ライフサイエンスコーパス: normal tissue

1 genes in ccRCC samples compared to adjacent normal tissue.

2 ficacy while abrogating its toxic effects on normal tissue.

3 increased 7.8 +/- 2.6-fold when compared to normal tissue.

4 to be depleted of mtDNA, relative to matched normal tissue.

5 ofiles for distinguishing between cancer and normal tissue.

6 on radiotherapy by reducing toxic effects to normal tissue.

7 rom clinical lung cancer samples and matched normal tissue.

8 encoding HIF-2alpha) expression relative to normal tissue.

9 was 415 times greater in CRC versus adjacent normal tissue.

10 ated apoptosis in cancer cells while sparing normal tissue.

11 tive human HNSCC tumors relative to adjacent normal tissue.

12 ) preferentially within tumors as opposed to normal tissue.

13 al to autonomously distinguish diseased from normal tissue.

14 ze can selectively target tumour tissue over normal tissue.

15 downregulated in breast tumor compared with normal tissue.

16 organoids were also generated from adjacent normal tissue.

17 ssive cells to grow toward blood vessels and normal tissue.

18 detected in adenomas compared with adjacent normal tissue.

19 efitinib, also preexists in cancer cells and normal tissue.

20 arious cancer cells, but is not expressed in normal tissue.

21 cted for any two cells randomly taken from a normal tissue.

22 large cargo traverse epithelial barriers in normal tissue.

23 Notably, only limited effects were seen in normal tissue.

24 trations in the tumor and in the surrounding normal tissue.

25 sociated lymph node metastases compared with normal tissue.

26 can help the surgeon distinguish tumor from normal tissue.

27 11betaHSD2 protein expression compared with normal tissues.

28 evelopment and then becomes silenced in most normal tissues.

29 3 and A3AR is lower in human OS tissues than normal tissues.

30 xplain much of the differences compared with normal tissues.

31 multiple samples of colon tumor and matched normal tissues.

32 nificantly higher in AVM tissues compared to normal tissues.

33 l for treating micrometastases while sparing normal tissues.

34 t a surgeon in differentiating cancerous and normal tissues.

35 was differentially expressed in SONFH versus normal tissues.

36 T family genes are ubiquitously expressed in normal tissues.

37 r site with reduced side effects to adjacent normal tissues.

38 ROS-mediated cytotoxicity of the drug toward normal tissues.

39 the estimated rate of stem cell division in normal tissues.

40 ues, showing higher levels of correlation in normal tissues.

41 complex presents as a major form detected in normal tissues.

42 asis or intrahepatic metastasis, compared to normal tissues.

43 st and prostate tumours and in corresponding normal tissues.

44 ferent calcium content in tumor cells versus normal tissues.

45 y lower in colorectal tumours than in paired normal tissues.

46 the target complex in cells from essential, normal tissues.

47 and another expression dataset from matching normal tissues.

48 of the mitochondrial and nuclear genomes in normal tissues.

49 uman breast tumors but not in tumor-adjacent normal tissues.

50 tumor targeting thus aborting its effect on normal tissues.

51 d RNA-editing patterns in tumors relative to normal tissues.

52 eir matched primary tumors and corresponding normal tissues.

53 ular hypoxia that it is not produced in most normal tissues.

54 er, it is not expressed in most nonlipogenic normal tissues.

55 s, but it is not constitutively expressed on normal tissues.

56 rity of the 12 tumors examined but not in 18 normal tissues.

57 uces apoptosis in cancer cells while sparing normal tissues.

58 target tumors more accurately while sparing normal tissues.

59 lly, TSLPR has limited surface expression on normal tissues.

60 rous and metastatic cancers, although not in normal tissues.

61 ls are higher in lung adenocarcinoma than in normal tissues.

62 ut three-fold without a parallel increase in normal tissues.

63 e for treating micrometastases while sparing normal tissues.

64 acranial DBTs up to 24 h with clearance from normal tissues.

