ライフサイエンスコーパス: cancerous

1 remalignant cells that can eventually become cancerous.

2 ofiles of 94 fresh breast tissue samples (84 cancerous/10 non-tumor adjacent samples) were analyzed u

3 apoptosis in contrast to radiosensitive non-cancerous A-T cells.

4 lead compound of this series, displayed anti-cancerous activity on all melanoma cells tested, includi

5 Non-cancerous acute neurological insults also induced signif

6 strategy that targets miR-199a to interrupt cancerous aerobic glycolysis.

7 Etoposide, which is largely used as an anti-cancerous agent against testicular, ovarian, small cell

8 assay to 70 clinical plasma samples (42 non-cancerous and 28 ovarian cancer patient samples) enabled

9 of TP73 expression was also performed in non-cancerous and adjacent cancerous liver tissues of HCC pa

10 ons ranged from 0.0 to 95.6 ng/mL across non-cancerous and cancer plasma specimens.

11 a HCC/hepatocyte co-culture model, in which cancerous and healthy cells share the same micro-environ

12 ence in functional K(Ca)3.1 activity between cancerous and healthy cervical epithelial cells, which c

13 enges stemming from the similarities between cancerous and healthy tissue.

14 from a wide variety of cell types, including cancerous and infected cells and those from tissues, wit

15 nd vaginal environment), tissue level (e.g., cancerous and inflamed tissues), and cellular level (e.g

16 into purine nucleotides in freshly resected cancerous and matched noncancerous lung tissues from non

17 stone modification data-sets from variety of cancerous and non-cancerous cell-lines.

18 Further assay was performed to differentiate cancerous and non-cancerous cells by measuring lipid and

19 get miRNA in total RNA (RNAt) extracted from cancerous and non-cancerous cells.

20 Higher displacement contrast between cancerous and non-cancerous tissue was found ex vivo, po

21 e literature as varying in abundance between cancerous and noncancerous areas in various human tissue

22 for an instantaneous differentiation between cancerous and noncancerous breast tissues utilizing meta

23 ential methylation and accessibility between cancerous and noncancerous cells.

24 induced PD-L1 expression in human and murine cancerous and noncancerous cells.

25 n abundances of selected metabolites between cancerous and noncancerous regions of the kidney tissue.

26 Four tissue samples containing both cancerous and noncancerous regions, obtained from three

27 d fatty acids (PUFAs) was identified in both cancerous and normal appearing breast tissue obtained fr

28 racellular and intracellular environments of cancerous and normal cells and the particular characteri

29 etabolic labelling process can occur in both cancerous and normal cells, cancer-selective labelling n

30 ometry imaging (DESI-MSI) on 54 banked human cancerous and normal prostate tissue specimens to invest

31 -prone owing to the limited contrast between cancerous and normal skin.

32 The genome-wide transcriptome profiling of cancerous and normal tissue samples can provide insights

33 n of the anticancer drug doxorubicin in both cancerous and normal tissues.

34 dance to assist a surgeon in differentiating cancerous and normal tissues.

35 plasmic viral assembly center (cVAC) in both cancerous and primary neuronal cells that concentrates v

36 Cancerous and the paired non-cancerous lung tissue miRNA

37 nces were differentially methylated in MCF7 (cancerous) and MCF10A (non-cancerous) cell lines.

38 ll types and discrimination between healthy, cancerous, and metastatic cells, with the same genetic b

39 capable of effectively identifying healthy, cancerous, and metastatic human breast cells.

40 to understand how curcumin induces its anti-cancerous, anti-inflammatory, and anti-microbial effects

41 o randomly selected cells, whether normal or cancerous, are therefore genetically different.

42 d to inflammatory cells in the stroma, while cancerous areas were dominated by nonessential fatty aci

43 s (HCT116 p53(+/+) ) with respect to the non-cancerous ARPE-19 cell line.

44 collecting a total of 164 Raman spectra from cancerous, benign, and transitional regions of resected

45 genomic data, albeit initially from only two cancerous brain cell lines for a limited number of epige

46 rmalization of NO levels in precancerous and cancerous breast cells downmodulates TGFbeta and ERBB2 a

47 enefiting from these cytosensors to identify cancerous breast cells.

