ライフサイエンスコーパス: normal tissue

1 c, upstream regulators, mitigating damage to normal tissue.

2 urs in most cancer types but not in blood or normal tissue.

3 led due to low specificity and disruption of normal tissue.

4 sion signatures without the need for matched normal tissue.

5 , which in tumors is more restricted than in normal tissue.

6 nd pancreatic cancer, with low expression in normal tissue.

7 enabling comparisons between tumor, TNT, and normal tissue.

8 on akin to what occurs in cancer, but within normal tissue.

9 changes ( p < 1 x 10(-5)) in NPC compared to normal tissue.

10 1 d to determine the dosimetry in tumors and normal tissue.

11 in open-sea regions in BCVY against BCO and normal tissue.

12 ) concentrations in tumor tissue relative to normal tissue.

13 by analyzing co-expressed genes in tumor vs. normal tissue.

14 atched BMs, primary CRC tumors, and adjacent normal tissue.

15 of water to distinguish between tumorous and normal tissue.

16 in PDAC patient samples compared to adjacent normal tissue.

17 , providing a natural therapeutic index over normal tissue.

18 Radiotherapy (RT) is limited by dose to normal tissue.

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

20 ofiles for distinguishing between cancer and normal tissue.

21 rom clinical lung cancer samples and matched normal tissue.

22 rates significant differences between PN and normal tissue.

23 n prostate tumours compared to corresponding normal tissue.

24 and defining the margins between lesions and normal tissue.

25 es and low or absent expression in essential normal tissues.

26 placental trophoblasts, but not on any other normal tissues.

27 cancer patients, plus 200 primary tumor and normal tissues.

28 se on antigen binding and reduce toxicity to normal tissues.

29 isoforms with varied expression in multiple normal tissues.

30 (iPSC) differentiation and in tumors versus normal tissues.

31 nduction of radiation-associated fibrosis in normal tissues.

32 umors without distant metastasis and matched normal tissues.

33 ion of aberrantly expressed young LINE-1s in normal tissues.

34 ved dose and reducing the possible damage to normal tissues.

35 d in gastric cancer compared to the adjacent normal tissues.

36 es, as compared to non-cancer histologically normal tissues.

37 bolite, WR-1065, by alkaline phosphatases in normal tissues.

38 od was applied to a wide range of tumors and normal tissues.

39 red resistance more difficult, while sparing normal tissues.

40 in tumors and their patient-matched adjacent normal tissues.

41 that macroscopic clones can be found in many normal tissues.

42 ancer drug doxorubicin in both cancerous and normal tissues.

43 elationship between tumors and corresponding normal tissues.

44 ressed in glioblastoma but also expressed in normal tissues.

45 ain inactive during blood circulation and in normal tissues.

46 X-ray irradiation, while minimally affecting normal tissues.

47 ing their non-specific off-target effects on normal tissues.

48 higher levels of Nrf2 and HO-1 compared with normal tissues.

49 of tumors, but has restricted expression in normal tissues.

50 rger absorbed doses in the tumor compared to normal tissues.

51 tumor uptake, and minimal retention in other normal tissues.

52 sed gene in TNBC with low expression in most normal tissues.

53 8 human soft tissue tumors and 60 respective normal tissues.

54 regulated in human NSCLC tissues relative to normal tissues.

55 inhibitor that is ubiquitously expressed in normal tissues.

56 951 tumours, 786 cancer cell lines and 6,119 normal tissues.

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

58 gulated in human CRC tissues versus adjacent normal tissues.

59 xplain much of the differences compared with normal tissues.

60 ferent calcium content in tumor cells versus normal tissues.

61 may play important roles in mIBG uptake into normal tissues.

62 may play important roles in mIBG uptake into normal tissues.

63 in solid tumors but not in the corresponding normal tissues.

64 about APA events in a large number of human normal tissues.

65 most other tumors relative to their pairing normal tissues.

66 or-associated antigens are also expressed in normal tissues.

67 is accompanied by unavoidable irradiation of normal tissues.

68 lin levels were found to be high in adjacent normal tissues.

69 Acquired mutations are pervasive across normal tissues.

70 across many cancers but not in corresponding normal tissues.

71 are ubiquitously expressed in both tumor and normal tissues.

72 hose arising in benign tumors or shared with normal tissues.

73 in in human and mouse pancreatic lesions and normal tissues.

74 r growth without any obvious side effects in normal tissues.

75 expressed miRNA between tumorous and matched normal tissues.

76 tes in tumor tissues as compared to adjacent normal tissues.

