ライフサイエンスコーパス: cancerous

1 n cervical epithelial cells (both normal and cancerous).

2 he vulva that, if left untreated, can become cancerous.

3 rn can predispose cellular tissues to become cancerous.

4 remalignant cells that can eventually become cancerous.

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

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

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

8 Cancerous and aging cells have long been thought to be i

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

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

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

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

13 levels of endogenous, activated p53 in both cancerous and non-cancerous cells, which led to signific

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

15 related derivatives, which were screened in cancerous and noncancerous cell lines.

16 alyzing cell subsets to discriminate between cancerous and noncancerous cells.

17 his approach has been expanded to study both cancerous and noncancerous prostate cells.

18 PER3, CRY1, CRY2, CKI, CLOCK, and BMAL1) of cancerous and noncancerous tissues from 29 GC patients w

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

20 indings prove the feasibility of classifying cancerous and normal breast tissues using ambient ioniza

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

22 enotypical differences were observed between cancerous and normal cells in both their untreated state

23 tric imaging (DESI-MSI), for 62 banked human cancerous and normal gastric-tissue samples.

24 ading-induced electrical differences between cancerous and normal lung cells in an integral fashion.

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

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

27 arge amounts of multi-tag bioimage data from cancerous and normal tissue specimens to begin to infer

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

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

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

31 extent of gene expression in cancerous, non-cancerous, and stem cells, up to 1500-fold higher than t

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

33 aks with intensities significantly larger in cancerous bladder cells compared to nonmalignant cell ca

34 mass cytometry with viSNE to map healthy and cancerous bone marrow samples.

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

36 Preoperative MRI for staging the cancerous breast does not reduce the risk of LR or DR.

37 re than 600 kb away) promoters in normal and cancerous breast epithelial cells.

38 tle effect on the survival and growth of non-cancerous breast epithelial cells.

39 t MCF-7 breast cancer cell lines and one non-cancerous breast line MCF-10A.

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

41 r stage and nodal stage in paired normal and cancerous breast tissue samples from 93 patients using r

42 of some of the compounds considered to treat cancerous breast tissue.

43 e ability to discriminate between benign and cancerous breast tissues, further investigation is neces

44 redict drug targets that selectively inhibit cancerous but not normal cell proliferation.

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

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

47 capable of inducing a KC phenotype even in a cancerous cell line, highlighting their importance for e

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

49 c activities in the micromolar range on many cancerous cell lines and do not cross-react with cisplat

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

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

52 isplays highest phototoxicity toward several cancerous cell lines.

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

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

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

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

57 jugates were 6-10 times selective for breast cancerous cells (MCF-7 and MDA-MB-435) over noncancerous

58 sections showed the selective destruction of cancerous cells and high numbers of tumour-infiltrating

59 DNA methylation is frequently altered in cancerous cells and likely results in transcriptional si

60 oits live viruses with selective tropism for cancerous cells and tissues to treat cancer.

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

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

63 xic lymphocytes eliminate virus-infected and cancerous cells by immune recognition and killing throug

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

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

66 tein polymers made possible the isolation of cancerous cells expressing lower levels of tumor antigen

67 selectively recognize and kill contaminating cancerous cells from autologous bone marrow transplants

68 processes involved in mitosis of healthy and cancerous cells from its molecular perspectives.

69 This attribute of cancerous cells has been targeted herein for the control

70 Cancerous cells have an acutely increased demand for ene

71 the mechanisms of PKCzeta down-regulation in cancerous cells have not been previously described.

72 38 may reprogram these cancer cells into non-cancerous cells in a FOXO3-dependent manner, and may all

73 he D3 platform to screen for precancerous or cancerous cells in cervical specimens and to detect huma

74 applied to sense the pH gradient induced by cancerous cells in stagnant fluids inside human body and

75 e of the main differences between normal and cancerous cells is the low extracellular pHe and the rev

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

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

78 The tumour microenvironment is the non-cancerous cells present in and around a tumour, includin

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

80 face of nanoparticles to specifically target cancerous cells through selective binding to the recepto

81 e host defense by killing viral-infected and cancerous cells through the secretion of preformed lytic

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

83 e of CYGB, its influence on the phenotype of cancerous cells under stress conditions and the clinical

84 nt viruses to selectively infect and destroy cancerous cells while sparing normal cells and tissues.

85 (non-cancerous) cells and subpopulations of cancerous cells with different complements of somatic ab

86 tein Dectin-1 recognizes structures found on cancerous cells, and then triggers an anti-tumor immune

87 irtue of their potential therapeutic role in cancerous cells, have been a major focus of research for

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

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

90 ous, activated p53 in both cancerous and non-cancerous cells, which led to significant levels of cell

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

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

93 ological changes in the lipid composition of cancerous cells.

94 radioprotector to protect normal cells over cancerous cells.

95 e BER deficient cells may be a source of pre-cancerous cells.

96 cient to drive tumorigenic properties of non-cancerous cells.

97 nts in parts of the body that do not contain cancerous cells.

