L1 and Galectin-9 and their intra-tumoral expression levels.

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

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

112 ned analysis of circulating levels and intra-tumoral expression of PD-L1 (HR 0.33, 95%CI 0.16-0.68, p

113 tochemistry was performed to determine intra-tumoral expression of PD-L1 and Galectin-9, while ELISA

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

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

116 SYK inhibition resulted in increased intra-tumoral expression of the p16 and p53 but decreased expr

117 ly-reported risk variant) and with increased tumoral expression of the TMPRSS2:ERG fusion-oncogene in

118 e their prognostic significance to the intra-tumoral expression of these same molecules.

119 d HCC patients, independently of their intra-tumoral expression.

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

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

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

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

124 monstrate the efficacy in reverting the anti-tumoral function of T cells, highlighting the therapeuti

125 mor-associated macrophages (TAMs) showed pro-tumoral functions without signature gene expression of d

126 Intra-tumoral genetic and functional heterogeneity correlates

127 Intra-tumoral genetic heterogeneity has been characterized acr

128 mics in dissecting, in its many forms, intra-tumoral genetic heterogeneity of CNAs, the magnitude wit

129 However, our knowledge of intra-tumoral genetic heterogeneity of this important class of

130 siveness of PLC may be achieved by enhancing tumoral genomic complexity that alters tumor biology.

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

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

133 uding prostate cancer by suppressing various tumoral growth factors.

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

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

136 Intra-tumoral heterogeneity (ITH) could represent clonal evolu

137 Intra-tumoral heterogeneity and dramatic improvement in spatia

138 veals a central principle underpinning intra-tumoral heterogeneity and motivates therapeutic targetin

139 hat such static classification ignores intra-tumoral heterogeneity and the potential for cellular pla

140 SI-H tumors associated with diminished intra-tumoral heterogeneity as well as higher expression of ch

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

142 Genetic and epigenetic intra-tumoral heterogeneity cooperate to shape the evolutionar

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

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

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

146 nders such as patient co-morbidities, by the tumoral heterogeneity of molecular and cellular markers,

147 dels that recapitulate both intra- and inter-tumoral heterogeneity to gain new insights into tumorige

148 Glioblastomas exhibit vast inter- and intra-tumoral heterogeneity, complicating the development of e

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

150 sight into cancer evolution, including intra-tumoral heterogeneity, metastasis, and immune evasion, p

151 e BC microenvironment, indicating high intra-tumoral heterogeneity.

152 immune cells and we observed intra and inter tumoral heterogeneity.

153 allowing for improved visualization of intra-tumoral heterogeneity.

154 crophage infiltration as well as lower intra-tumoral heterogeneity.

155 ed on the rescue and enhancement of the anti-tumoral host response.

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

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

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

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

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

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

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

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

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

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

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

167 of immunosuppressive mechanisms that promote tumoral immune escape.

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

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

170 1,224 single cells from peripheral and intra-tumoral immune populations from patients with HPV(-) and

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

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

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

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

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

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

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

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

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

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

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

182 es (cGAS-STING) pathway activation, and anti-tumoral immunity is critical for the development of effe

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

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

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

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

187 ated by radiation as a function of increased tumoral immunogenicity, underscoring the potential of AT

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

189 ted aorta (40%), and the right atrium pseudo-tumoral infiltration (36%).

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

191 an immunoreactive microenvironment exhibited tumoral infiltration of granzyme B+CD8+ T cells (GzmB+CD

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

193 mmatory processes were altered, with reduced tumoral infiltration of neutrophils and CD4 positive T c

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

195 gested that hydrogel administrated via intra-tumoral injection could prolong both PDT agents retentio

196 The dose of R848 (10 mug for intra-tumoral injection or 6 mg/kg for intravenous injection d

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

198 a target for inhibition of Snail1-dependent tumoral invasion and chemoresistance.

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

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

201 atasets (3D) revealed variation in the intra-tumoral Ki67 expression that was not evident in individu

202 HCC-specific survival independently of intra-tumoral levels and baseline clinicopathologic characteri

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

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

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

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

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

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

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

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

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

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

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

214 of this is pancreatic cancer, in which intra-tumoral microbes such as bacteria and fungi have been sh

215 iome of LTS patients and identified an intra-tumoral microbiome signature (Pseudoxanthomonas-Streptom

216 These features may be determined by the tumoral microenvironment.

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

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

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

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

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

222 rmline and is associated with variable inter-tumoral MYBL2 expression.

223 biliary cancers have distinct peripheral and tumoral myeloid signatures.

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

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

226 ry cytokines (interleukin, [IL]-6, IL-8, and tumoral necrosis factor-alpha [TNF-alpha]), and oral Can

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

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

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

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

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

232 the use of nanotechnology to harmonize intra-tumoral oxygen or suppress hypoxia-related signaling for

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

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

235 hanced vascular permeability specifically in tumoral/peritumoral areas, which resulted in fast and su

236 lectively increased vascular permeability in tumoral/peritumoral areas, without interfering with drug

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

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

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

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

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

242 explained, in part, by the presence of intra-tumoral platelets.

243 ned for their selective toxicity against non tumoral primary cells (fibroblasts) and against a breast

244 sed to describe an inflammatory or fibrosing tumoral process of an undetermined cause that may involv

245 stages of initiation and progression of this tumoral process.

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

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

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

249 ge and were strongly correlated with mammary tumoral progression.

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

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

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

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

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

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

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

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

258 fective at-site siRNA release resulting from tumoral reactive oxygen species (ROS)-triggered sequenti

259 ng antivirals (DAA) on the risk of death and tumoral recurrence in patients with hepatitis C virus (H

260 SCC received mitomycin in case of tumoral resection margins, respectively (P = .018).

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

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

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

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

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

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

267 Although inappropriate tumoral secretion of calcitriol is typically associated

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

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

270 otency at the low nanomolar level in several tumoral settings, and to the selectivity toward IDO1 ove

271 fluid pressure in both interstitial and peri-tumoral spaces.

272 he models may also fail to account for intra-tumoral spatial and microenvironmental heterogeneity.

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

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

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

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

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

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

279 at the T cell clones that dominate the intra-tumoral T cell landscape after ICB are distinct from tho

280 ous CRPC model significantly increases intra-tumoral T(h)1 subsets and improves survival.

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

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

283 Inhibition of ATM increased tumoral T1IFN expression in a cGAS/STING-independent, bu

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

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

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

287 L is often overexpressed in human colorectal tumoral tissues.

288 ze during animal development and to restrict tumoral transformation.

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

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

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

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

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

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

295 Conclusion: Since tumoral uptake of (18)F-FES is not significantly impacte

296 ents, a correlation was observed between the tumoral uptake of [(64)Cu]Cu-MeCOSar-Tz and the subseque

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

298 ound (US) imaging provides information about tumoral vessel structures and blood flow.

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

300 High tumoral ZNF304 expression is associated with poor overal