65 TL7 underexpression in cancerous compared to normal tissues.

66 ed migration of cytolytic CD8 T cells within normal tissues.

67 UGT1A_i2 mRNA in colon tumors compared with normal tissues.

68 in lung tumors as compared to their adjacent normal tissues.

69 transcriptional programs relative to matched normal tissues.

70 ed in colorectal cancer biopsies compared to normal tissues.

71 owth without evident significant toxicity to normal tissues.

72 eat me" signal CD47 expressed on tumors and normal tissues.

73 o cancer cells without incurring toxicity to normal tissues.

74 age tumors with and without STIC lesions and normal tissues.

75 ion in mouse models with little toxicity for normal tissues.

76 in a cohort of 42 tumor tissues and adjacent normal tissues.

77 gulated in human CRC tissues versus adjacent normal tissues.

78 or cells, it also has significant effects on normal tissues.

79 h limited deleterious effects on surrounding normal tissues.

80 ry patient-derived tumors, without affecting normal tissues.

81 e elevated in a wide variety of unirradiated normal tissues.

82 ocytes, within HO-containing tissues but not normal tissues.

83 ially expressed between the paired tumor and normal tissues (1048 up and 1997 down).

84 r expression of mtRNA in tumors (relative to normal tissue) across a majority of cancer types.

85 cellular heterogeneity and demonstrate that normal tissue adjacent to breast cancer is characterized

86 Identifying molecular alterations in normal tissue adjacent to cancer is important for unders

87 Histologically normal tissue adjacent to the tumor (NAT) is commonly us

88 eded during RT, leading to severe damages to normal tissues adjacent to tumors.

89 breast cancer, and equivalent or fewer late normal-tissue adverse effects were seen.

90 enhanced risk for late radiation toxicity to normal tissues after radiotherapy.

91 f CDC6 mRNA expression in tumour compared to normal tissue and a correlation between CDC6 and CHEK1 m

92 dearth of information on its localization in normal tissue and by the lack of antibodies suitable for

93 to also be differentially expressed between normal tissue and cancer.

94 that cancer cells take up more glucose than normal tissue and favor incomplete oxidation of glucose,

95 therapy, proton radiotherapy irradiates less normal tissue and might improve health outcomes associat

96 ition differently in prostate cancer than in normal tissue and prostate hyperplasia, whereas MMP2 is

97 nced oxidative stress compared with adjacent normal tissue and the contralateral kidney.

98 different degrees of receptor saturation for normal tissue and tumor.

99 ompanied by significant collateral damage to normal tissue and unwanted side effects.

100 eing expressed in HGS-OvCa tumors and not in normal tissues and analyzed 671 top-ranked isoforms by h

101 SUVmax and SUVmean were recorded for normal tissues and areas of uptake outside the expected

102 number and nature of genetic alterations in normal tissues and can be used to address a variety of f

103 levant functions that this protein exerts in normal tissues and cancer.

104 sequencing (RNA-seq) libraries from tumors, normal tissues and cell lines comprising over 43 Tb of s

105 immunogenic because they are not present in normal tissues and hence bypass central thymic tolerance

106 ules cross endothelial cell (EC) barriers in normal tissues and in solid tumors, including paracellul

107 in CRC tissues compared with their adjacent normal tissues and is an independent prognostic factor f

108 Telomeres were shorter in tumors than in normal tissues and longer in sarcomas and gliomas than i

109 esponding to differential gene expression in normal tissues and matching tumors.

110 atopoietic cell transplantation (HCT) injure normal tissues and may increase the risk of frailty even

111 ive positive RD3 immunoreactivity in various normal tissues and particularly strong dot-like perinucl

112 approaches to explore cell fate behavior of normal tissues and the initiation of preneoplasia remain

113 nvestigate the safety and biodistribution in normal tissues and uptake in tumor lesions.

114 xpressed in lung cancer compared to adjacent normal tissue, and exhibited a predominant nuclear locat

115 s and proteomics datasets from malignant and normal tissues, and developed an algorithm to identify p

116 tumor visualization, minimal accumulation in normal tissues, and rapid renal clearance.