48 method that allows propagation of normal and cancerous breast epithelial cells of luminal origin, flo

49 er in the more rigid environments similar to cancerous breast tissue (E = 4-12 kPa) as compared to he

50 and ranged between 1.0E05-1.2E06 W/m(3) for cancerous breast tissue.

51 by induction of cellular superoxide anion in cancerous but not normal cells.

52 n protein host complex resulted in increased cancerous cell death while noncancerous control cells we

53 iferation-tRNAs' are induced upon normal and cancerous cell division, while the 'differentiation-tRNA

54 molecular pathways by which oncogenes drive cancerous cell growth, and how dependence on such pathwa

55 Late diagnosis of a cancerous cell in patients is the major hurdle for the a

56 ct the viscoelastic properties of benign and cancerous cell lines (NIH 3T3 fibroblasts, NMuMG epithel

57 Furthermore, cell viability in a cancerous cell lines was evaluated by MTT assay in the p

58 toxicity (IC(50) = 0.07-0.7 muM in different cancerous cell lines), complex 1 was taken up by HeLa ce

59 mmadelta T cell immunotherapy, in a range of cancerous cell lines, using L-ZOL as a comparator.

60 isplays highest phototoxicity toward several cancerous cell lines.

61 for imaging intracellular Cys in normal and cancerous cell lines.

62 The ability to selectively kill cancerous cell populations while leaving healthy cells u

63 The ability to selectively kill cancerous cell populations while leaving healthy cells u

64 the complexity of a tumor biopsy, estimating cancerous cell purity, tumor ploidy, allele-specific cop

65 dels trained on matched -omics data from non-cancerous cell-lines are able to predict cancerous expre

66 data-sets from variety of cancerous and non-cancerous cell-lines.

67 proach allows efficient analysis of aged and cancerous cell-specific DNA methylation patterns for dia

68 thylated in MCF7 (cancerous) and MCF10A (non-cancerous) cell lines.

69 Because it is expressed in normal and cancerous cells alike, attempts at targeting ABCB1 direc

70 Interactions between cancer cells/non-cancerous cells and cells/non-cell components in the TME

71 this basis, probe 1 can be used to identify cancerous cells and tissues characterized by elevated NQ

72 strated that chimeric RNAs also exist in non-cancerous cells and tissues, although large-scale, genom

73 ogenicity and natural capabilities to target cancerous cells and to escape from the recognition and e

74 TM had limited effects on non-cancerous cells and tumor-free mice, suggesting that can

75 M1 macrophages target cancerous cells and, therefore, can be used as drug carr

76 d with powerful immune surveillance to clear cancerous cells as they emerge.

77 delivery, and photothermal therapy (PTT) of cancerous cells based on their physicochemical propertie

78 performed to differentiate cancerous and non-cancerous cells by measuring lipid and protein peak inte

79 al for the elimination of virus-infected and cancerous cells by NK cells.

80 Changes in the lipid metabolism of cancerous cells can provide important indications as to

81 ss the cellular and molecular changes in non-cancerous cells during ageing, and how these may contrib

82 Cancerous cells have an acutely increased demand for ene

83 s that the minimal dose required to kill all cancerous cells in a lung tumor can be reduced by roughl

84 A brain tumor is an uncontrolled growth of cancerous cells in the brain.

85 e report that in hypoxia, ASS1 expression in cancerous cells is downregulated further by HIF1alpha-me

86 otropy was found in cells without actin cap: cancerous cells MDA-MB-231, which naturally lack the act

87 well as the potential adverse effects on non-cancerous cells must be clarified.

88 Compared to healthy cells, cancerous cells often increase exposure of the negativel

89 ed on their lineage and in comparison to non-cancerous cells originating from the same tissue type.

90 the uptake of peptide-targeted liposomes by cancerous cells overexpressing VLA-4 to 15-fold over tha

91 itochondrial nucleic acid homeostasis in non-cancerous cells remain unclear.