77 f) was significantly higher for tumor versus normal tissue (0.47 +/- 0.42 vs. 0.30 +/- 0.22, p = 0.02

78 Normal tissues accumulate genetic changes with age, but

79 ome, studying 1526 tumors and their adjacent normal tissues across seven cancer types, including brea

80 equencing of retrospective tumor and matched normal tissue adjacent to tumor (NAT) samples collected

81 fied epigenetic field defects when comparing normal tissues adjacent to tumors and normal tissues fro

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

83 rom three large datasets consisting of adult normal tissue, adult cancer tissue, and pediatric cancer

84 ll markers, expression was lower in LCIS vs. normal tissue (all P <= 0.05).

85 nce depth was 712-fold for DNA isolated from normal tissue and 368-fold for FFPE tumors.

86 t diagnosis, thus providing samples spanning normal tissue and benign and malignant tumors from each

87 d differential community composition between normal tissue and cancerous tissue, paving the way for i

88 er injection may allow tracer clearance from normal tissue and hence improve image contrast and detec

89 ertoire sequencing on multi-regional tumors, normal tissues and blood samples from 39 ESCC patients.

90 nal antibodies (mAbs) to predict toxicity in normal tissues and efficacy in tumors.

91 f 0.44 and 0.93 were observed in 616 matched normal tissues and in 249 blood samples from children wi

92 an PC tissues as compared to paired adjacent normal tissues and its higher expression in PC patients

93 e of understanding the effects of hypoxia in normal tissues and malignant tumors.

94 ce [(131)I]mIBG accumulation and toxicity in normal tissues and organs.

95 demand of cancer is quite unique compared to normal tissues and this is an emerging hallmark of cance

96 nd to resistance, owing to TAA expression in normal tissues and to TAA expression loss in tumour cell

97 Volumes of interest were drawn on normal tissues and tumor to assess radiation dose, and a

98 oward quantification of target engagement in normal tissues and tumors using (89)Zr-immuno-PET.

99 ere detected in various tumors compared with normal tissues and were associated with poor clinical ou

100 cer tissue and in HEK293T cells derived from normal tissue, and (iv) HSV-1 replication was affected b

101 lecular subtypes of breast cancer, DCIS, and normal tissue, and add to the understanding of their pat

102 placental NOx would be increased in FGR vs. normal tissue, and be further increased in villitis vs.

103 mages to differentiate tongue neoplasia from normal tissue, and then correlate these discriminative p

104 expression was found in tumor versus matched normal tissue, and these findings were validated in larg

105 ertions in GI cancer tissues are absent from normal tissues, and 3) under certain conditions, somatic

106 copy numbers on neoplastic cells, absent on normal tissues, and contributes to the survival of cance

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

108 mall molecules, have minimum accumulation in normal tissues, and induce minimum toxicity.

109 m, 32 patients have primary tumors, adjacent normal tissues, and matched liver metastases.

110 successfully applied to distinguish cancers, normal tissues, and other potential traits with limited

111 Loss of normal tissue architecture is a hallmark of oncogenic tr

112 to examine somatic changes with paired tumor-normal tissue are needed.

113 ased on the skipped exon units in cancer and normal tissues are not available.

114 is study was to assess nonspecific uptake in normal tissues as a first critical step toward quantific

115 on most cancer yet rarely detected in adult normal tissues as reported in previous studies, featurin

116 trolling immune recognition and responses in normal tissues as well as the tumor microenvironment.

117 in the intestine, but not in tumors or other normal tissues, as determined by in vivo mass spectromet

118 tumor uptake and a very low accumulation in normal tissues, as well as a rapid clearance from the ci

119 expressed DEC205, which was not expressed by normal tissue-associated fibroblasts.

120 rs that can identify 21 types of cancers and normal tissues based on bulk RNA-seq as well as scRNA-se

121 he therapeutic index between tumor cells and normal tissues based on MGMT expression, as a means to e

122 okinetic model, which predicts the tumor vs. normal tissue biodistribution of the most studied pHLIP,

123 y somatic mutations shared between tumor and normal tissues but absent from blood cells.

124 n protein that have low uptake in almost all normal tissues but high uptake in most cancer types.

125 eased at tumor margins, which interface with normal tissue, but not in tumor margins at the edge of t

126 tein that is expressed at low levels in most normal tissues, but is overexpressed in various human ca

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

128 the kidney and high accumulation in several normal tissues, but the underlying molecular mechanisms

129 y restricted to the endoplasmic reticulum in normal tissues, but which is expressed on the cell surfa

130 small molecules to reduce acute toxicity to normal tissues by radiation and chemotherapy.