117 dases is often higher in tumor cells than in normal tissues, and such concentration gradients can be

118 ethal toxicity from on-target recognition of normal tissues, and there is a paucity of truly tumor-sp

119 Regenerative medicine aims to restore normal tissue architecture and function.

120 However, clonal tumor expansion from complex normal tissue architectures potentially obscures cancer-

121 Yet, paired normal tissues are not always available in clinical sett

122 nder both normoxic and hypoxic conditions in normal tissues as well as in a murine breast cancer mode

123 of cancer treatment, nonselectively damages normal tissues as well as tumor tissues.

124 y parallel RNA sequencing in GCs and matched normal tissues, as well as in GC-derived and normal gast

125 of the allelic composition of the tumor and normal tissue at each reference base.

126 y in both prostate cancer lesions as well as normal tissues at both time points.

127 The tumor and normal tissue biodistribution of (177)Lu-DOTA-Fab-PEG24-

128 stantially in the cancer with respect to the normal tissue but ultimately play an important role in p

129 d ligands, whose expression is negligible in normal tissues, but increased in stress and disease cond

130 cytoskeleton in prostate epithelial cells in normal tissues, but not in prostate cancers.

131 o be important for tight control of hTERT in normal tissues, but the molecular mechanisms leading to

132 CAR T cells can potentially damage normal tissues by specifically targeting a tumor-associa

133 Infiltration of gliomas into normal tissue can be detected by DESI-MS.

134 o which tumour samples are contaminated with normal tissue can be estimated and corrected for.

135 rrays, representing human gene expression in normal tissues, cancer cell lines and primary tumors.

136 and metastases, and the removal of important normal tissues causes excessive morbidity.

137 rther confirmed in liver cancer and adjacent normal tissue collected from in-house Chinese liver canc

138 85.7%) and right (91.7%) tumor and/or paired normal tissues compared with left and right control biop

139 The most optimal multivariable normal tissue complication probability model for ACEs co

140 cope with disease recurrence and a myriad of normal tissue complications brought on by radio- and che

141 sis of RD3 transcriptional expression across normal tissues confirmed tissue-specific RD3 mRNA levels

142 Highest tumor-to-normal tissue contrast was obtained at days 3 and 7 afte

143 umors with significantly enhanced disease-to-normal tissue contrast, as confirmed in three subtypes o

144 An increase in tumor-to-normal-tissue contrast was observed over the imaging tim

145 is a sensitive PET agent with high tumor-to-normal-tissue contrast.

146 sion in renal tumours compared with adjacent normal tissues correlates with enhanced binding of Hsp90

147 carcinoma cell lines as distinct from their normal tissue counterparts and the tumor microenvironmen

148 ed cytotoxicity while maintaining restricted normal tissue cross-reactivity and achieving substantial

149 is considered as a prime target in limiting normal tissue damage and improving tumor control in radi

150 cause of clinically observed variability of normal tissue damage following radiotherapy is poorly un

151 (PDT) can destroy local tumors and minimize normal tissue damage, but is ineffective at eliminating

152 pparent in studying cancer that tumors, like normal tissues, demonstrate metabolic cooperation betwee

153 nd regulation of the homeostatic dynamics of normal tissue development, proliferation, regeneration,

154 re present at high levels in morphologically normal tissue distant from the cancer, reflecting clonal

155 well as providing a better understanding of normal tissue dynamics.

156 epertoire that induces cross-reactivity with normal tissue, effectively breaking tolerance that is ac

157 hose from microbes, damaged tissues, and the normal tissue environment.

158 n having tumor-specific or highly restricted normal tissue expression by RT-qPCR analysis are enriche

159 Compared with normal tissue, expression of many DNA replication/repair

160 ement ratio [SER], and washout fraction) and normal tissue features (background parenchymal enhanceme

161 However, the mechanisms through which normal tissue fibroblasts are reprogrammed to tumor-prom

162 etermine frequency of cure and assess select normal tissues for treatment-related histopathologies.