98 hly expressed in the mitochondria of various cancerous cells.

99 cific interactions of the liposomes with non-cancerous cells.

100 hat controls redox homeostasis in normal and cancerous cells.

101 etermined that GPER is highly upregulated in cancerous cells.

102 es that can be exploited to selectively kill cancerous cells.

103 nd dependencies that can be targeted to kill cancerous cells.

104 arrest that limits the proliferation of pre-cancerous cells.

105 mammary acini and kidney cells but absent in cancerous cells.

106 , uncontrolled growth and differentiation of cancerous cells.

107 ls and the elimination of virus-infected and cancerous cells.

108 fragment of APP, as compared with normal non-cancerous cells.

109 ical and biologic changes both in normal and cancerous cells.

110 technique to discriminate between normal and cancerous cells.

111 d thereby assist in driving the formation of cancerous cells.

112 unctionally inhibited proliferation of these cancerous cells.

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

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

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

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

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

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

119 of cells, including admixture by normal (non-cancerous) cells and subpopulations of cancerous cells w

120 s degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) func

121 ls (SW48) in a mixed cell culture of primary cancerous colon cells (HT29) without any biochemical lab

122 roach analyzes cell phenotypes in normal and cancerous colon tissue imaged using the robotically cont

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

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

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

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

127 revealed striking ANGPTL7 underexpression in cancerous compared to normal tissues.

128 These non-cancerous components of the tumour may play an important

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

130 transitions in other epithelia in normal and cancerous conditions.

131 assist in the diagnosis of precancerous and cancerous conjunctival lesions.

132 ivotal role for HMGB1 in the development and cancerous contributions of MDSCs.

133 or (SiNW-ECIS) as an instrument that detects cancerous cultured living lung cells by monitoring their

134 ave been indicated to play a role in several cancerous disease states.

135 ication and treatment response assessment of cancerous disease.

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

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

138 been used for the theoretical study of anti-cancerous drugs scheduling optimization, with the aim of

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

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

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

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

143 erall 25% deletions within the OLFM4 gene in cancerous epithelial cells compared with adjacent normal

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

145 tumor tissues predominantly occurred in the cancerous epithelial cells.

146 sed in prostate cancer cells compared to non-cancerous epithelial cells.

147 espectively, for detection of dysplastic and cancerous esophageal lesions).

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

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

150 e feedback to optimize targeted treatment of cancerous foci and minimize quality-of-life side-effects

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

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

153 attering in the stroma immediately adjoining cancerous glands can be used to identify patients at hig

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

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

156 cellular oxidative stress is supportive for cancerous growth of cells, excessive levels of reactive

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

158 stem cells and their relevance to normal and cancerous growth.

159 rapeutic procedures for bleeding, polyps and cancerous growths.

160 key kidney fibroblasts (MKF) and human colon cancerous (HCT-8) cells in close proximity, as well as b

161 sed on HDAC6 based on its ability to inhibit cancerous Hsp90 chaperone activities by disrupting Hsp90

162 hromosomal data sets of both a healthy and a cancerous human B-cell to construct 3D models of individ

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

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

165 Cancerous human cells have also been discriminated from

166 etected cyclin D1 mRNA in RNA extracted from cancerous human cells, using ds-NIF methodology.

167 ry different oncolytic tropisms against some cancerous human leukocytes.

168 phogenesis and differentiation in normal and cancerous human prostate cells.

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

170 f Mcl-1 and of various senescence markers in cancerous human tissues.

171 f 1212 compliance measurements of normal and cancerous in vivo gastrointestinal tissues were taken.

172 all cells tested in vitro, noncancerous and cancerous, including patient-derived tumor samples.

173 ated PP2A by decreasing the transcription of cancerous inhibitor of PP2A (CIP2A), a chief inhibitor o

174 Cancerous inhibitor of PP2A (CIP2A), a guardian of oncop

175 A, Inhibitor-2 of PP2A (SET oncoprotein) and cancerous inhibitor of PP2A (CIP2A), inactivate PP2A and

176 uman breast cancer cells, we identify CIP2A (cancerous inhibitor of PP2A [protein phosphatase 2A]) as

177 Cancerous inhibitor of protein phosphatase 2A (CIP2A) is

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

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

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

181 cobacter-induced disease to precancerous and cancerous lesions in the absence of MyD88 signaling was

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

183 event in PDAC--develop a small number of pre-cancerous lesions that stochastically develop into PDAC

184 he fluorescent signal from pHLIP Var3 marked cancerous lesions with a very low false-positive rate.

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

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

187 mal tissue, but lower levels relative to pre-cancerous lesions.

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

189 multivariate clustering between the healthy/cancerous liver tissues and between the bacterial specie

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

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

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

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

194 ered cell-cell and cell-matrix adhesion, the cancerous mass can invade the neighbouring tissue.

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

196 based animal model of ExPEC translocation in cancerous mice, a system that can be readily used to ide

197 tatic cell line with the introduction of non-cancerous mitochondria.