92 echanisms that restrict viral replication in cancerous cells represent viral vulnerabilities that can

93 The hallmark of tumours is the ability of cancerous cells to promote vascular growth, to dissemina

94 oncogenic transformation by eliminating pre-cancerous cells with disrupted cell cycle checkpoints(1)

95 that protects against infection, eliminates cancerous cells, and regulates tissue repair, thus servi

96 tes the eradication of pathogen-infected and cancerous cells, as well as the production of antibodies

97 Chemokines promote/abrogate proliferation of cancerous cells, block/aid apoptosis, and are instrument

98 phocytes that eliminate virally infected and cancerous cells, but the mechanisms that control NK cell

99 urg effect has been characterized in certain cancerous cells, embryonic stem cells, and other rapidly

100 ch is expressed in healthy proliferating and cancerous cells, is a serine/threonine protein kinase, w

101 A major concern in the area is the spread of cancerous cells, technically refered to as metastasis in

102 riginates mainly in apoptotic, senescent and cancerous cells, this approach allows efficient analysis

103 ch vesicle type can originate from normal or cancerous cells, transfer molecular cargo to both neighb

104 Contrary to non-cancerous cells, where BRCA2 deletion causes cell cycle

105 HCMV cannot replicate in most cancerous cells, yet the causes of this restriction are

106 RNA-based cell classifier for discriminating cancerous cells.

107 moeostasis by eliminating virus-infected and cancerous cells.

108 of what triggers and maintains the growth of cancerous cells.

109 quired for removal of infected, damaged, and cancerous cells.

110 hly expressed in the mitochondria of various cancerous cells.

111 the three acids to produce glutamic acid in cancerous cells.

112 RNA (RNAt) extracted from cancerous and non-cancerous cells.

113 meter in the membranes of virus-infected and cancerous cells.

114 rtic acid and proline are nitrogen donors in cancerous cells.

115 ancer cells and have minimal activity on non-cancerous cells.

116 in adaptive immunity by killing infected or cancerous cells.

117 e capable of killing virally infected and/or cancerous cells.

118 toxic T lymphocytes (CTLs) kill infected and cancerous cells.

119 tional relevance of two chimeric RNAs in non-cancerous cells.

120 ive T cells to eliminate virally infected or cancerous cells; however, they are plagued by low stabil

121 ome of the proteins with implications in the cancerous cellular states were showing the structural or

122 In contrast to the results from cancerous cervical cells, K(Ca)3.1-dependent H33258 upta

123 e DNA damage biomarker 8-oxodG in normal non-cancerous cervical tissues and cells obtained from women

124 e data at sub-cellular level for healthy and cancerous colon tissue, where the cells have different c

125 We propose a model of the healthy and cancerous colonic crypt microenvironment.

126 ed a cellular-level model of the healthy and cancerous colonic crypt microenvironments.

127 specific for EGFR to the cell surface of pre-cancerous colonocytes within the epithelium of dysplasti

128 Though the presence of hypoxia under cancerous condition has been associated with the overexp

129 need to be further tailored and improved for cancerous data, which often features quite diverse expre

130 ication and treatment response assessment of cancerous disease.

131 ber of fatal death caused by the world's top cancerous disease.

132 pathways become aberrant, and autoimmune or cancerous diseases ensue.

133 rug, on gene-disease data from 22 common non-cancerous diseases in OpenTargets.

134 of cells with abnormal karyotypes to become cancerous, do pathways that limit the prevalence of such

135 identify novel proteins that are involved in cancerous EGFR signaling.

136 To date, applications of non-cancerous enhanced permeation have been relatively unexp

137 ssification of some low-grade lesions as non-cancerous entities.

138 tency into lytic replication in a variety of cancerous epithelial cell types as well as in some, but

139 h suppression in cancer cells but not in non-cancerous epithelial cells.

140 l cells is driven by ligands produced by the cancerous epithelial.

141 ession model to estimate the distribution of cancerous epithelium within slides.

142 There is a growing need for cancerous exosome detection towards potential non-invasi

143 efficient quantification approach to detect cancerous exosomes and offers an avenue toward future di

144 Sensitive detection of cancerous exosomes is critical to early diseases diagnos

145 non-cancerous cell-lines are able to predict cancerous expression with equivalent genome-wide fidelit

146 y, YAP was overexpressed in inflammatory and cancerous fallopian tube tissues.

147 sity to be multifocal with several different cancerous foci per gland.

148 To discriminate cancerous from non-cancerous nodules at the time of diag

149 at which features are able to best separate cancerous from non-cancerous regions on both radiologic

150 sed in the tumor samples relative to the non-cancerous gastric tissues (FC = 2.441; P = 0.0002).

151 se imaging, in the stromal layer adjacent to cancerous glands, is predictive of recurrence.