131 iation to target and kill tumour tissue, but normal tissue can also be damaged, leading to toxicity.

132 In normal tissues, CD30 is expressed on some activated B an

133 Here, we report that each of 21 normal tissue cell lines from seven different organs was

134 Recently, non-professional phagocytosis by normal tissue cells has been reported, which prompted us

135 ssional phagocytosis is a general feature of normal tissue cells.

136 Vs in prostate tumors as opposed to adjacent normal tissue cistromes of master transcription regulato

137 onfirmed excellent tumor targeting and rapid normal tissue clearance of the PET imaging analog (86)Y-

138 Results: Excellent tumor targeting and rapid normal-tissue clearance of (86)Y-NM600 were noted in bot

139 in small targets with reduced damage to the normal tissue compared to conventional X-rays.

140 diatric brain tumors by reducing the dose to normal tissue compared with that of photon radiotherapy

141 Normal tissue complication probability (NTCP) models cou

142 Multiple competing normal tissue complication probability (NTCP) models hav

143 der to develop several approximations to the normal tissue complication probability (NTCP): a problem

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

145 unique splice variant of beta4 expressed in normal tissue, contains a cytoplasmic domain of 231 amin

146 ithout normal controls, different sources of normal tissue contaminations.

147 he severity of radiation-induced fibrosis in normal tissue correlates to damaged fat reservoirs in th

148 eceptor positive tumors (ER + 85%) and their normal tissue counterparts (n = 61) were sequenced to ~

149 ormal-like state', having characteristics of normal tissue counterparts.

150 cific gene networks in 39 human tumor and 27 normal tissue datasets.

151 Both normal tissue development and cancer growth are driven b

152 h tightly regulated and pleiotropic roles in normal tissue development and homeostasis.

153 omplex network of blood vessels that promote normal tissue development and physiology.

154 cts of screening (68)Ga-PET/CT and tumor and normal tissue dose were observed, providing a rationale

155 ed to adult and pediatric humans to estimate normal-tissue dosimetry.

156 e the ability to reduce collateral damage on normal tissue due to pan-toxic effects of drugs.

157 Meanwhile, there are no side effects on normal tissues due to the local treatment.

158 cies are increased in cancers versus matched normal tissues, due to widespread allele-specific hypome

159 t and photographic assessments showed higher normal tissue effect risk for 27 Gy versus 40 Gy but not

160 The FAST Trial (CRUKE/04/015) evaluated normal tissue effects (NTE) and disease outcomes after 5

161 s, any moderate or marked clinician-assessed normal tissue effects in the breast or chest wall was re

162 l tumour control, and is as safe in terms of normal tissue effects up to 5 years for patients prescri

163 Normal tissue effects were assessed by clinicians, patie

164 Other normal tissue effects were minimal, with similar or less

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

166 ome-wide methylation features, compared with normal tissues (esophageal, gastric, and duodenum; contr

167 ar spectra of scattering coefficient maps of normal tissues exhibit a spatial feature distinct from t

168 essing high levels of antigen while avoiding normal tissues expressing basal levels of the same antig

169 astric and pancreatic adenocarcinomas, while normal tissue expression is limited to the epithelium of

170 it is possible to target proteins with broad normal tissue expression.

171 014, were included; 44 had sufficient paired normal tissue for analysis.

172 racellular pH differences between cancer and normal tissues for clinical use has been challenging.

173 and was also increased in tumor relative to normal tissue from HPV-positive OPSCC tumor samples.

174 umor samples than in the respective adjacent normal tissue from patients with colon cancer.

175 on (DE) of GPCRs by comparing tumors against normal tissue from the Gene Tissue Expression Project (G

176 paring normal tissues adjacent to tumors and normal tissues from age-matched cancer-free women from t

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

178 epared from tumor patients (tumor and paired normal tissues from surgical resections) or biofilm-posi

179 845 ES events across 33 cancer types and 31 normal tissues from The Cancer Genome Atlas (TCGA) and G

180 alk with specific stromal elements to impair normal tissue function and thereby enable emergent cance

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

182 egrin extracellular region, not required for normal tissue function, can generate a new biophysical c

183 immune cells, which are critical to maintain normal tissue functions.

184 tress by steering progenitor fate to prolong normal tissue growth.

185 HRAS-driven tumorigenesis while maintaining normal tissue growth.

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

187 High glucose uptake by cancer compared to normal tissues has long been utilized in fluorodeoxygluc

188 as early as the 1950s, somatic mutations in normal tissue have been difficult to study because of th

189 hole-genome sequencing efforts of tumors and normal tissues have identified numerous genetic mutation

190 erable on-target toxicities in more prolific normal tissues have led to repeated failures in the clin

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

192 nriched in tumors with minimal expression in normal tissues holds the potential to develop tumor-spec

193 s a multifaceted factor contributing to both normal tissue homeostasis and disease development.