163 d RNA-seq data of matched tumor and adjacent normal tissue from 50 breast cancer patients as well as

164 ly increased in human atheroma compared with normal tissue from the same carotid arteries.

165 ferentially expressed between PTC tissue and normal tissue from the same patient.

166 d from peripheral blood, tumor, and adjacent normal tissues from six hepatocellular carcinoma patient

167 f model systems that accurately recapitulate normal tissue function of human organs and their respons

168 ytoskeletal systems is important to maintain normal tissue function, knowing the relative contributio

169 nic low-grade inflammation and disruption of normal tissue functions in metabolic diseases.

170 in cancer and more ubiquitously expressed in normal tissues, GLUT4 exhibits more limited normal expre

171 Fission drives normal tissue growth and maintenance.

172 ha and beta diversity analyses revealed that normal tissues had the greatest richness in community di

173 In normal tissues, Hh pathway activation via PTCH/SMO cause

174 ferocytosis, is essential for maintenance of normal tissue homeostasis and a prerequisite for the res

175 tood, yet the ECM plays an important role in normal tissue homeostasis and disease processes.

176 tood, yet the ECM plays an important role in normal tissue homeostasis and disease processes.

177 raordinary ability to respond differently to normal tissue homeostasis, to tissue repair, or when cha

178 tions at the site of inflammation to restore normal tissue homeostasis.

179 The average CEST contrast between tumors and normal tissue in 17 patients was 7.58% (P = 0.006) in th

180 iation-induced tumorigenic transformation of normal tissue in astronauts, and in cancer patients unde

181 expression in cancerous tissue and adjacent normal tissue in patients with invasive ductal carcinoma

182 has the potential to differentiate tumor and normal tissue in real time during surgical excision.

183 radiation-induced toxicity due to damage to normal tissue in the irradiation field.

184 sfully repurposed to distinguish cancer from normal tissue in the preoperative clinic and throughout

185 chieved between tumor tissue and surrounding normal tissues in adenocarcinomas, squamous cell carcino

186 Low uptake in normal tissues in conjunction with high tumor uptake res

187 s in the differentiation status of tumor and normal tissues in different patients.

188 cancer tissues as compared with the adjacent normal tissues in human patients.

189 ctive form of ADAM10 in tumors compared with normal tissues, in mouse models and humans, identified b

190 logical treatment modality that also damages normal tissue, including the skin, and causes radiation

191 However, the extent of normal tissue injury in the lungs following high-LET rad

192 Normal tissue injury resulting from cancer radiotherapy

193 Charting differences between tumors and normal tissue is a mainstay of cancer research.

194 Severe late damage to normal tissue is a major limitation of cancer radiothera

195 ments while minimizing injury to surrounding normal tissue is an important clinical goal.

196 ogramming towards reduced differentiation in normal tissue is an important step in breast carcinogene

197 e-positive cancer cells over single-positive normal tissue is believed to enhance the therapeutic eff

198 optimal therapeutic index to avoid damage to normal tissue is extremely important.

199 oreover, the probability of complications to normal tissues is predicted using anatomic or functional

200 ficantly upregulated in cancer compared with normal tissues, is a major determinant of mutp53 stabili

201 deletion prevents the embryonic lethality of normal tissues lacking Mdm2, suggesting that cells can s

202 idly cycling SCs function principally during normal tissue maintenance and are highly sensitive to st

203 e progression, underlining its relevance for normal tissue maintenance.

204 es, compared against primary CRCs (n=95) and normal tissues (n=60), and integrated with genomic and d

205 ay with SONFH tissues (ONs) and the adjacent normal tissues (NLs) to select the angiogenic miRNA.