198 ry chain activities compared to cybrids with cancerous mitochondria.

199 tochondria are inhibited in cybrids with non-cancerous mitochondria.

200 he epithelial cell is induced to undergo pre-cancerous molecular changes that render it prone to furt

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

202 th ELISA for the analysis of the MDM2 in the cancerous mouse brain tissue homogenates.

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

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

205 ecies but in humans appeared only as somatic cancerous mutations.

206 ributing to relapse, and the identity of pre-cancerous mutations.

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

208 press markers that are also expressed in non-cancerous neural stem cells, including nestin and Sox2.

209 improve diagnostic accuracy for identifying cancerous nodules.

210 accompanied by increases in the diagnosis of cancerous nodules.

211 x) enhanced the extent of gene expression in cancerous, non-cancerous, and stem cells, up to 1500-fol

212 In spite of the uniform cancerous nuclear background, as observed with the mitoc

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

214 eins to predict the subcellular locations of cancerous ones is arbitrary because the protein distribu

215 identify reference, human bladder cells from cancerous ones.

216 derived HeLa and SiHa cells but not in other cancerous or normal cell lines.

217 nome Imaging System image stacks from either cancerous or normal human colorectal specimens.

218 ted with concurrent detection of potentially cancerous oral lesions among HIV-negative patients but n

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

220 to cases of postmenopausal osteoporosis and cancerous osteolysis.

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

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

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

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

225 Despite higher HLA-A and HLA-D expression, cancerous pDCs did not exert cytotoxic activity against

226 In this scenario, cancerous pDCs were able to produce high levels of IL-1a

227 ules to recipient cells thereby conferring a cancerous phenotype.

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

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

230 ility of MYC, which contributes to promoting cancerous phenotypes.

231 PEL, a cancerous proliferation of B cells, is caused by Kaposi'

232 wnregulation is a novel mechanism supporting cancerous proliferation, and they provide a metabolic li

233 ration and invasion in both immortalized and cancerous prostate cells.

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

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

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

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

238 l epithelial populations from the benign and cancerous regions of primary human prostates.

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

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

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

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

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

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

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

246 latory nuclear activities may be specific to cancerous squamous epithelial cells, as normal keratinoc

247 ign tumor is a key challenge to diagnose the cancerous stage of the patients tested by clinical human

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

249 ve the transformation of normal cells to the cancerous state.

250 stribution patterns may differ in normal and cancerous states.

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

252 s capable of destroying virally infected and cancerous targets by polarized release from secretory ly

253 tistically higher for normal tissue than for cancerous tissue (p=0.00).

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

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

256 Here, we compared GPER expression in cancerous tissue and adjacent normal tissue in patients

257 Differences between metrics for cancerous tissue and those for normal tissue were assess

258 improved differentiation between normal and cancerous tissue at the tumor margins.

259 re indented using PMC to identify benign and cancerous tissue cores.

260 Normal colorectal mucosa and paired cancerous tissue from 60 patients with colorectal cancer

261 were used to calibrate the CRTCMS to predict cancerous tissue in a further 12 patients (3 cancer esop

262 The complete removal of cancerous tissue is a central aim of surgical oncology,

263 0-1), and minimum microscopic margins of non-cancerous tissue of 2 mm or more, were recruited.

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

265 icantly higher/lower co-expression levels in cancerous tissue samples when compared with normal colon

266 luding oleic acid, were more abundant in the cancerous tissue than in normal tissues.

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

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

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

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

271 lmost perfect distinction between normal and cancerous tissues based solely on EDGE results.

272 specimens can distinguish between normal and cancerous tissues by identifying the heterogeneous and d

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

274 onsider genes that mutate between normal and cancerous tissues or changes in protein or RNA expressio

275 Targeted delivery of anticancer drugs to cancerous tissues shows potential in sparing unaffected

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

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

278 ssues, PC expression was greatly enhanced in cancerous tissues, whereas GLS1 expression showed no tre

279 selective photodynamic therapy (PDT) to the cancerous tissues, with minimal harm to the adjacent nor

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

281 eded microRNA abundance in most infected non-cancerous tissues.

282 n transcripts are present in both benign and cancerous tissues.

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

284 pancreatic cancer tissues compared with non-cancerous tissues.

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

286 To investigate the transition from non-cancerous to metastatic from a physical sciences perspec

287 imental model for studying the age-dependent cancerous transformation of hMSCs.

288 endoplasmic reticulum frequently occurs upon cancerous transformation to enhance tumor cell migration

289 e passage-dependent response of hMSCs toward cancerous transformation.

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

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

292 nulomas are morphologically similar to solid cancerous tumors in that they contain hypoxic microenvir

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

294 , FerT, are coexpressed in normal testes and cancerous tumors, but whether they exert related roles i

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

296 erization of the state and aggressiveness of cancerous tumors.

297 hallenge in the effective treatment of solid cancerous tumours using conventional approaches.

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

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

300 erence between the expressions of glycans in cancerous versus noncancerous cells of the same origin,