194 ced Tctp levels failed to proliferate during normal tissue homeostasis and regeneration.

195 ue microenvironment plays a critical role in normal tissue homeostasis and tumor development.

196 xtracellular ligands have essential roles in normal tissue homeostasis by coordinately regulating cel

197 of primary hepatocytes in vitro, as well as normal tissue homeostasis in mice.

198 mmation for tissue repair and restoration of normal tissue homeostasis once an infection is controlle

199 and cross-talk between autophagy and Lkb1 in normal tissue homeostasis, we generated genetically engi

200 flexibility of the intestine in maintaining normal tissue homeostasis.

201 y accurate targeting of tumor and sparing of normal tissue; however, in the pelvic region it is anato

202 es and 640 normal samples from 21 tumors and normal tissues in TCGA based on the 300 most significant

203 Gene expression data of breast tumors and normal tissues in the TCGA database were analyzed with o

204 DeltaN146 is undetectable in normal tissues in vivo Targeted HSV-1 editing results in

205 L-17RA expression in tumors than in adjacent normal tissues; in pancreatic adenocarcinoma, increased

206 ly increased in specimens of EOC compared to normal tissues, including in the serous subtype (p < 0.0

207 or, and osteosarcoma, in addition to several normal tissues, including kidney podocytes and lymphatic

208 Uptake in normal tissues, including the blood, spleen, liver, hear

209 present at an age of 3 and 12 months despite normal tissue integrity.

210 c changes-which may occur in morphologically normal tissue-is comparatively limited, as for most canc

211 P is virtually absent in the interstitium of normal tissues, it can be present in the hundreds of mic

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

213 ple tumor types and restricted expression in normal tissues make B7-H3 an attractive target for immun

214 to maintain an appropriate cell density for normal tissue morphogenesis and homeostasis.

215 (n = 5) compared to N0 cancers (n = 10) and normal tissue (n = 5).

216 n of Rig-G between lung cancer (n = 138) and normal tissues (n = 23), from public-available data sets

217 alysis of patient colon tumors (n = 197) and normal tissues (n = 39) revealed sex-specific metabolic

218 For the normal tissue of 16 organs, a 2-cm spheric volume of int

219 lls, similar to findings in genomic DNA from normal tissues of GI tumor patients.

220 types are more densely innervated than their normal tissues of origin.

221 advanced primary prostate tumors compared to normal tissue or tumors with low Gleason scores.

222 ta, the reference samples may represent e.g. normal tissue or tumour samples with a particular genoty

223 were found hypermethylated in CRC but not in normal tissues or effluents from fecal donors.

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

225 tumor tissues when compared to the adjacent normal tissues (p < 0.01).

226 Tumor-normal tissue paired analysis revealed genotype concorda

227 For normal tissues, parotid gland factors were 6.7, 9.4, 13.

228 For normal tissues, parotid gland factors were 6.7, 9.4, 13.

229 utational landscapes differ markedly between normal tissues-perhaps shaped by differences in their st

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

231 tivities might provide us with insights into normal tissue physiology, development of disease, and ne

232 cells in solid tumors are expressed in some normal tissues, raising concern for off-tumor toxicity.

233 expressed in haematopoietic cells and other normal tissues, raising safety challenges to the develop

234 The high tumour-to-normal tissue ratio offered by TMRET in combination with

235 1- to 3-h imaging window, the mean tumor-to-normal-tissue ratio remained high in all key organs: liv

236 Tumor-to-normal-tissue ratios and tumor distribution volume ratio

237 Normal-tissue ratios as represented by tumor-to-liver, t

238 mal-organ or -tissue SUV(mean), and tumor-to-normal-tissue ratios calculated from SUV(max) and SUV(me

239 ete response in 86% of tumors, with tumor-to-normal-tissue ratios that predict an improved therapeuti

240 Developmental processes underlying normal tissue regeneration have been implicated in cance

241 ugh angiogenesis is critically important for normal tissue regeneration, it is also a hallmark of pat

242 d N-glycans among the tumor region, adjacent normal tissue region, and tumor proximal collagen stroma

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

244 cesses that underpin mutational selection in normal tissues remain poorly understood.