206 We show that, in comparison with normal tissues, NPTX2 and NPTXR are overexpressed in viv

207 r susceptibility genes, in DNA prepared from normal tissue obtained from 854 patients with pancreatic

208 tors (RANK(+) and RANK(-)) in histologically normal tissue of BRCA1-mutation carriers and showed that

209 n has recently been demonstrated to occur in normal tissue of individuals ascertained with varied phe

210 KG2D ligands was not induced persistently on normal tissues of allogeneic HSCT-recipient mice treated

211 Arf is not expressed in most normal tissues of young mice but is induced by high thre

212 .g. tumor size) with a reference group (e.g. normal tissue) on the basis of thousands of features (e.

213 multiregion tumor specimens, and uninvolved normal tissues or blood from 45 patients with early-stag

214 n the tissues, which may inherently exist in normal tissues or may be formed by inflammation or injur

215 tion and rapid distribution and excrete from normal tissue/organ via renal excretion after complete t

216 sitioning at anaphase onset is essential for normal tissue organization and function.

217 dose and irradiated area in the response of normal tissues outside the irradiated field at 1 and 4 d

218 s (including those of primary tumors, paired normal tissues, PBMC, recurrent tumors, and metastatic t

219 Apoptosis is an important component of normal tissue physiology, and the prompt removal of apop

220 erexpressed in various cancers compared with normal tissues, plays a pivotal role in adhesion, angiog

221 specific T cells that interact directly with normal tissues, potentially causing specific organ damag

222 in human bone metastases when compared with normal tissues, primary tumors or lymph node metastases.

223 rediction idea of applying models trained on normal tissue proteins to predict the subcellular locati

224 pathways active in tumor cells but absent in normal tissues provide opportunities to develop effectiv

225 HER2-expressing tumors, with a high tumor-to-normal tissue ratio in xenograft models of human cancer.

226 Consequently, tumor-to-normal tissue ratios of distribution were superior for 2

227 Tumor-to-normal-tissue ratios obtained with (111)In-3BP-227 and (

228 ulation of apoptosis during infection versus normal tissue regeneration.

229 iological variations in metabolite levels in normal tissues regulate stem-cell function in vivo.

230 reg cells and those present in corresponding normal tissue remain largely unknown.

231 hanism for regulating insulin sensitivity in normal tissue remains unclear.

232 the biosynthesis of collagen ECM at sites of normal tissue repair and fibrosis, with enormous implica

233 During normal tissue repair, stromal niche signals, often Hedge

234 n lead to chronic inflammation that prevents normal tissue repair.

235 n tumor-resident Treg cells in comparison to normal tissue-resident ones.

236 ll response with reactivity directed against normal tissue, resulting in the generation of high level

237 lly resected HCCs and matched tumor-adjacent normal tissues revealed an overexpression of RPS15A in H

238 context between tissues could contribute to normal tissue risk assessment and planning of remedial m

239 nctional roles in cancer cell and absence in normal tissue, SALL4 is a potential novel therapeutic ta

240 sive breast cancer, breast tumor and matched normal tissue sample data (as of September 18, 2015) wer

241 Although normal tissue samples adjacent to tumors are sometimes c

242 regulated in HPV-positive tumors compared to normal tissue samples and HPV-negative cases, and thus c

243 ide transcriptome profiling of cancerous and normal tissue samples can provide insights into the mole

244 iant calling typically requires paired tumor-normal tissue samples.

245 gene (SUFU) was identified in all tumor and normal tissue samples.

246 as performed on 46 HPV-positive OPSCC and 25 normal tissue samples.

247 ferentially correlated in cancer compared to normal tissues, showing higher levels of correlation in

248 Analogies between TICs and normal tissue stem cells have led to the proposal that a

249 presence of cancer cells with properties of normal tissue stem cells.

250 suggesting that these cells have features of normal tissue stem cells.

251 In normal tissue, STn is not detectable, which is critical

252 ression of specialized keratins required for normal tissue structure and integrity.

253 xpress tumor-associated antigens relative to normal tissue, such as EGFR.

254 n usage of individual genes when compared to normal tissue, suggesting that alternative splicing may

255 Diabetic muscles collected at the rim of normal tissue surrounding the plane of dissection showed

256 distinct areas of cancer and morphologically normal tissue taken from the prostates of three men.