152 powerful and effective strategy for inducing cancerous growth arrest through the direct epigenetic re

153 R2 in the absence of EGF both for normal and cancerous growth.

154 calculated in order to determine risk of non-cancerous health effects for adults consuming tea on a d

155 HQ greater than 1, indicating no risk of non-cancerous health effects.

156 not find evidence of expression in normal or cancerous human breast.

157 ficient mice engrafted with either normal or cancerous human cells are widely used in basic and trans

158 rized rat intestines and arborize healthy or cancerous human colon organoids.

159 e found both DN T cell subsets in normal and cancerous human kidneys, indicating possible clinical re

160 ed to studying FA changes between normal and cancerous human prostate cells.

161 not only host defense immunity, but also pro-cancerous immune cells and immune cell cytolytic activit

162 to increased expression of periostin in non-cancerous inflammatory conditions.

163 complexes are modulated by proteins such as cancerous inhibitor of protein phosphatase 2A (CIP2A), p

164 curs during tissue formation, wound healing, cancerous invasion, and viral infection.

165 oprotein transporter while being retained in cancerous kidney tissues with low P-glycoprotein express

166 used to image, alleviate, and ablate harmful cancerous legions with good specificity versus healthy t

167 ccuracy of needle deployment to the targeted cancerous lesion site.

168 l conditions, long before the formation of a cancerous lesion.

169 d biopsy detected 14 previously undiscovered cancerous lesions (clinically significant cancers [CSCs]

170 rapid in vivo detection and localization of cancerous lesions (generally exhibiting a higher water c

171 SERRS nanoparticles such that delineation of cancerous lesions can be achieved in vivo and ex vivo on

172 that usually eliminates defective cells, pre-cancerous lesions signal the death of surrounding tissue

173 ng has enabled early-stage identification of cancerous lesions that require needle biopsy for minimal

174 ersally accelerated in cancer, including pre-cancerous lesions, and that it is also accelerated in no

175 onists are effective at treating superficial cancerous lesions, but their use internally for other ty

176 enting replication stress, a hallmark of pre-cancerous lesions.

177 tive detection rates in a mouse model of non-cancerous lipopolysaccharide-induced inflammation.

178 also performed in non-cancerous and adjacent cancerous liver tissues of HCC patients.

179 the 12 patients in group A had no NSN in the cancerous lobe whereas the remaining six patients had a

180 iew, 21 of the 48 patients had no NSN in the cancerous lobe, which left 27 patients whose CT scans we

181 Cancerous and the paired non-cancerous lung tissue miRNAs display different pattern o

182 harness amino acid auxotrophy so as to block cancerous lymphocyte growth have been attempted for deca

183 he markedly atypical glycomic profile of the cancerous mammalian cell membrane and successfully made

184 However, the pro-cancerous mechanisms finally took the ascendency by boos

185 r-cellular network obtained from normal, non-cancerous molecular interactions such as signal transduc

186 ribed an elevated level of mutant p53 in non-cancerous mouse tissues.

187 tional impact on fields such as genetics and cancerous mutation detection Here we report an ultrasens

188 of the formation of tumors as a fixation of cancerous mutations in tissues.

189 tructures of rat brain, and in human ovarian cancerous, necrotic, and normal tissues was achieved.

190 To discriminate cancerous from non-cancerous nodules at the time of diagnosis, a combinatio

191 es between nonmalignant cancer cells and the cancerous ones for both of preprocessing approaches.

192 tional human-derived nonneuronal cell lines (cancerous or immortalized) and found significant subpopu

193 e-specific signaling analysis of healthy and cancerous organoids.

194 esent in 197 samples from 18 sample types of cancerous origin.

195 ersion to a more stem-like state upstream of cancerous osteoblastic cells.

196 ors must subvert these mechanisms to achieve cancerous overgrowth [3-7].

197 ack into feed-forward activation that drives cancerous overgrowth.

198 n: 20.6 ng/ml for cancer; 5.94 ng/ml for non-cancerous) (p value < 0.001).

199 eatic cancer cells, but not by adjacent, non-cancerous pancreatic tissue.

200 images have discriminated between normal and cancerous Pap smears with 100% accuracy.

201 ound to have greatly elevated intensities in cancerous part of analyzed tissue specimen.