245 een early inflammation that is essential for normal tissue repair and the pathologic inflammation tha

246 ollowing executioner caspase activation is a normal tissue repair mechanism usurped to promote oncoge

247 Macrophage plasticity is critical for normal tissue repair to ensure transition from the infla

248 ts at sites of tissue injury is critical for normal tissue repair.

249 e homology, and fusions occurring in healthy normal tissue require informed filtering, making it diff

250 ssed with M2/M2-like molecules in subsets of normal tissue-resident macrophages, infiltrating macroph

251 exaggerated T-cell response directed against normal tissue, resulting in the generation of high level

252 gen analysis, and mechanical measurements in normal tissue revealed that stroma in the high-density b

253 sequencing data from ~6700 samples across 29 normal tissues revealed multiple somatic variants, demon

254 ) have enabled the detection of mutations in normal tissue, revealing an unanticipated high level of

255 nd visceral organs as well as representative normal tissues (salivary glands and spleen) were segment

256 d visceral organs, as well as representative normal tissues (salivary glands and spleen), were segmen

257 e (repairome) genes in 63 tumors and matched normal tissue samples in African Americans and Caucasian

258 nations that differentiate between tumor and normal tissue samples with 91% sensitivity (95% Confiden

259 gastric cancer tissue samples compared with normal tissue samples.

260 dataset including 26 tumour and 26 adjacent normal tissue samples.

261 cing was performed on 62 HGT1 and 15 matched normal tissue samples.

262 model of colon cancer and achieved tumor-to-normal tissue signal ratios of ~40.

263 The remarkable normal tissue sparing afforded by FLASH may someday prov

264 pered by its biodistribution and toxicity to normal tissues, specifically gastrointestinal (GI) tissu

265 As humans age, normal tissues, such as the esophageal epithelium, becom

266 ression was not higher in LCIS compared with normal tissue, suggesting collagenase MMP expression doe

267 ll interactions that mediate size control in normal tissues, than to any cell-autonomous, 'oncogene-i

268 By contrast, tumours that arise from normal tissues that do not express NAPRT highly are enti

269 Because of low background activity in normal tissue, there was a high tumor-to-background rati

270 In LCIS and normal tissue, there was a strong correlation between MM

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

272 ours and inflammatory diseases compared with normal tissues, thus contributing to the establishment o

273 esenting a range of prostate phenotypes from normal tissue to drug-resistant metastases.

274 n cancer chemotherapy; however, responses of normal tissues to these agents have not been widely inve

275 ghts for evaluating the pharmacokinetics and normal -tissue toxicity and in determining dosing rate o

276 However, this approach risks enhancing normal tissue toxicity as much as tumor toxicity, thereb

277 nd validation including the incorporation of normal tissue toxicity is necessary to properly balance

278 However, normal tissue toxicity limits the radiation dose and the

279 tration, less energy dissipation and minimal normal-tissue toxicity over traditional first NIR PTT (7

280 No effects were observed in the normal tissue traversed by the particle beam, suggesting

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

282 the mouse epidermis taken over 1 week during normal tissue turnover [13].

283 D synthesis, NAPRT, is highly expressed in a normal tissue type, cancers that arise from that tissue

284 a from 17 studies on the ECM of 15 different normal tissue types, six cancer types (different grades

285 mpsia secreted significantly more STC-1 than normal tissue under the same conditions.

286 ed a clear differentiation between tumor and normal tissue up to a microscopic level, with a tumor-to

287 sues can only be distinguished from adjacent normal tissues using quantitative results of both lipid

288 If available, normal tissue was also exome sequenced.

289 talytically inactive LF mutant) in tumor and normal tissues was measured using SPECT/CT imaging in vi

290 g pipelines applied to 6,690 human tumor and normal tissues, we show that nearly 88% of protein-codin

291 In total, 142 pathologic lesions along with normal tissues were analyzed.

292 Finally, normal tissues were found to harbor mutations in known c

293 highest absorbed dose estimates (mGy/MBq) in normal tissues were to the right colon (0.167 +/- 0.04)

294 ond) referred to as FLASH tends to spare the normal tissues while retaining the therapeutic effect on

295 inferred differential GRNs in cancer versus normal tissues, whose genes with largest network degrees

296 TNC, and THBS2) that distinguish tumors from normal tissues with 90% sensitivity/94% specificity.

297 ucose availability to tumours while fuelling normal tissues with ketone bodies.

298 splicing of SLC2 mRNA isomers in tumors and normal tissues, with a focus on breast tumors and cell l

299 ular level, and their reduced penetration in normal tissue would be expected to lower off-target toxi

300 reating NRAS mutant cancers, particularly as normal tissues would retain K-Ras4b function for physiol