257 The hypothesis is that in normal tissue the estrogenic SERM activity of a dual AI/

258 tumor environment and absent or inactive in normal tissues; therefore they represent viable targets

259 Unfortunately, these cells also attack host normal tissues through the often fatal graft-versus-host

260 at can induce damaging cross-reactivity with normal tissue to checkpoint protein inhibitors that indu

261 sitivity of different human tumor models and normal tissues to calcium electroporation.

262 benefit of collecting and profiling matched normal tissues to gain more insights on disease etiology

263 l approaches aimed at reducing or preventing normal tissue toxicity induced by radiotherapy is a long

264 therapy experience more frequent and greater normal tissue toxicity relative to younger patients.

265 h risk in space or protracted post-treatment normal tissue toxicity.

266 IR would improve tumor control and decrease normal tissue toxicity.

267 could be used as an in vivo marker to assess normal-tissue toxicity after extended internal irradiati

268 ing simultaneous sequencing of the tumor and normal tissue ("tumor-normal sequencing") compared with

269 However, both normal tissue types exhibited significant positive corre

270 d epigenomic activity patterns in cancer and normal tissue types more accurately than alternative met

271 s also implicated in self-renewal in several normal tissue types.

272 HERVs are silenced in most normal tissues, up-regulated in stem cells and in placen

273 The high stability and bioavailability, low normal-tissue uptake of [(64)Cu]Cu-NOTA-HsTX1[R14A], and

274 and blood clearance data, lesion uptake, and normal-tissue uptake were determined, and radiation-abso

275 ctal cancer (CRC) cells compared to adjacent normal tissues using deep RNA-sequencing (RNA-seq).

276 r individualised treatments that address the normal tissue variants visible on MRI.

277 rols in both the sonicated tumors and in the normal tissue volumes at 1 and 24h after sonication.

278 imens, whereas the expression of nectin-4 in normal tissue was more limited.

279 d during surgical procedures where otherwise normal tissue was removed to gain access to deeper hippo

280 uptake in infarcted heart tissue compared to normal tissue was significantly higher in non-diabetic r

281 nd in human ovarian cancerous, necrotic, and normal tissues was achieved.

282 Uptake in normal tissues was low, except for the kidneys, where up

283 Differential expression (tumor vs. adjacent normal tissue) was detected for more than 3,500 genes (l

284 gulating tissue protection and physiology in normal tissues, we hypothesized that CD73-generated aden

285 ational processes at work in morphologically normal tissue were also at work in cancer.

286 n metrics for cancerous tissue and those for normal tissue were assessed by using a two-tailed two-sa

287 ents of defined regions (ROIs) of tumour and normal tissue were quantified as percentage change in me

288 Colorectal carcinoma specimens and matched normal tissues were collected from patients at the Mayo

289 Lastly, the mutation spectra of normal tissues were different from each other, but simil

290 Radiation-absorbed doses to tumors and normal tissues were estimated and compared for (111)In-

291 t 2-fold higher concentrations in tumors vs. normal tissues, were observed for interstitial Pi - the

292 demic center for paired metastatic tumor and normal tissue WES during a 19-month period (February 201

293 vel findings on radiogenic transformation of normal tissue when exposed to particle radiation, it als

294 belled lectins to distinguish dysplasia from normal tissue when sprayed on to the luminal surface epi

295 eam radiation therapy (PBRT) reduces dose to normal tissues, which may lead to better neurocognitive

296 get because blocking CD47 signaling protects normal tissues while sensitizing tumors to ionizing radi

297 GC cells and primary GC tissues compared to normal tissues, while the expression of P2Y2 and P2Y4 re

298 d tracers cleared rapidly from the blood and normal tissues, with excretion mainly via the renal path

299 GSC and all tumor samples in comparison with normal tissues, with overall agreements of 96.4% and 96.

300 Cancer-specific targeting sparing normal tissues would significantly enhance cancer therap