202 hanced vascular permeability in multiple non-cancerous pathological tissues.

203 er cells, multicellular tumor spheroids, and cancerous patient tissues.

204 gher hepcidin concentrations compared to non-cancerous patients (mean: 20.6 ng/ml for cancer; 5.94 ng

205 t is unknown how the ERG oncogene promotes a cancerous phenotype and maintains downstream androgen re

206 , alters tissue mechanics, and drives a more cancerous phenotype.

207 At the molecular level, cancerous phenotypes are the outcome of cellular functio

208 potential inhibitor of citrin that restricts cancerous phenotypes in cells.

209 ngage a core survival pathway to support its cancerous phenotypes, and reveal new facets of MTA1-SGK1

210 ower (~12% additive variance) for predicting cancerous phenotypes, beyond PCAWG-identified driver mut

211 an cancer cell line (MCF7) and in mouse, non-cancerous, primary cells (mouse embryonic fibroblasts, M

212 clinically useful biosensor would detect the cancerous probability of any suspicious breast mass with

213 colytic enzyme and appears on the surface of cancerous proliferating cells, has been used as a diagno

214 or the first time have demonstrated the anti-cancerous properties of ormeloxifene in cervical cancer.

215 emonstrate the discrimination of healthy and cancerous prostate cell lines based on the whole-cell, t

216 at consensus ETS sites both in normal and in cancerous prostate cells.

217 were found at elevated levels or uniquely in cancerous prostate tissue.

218 otype resembling stromal cells isolated from cancerous prostate tissue; supporting angiogenesis in vi

219 Both normal and cancerous prostate tissues were sliced and cultured in t

220 reast epithelial cell line (MCF10A) from its cancerous PTEN mutants (MCF10 PTEN-/-).

221 The overall intensity of scattering from cancerous regions is a degree of magnitude greater in ca

222 are able to best separate cancerous from non-cancerous regions on both radiologic and digital patholo

223 automatically pre-screening and highlighting cancerous regions prior to review.

224 taT cells, were significantly lower, and pro-cancerous regulatory T cells were significantly higher i

225 maging, can differentiate between normal and cancerous renal tissue.

226 n uptake of the Glc-Pts were observed in non-cancerous RWPE2 cells.

227 oscopy (EIS) of the secretomes to detect the cancerous samples due to the lipidic content of their se

228 y higher in HCC samples than in adjacent non-cancerous samples.

229 g the extracellular matrix and promoting pro-cancerous signaling pathways by activating growth factor

230 rturbation in the presence of drugs, and (3) cancerous single-cells transitioning from a blebbing to

231 Recent research shows that potentially cancerous, somatic mutations can reside in normal cells.

232 RelB mRNA levels were strongly increased in cancerous specimens compared to tumor-adjacent non-neopl

233 ovel method is useful for distinguishing non-cancerous specimens from those in need of careful examin

234 g electron microscopy (FE-SEM) of benign and cancerous specimens showed marked differences in the tis

235 nfected and early-stage (1 and 2 months) and cancerous-stage (3 and 6 months) tissues.

236 man papillomavirus infection and related pre-cancerous stages in Kenya were carried out.

237 monstrated robust EGFR activation in the pre-cancerous stages of colitis and dysplasia.

238 sely model the transition between normal and cancerous states in chronic myeloid leukemia (CML).

239 oned pharmaceutical treatment as observed in cancerous stromal fibroblasts.

240 ctivity based on passive accumulation in non-cancerous target tissues, their challenges, and prospect

241 tumors (3.6 +/- 1.5 um) and the adjacent non-cancerous tissue (6.4 +/- 2.5 um), which allowed to diff

242 ly acidic pH values that separate normal and cancerous tissue (pH < 7).

243 lass classification of images into normal or cancerous tissue and a three-class classification into n

244 ppressor cells (MDSCs), populate inflamed or cancerous tissue and block immune cell effector function

245 couraged us to exploit the more acidic pH of cancerous tissue and design pH-controllable singlet oxyg

246 TRFS enables identification of cancerous tissue by its distinct autofluorescence signat

247 r matrix gels, which better mimic normal and cancerous tissue development than cells maintained on co

248 during operations to precisely separate out cancerous tissue due to augmented fluorescence brightnes

249 me to visualize picosecond laser ablation of cancerous tissue in a clinically relevant model.

250 0-1), and minimum microscopic margins of non-cancerous tissue of 2 mm or more, were recruited.

251 omarkers due to their specific expression in cancerous tissue only.

252 placement contrast between cancerous and non-cancerous tissue was found ex vivo, potentially due to t

253 ed structural differences between normal and cancerous tissue within the resection bed following WLE

254 y utilize hyperthermia and ablation to treat cancerous tissue, but for drug delivery applications the

255 munity composition between normal tissue and cancerous tissue, paving the way for investigations focu

256 In the case of cancerous tissue, stromal cell-derived differentiation s

257 cues and palpation to delineate healthy from cancerous tissue.

258 ology, perceived to operate only on prolific cancerous tissue.

259 anisms by which MDSCs disseminate/infiltrate cancerous tissue.

260 proliferation and DNA repair from normal to cancerous tissue; (2) a transitory increase of metabolis

261 the tumor samples in comparison with the non-cancerous tissues (median fold change (FC) = 0.3143; P =

262 croarray sections containing both normal and cancerous tissues and by evaluating findings deposited i

263 l tract, displays differential expression in cancerous tissues and is considered a potential drug tar

264 hance the classification of noncancerous vs. cancerous tissues and the prediction of cancer patient s

265 However, this mechanism also protects cancerous tissues by inhibiting antitumor immune cells i

266 n 24 paired GC tissues and corresponding non-cancerous tissues by quantitative Real-Time PCR.

267 ore tissue resection and determined that the cancerous tissues in these patients had enhanced PC acti

268 However, its application to studying cancerous tissues is currently hampered by the lack of c

269 The microenvironment in cancerous tissues is immunosuppressive and pro-tumorigen

270 sels and enhances their passive targeting to cancerous tissues through an enhanced permeability and r

271 at the integration of molecular profiling of cancerous tissues with deep, longitudinal profiling of t

272 transport of anticancer drugs in normal and cancerous tissues with engineered nanoparticles is key t

273 tein adsorption, escape liver uptake, target cancerous tissues, and report kidney dysfunction at earl

274 ng cancer tissues compared with adjacent non-cancerous tissues, and the levels of miR-218 were signif

275 udied Ub phosphoform exclusively observed in cancerous tissues, and ZAP70-pY248, a kinase phosphoform

276 f cancer cells, or specifically delivered to cancerous tissues.

277 of the distinct molecular characteristics of cancerous tissues.

278 ach sample contained a mixture of normal and cancerous tissues.

279 ells to migrate to sites of inflammation and cancerous tissues.

280 pancreatic cancer tissues compared with non-cancerous tissues.

281 pholipid (GP) species between the normal and cancerous tissues.

282 omatic L1 insertions in paired normal and GI cancerous tissues.

283 x protein spatial distribution in normal and cancerous tissues.

284 biomarker profiles often seen in inflamed or cancerous tissues.

285 Mechanistic insights into cancerous transformation and especially metastatic progr

286 e of nanoparticle size in ROS generation for cancerous tumor growth control was elucidated, and an op

287 ticles in situ was recently shown to control cancerous tumor growth.

288 Alport syndrome, Goodpasture's disease, and cancerous tumor growth.

289 blasts have been observed in the vicinity of cancerous tumors and can be recapitulated with in vitro

290 pi 1 (GSTP1) is frequently overexpressed in cancerous tumors and is a putative target of the plant c

291 can help scientists to better understand how cancerous tumors grow and spread in the body.

292 echanisms valid to all scales, from cells in cancerous tumors to animals in large communities.

293 protein (1% hypoxia or ischemic diseases and cancerous tumors), and where both cap-binding proteins a

294 e molecular composition of ex vivo slices of cancerous tumors, little is known about how variations i

295 erization of the state and aggressiveness of cancerous tumors.

296 at hypoxia is a characteristic of most solid cancerous tumours, treating hypoxic tumours using PDT ca

297 ed to automatically differentiate normal and cancerous urothelial cells with 100% accuracy.

298 d in cancer, new technologies to interrogate cancerous UTRs, and potential therapeutic opportunities

299 pre-specified classes, such as normal versus cancerous, we develop a deep-neural-network based SI cla

300 Thus, disruption of CDCP1 perturbs pro-cancerous Wnt signaling including nuclear localization o