ライフサイエンスコーパス: multiple cancer

1 on (PNI) is an indicator of poor survival in multiple cancers.

2 a source of broad therapeutic resistance in multiple cancers.

3 -nick in cell lines and tissues derived from multiple cancers.

4 ed virus (KSHV) and EBV, are associated with multiple cancers.

5 evated levels of 2-hydroxyglutarate (2HG) in multiple cancers.

6 PRC1) and is involved in the pathogenesis of multiple cancers.

7 draining lymph nodes has been documented in multiple cancers.

8 rtant human pathogen that is associated with multiple cancers.

9 sistance, rapid relapse, and poor outcome in multiple cancers.

10 23-H1 is associated with aggressive forms of multiple cancers.

11 ssociated with progression and metastasis of multiple cancers.

12 single catastrophic event, was described in multiple cancers.

13 s the formation and malignant progression of multiple cancers.

14 (RAGE) and its ligands are overexpressed in multiple cancers.

15 T locus on 5p15.33, which is associated with multiple cancers.

16 s measure to create an evolutionary tree for multiple cancers.

17 promoting cell survival and tumorigenesis in multiple cancers.

18 s have implicated a role for this pathway in multiple cancers.

19 e genes, all of which were highly mutated in multiple cancers.

20 on, propagation, and treatment resistance of multiple cancers.

21 rs and loss of p53 results in early onset of multiple cancers.

22 tial factors in organ-specific metastasis of multiple cancers.

23 IFN-alpha is approved for the treatment of multiple cancers.

24 mal growth factor family and is amplified in multiple cancers.

25 stasis, and its expression is upregulated in multiple cancers.

26 l division and exerts oncogenic functions in multiple cancers.

27 enome integrity, and FEN1 mutations arise in multiple cancers.

28 hat MiSL predictions are enriched for SLs in multiple cancers.

29 tative immunogenic cancer/testis antigens in multiple cancers.

30 hways and a validated chemotherapy target in multiple cancers.

31 5 as an alternative cancer vaccine target in multiple cancers.

32 d with epithelial-mesenchymal program across multiple cancers.

33 and persistent infection is associated with multiple cancers.

34 cating cells and is used in the treatment of multiple cancers.

35 ciated with the risk of Type II diabetes and multiple cancers.

36 ed cellular regulators of MGMT expression in multiple cancers.

37 promoter mutations to aberrant expression in multiple cancers.

38 hare loci with coaltered copy numbers across multiple cancers (19 cancer types from The Cancer Genome

39 tains over 52 biomarkers that are related to multiple cancers, according to the literature.

40 deregulated cellular translation, evident in multiple cancers and 'ribosomopathies'.

41 A patient is described with multiple cancers and compound heterozygous mutations in

42 MPC1 is deleted or underexpressed in multiple cancers and correlates with poor prognosis.

43 ubiquitous naturally occurring fiber causing multiple cancers and fibroproliferativedisease.

44 B-RAF serine-threonine kinase is mutated in multiple cancers and functions as an oncogene in melanom

45 os related antigen-1 (Fra-1) is activated in multiple cancers and gene ablation can suppress the inva

46 O-GlcNAc transferase (OGT) is elevated in multiple cancers and inhibition of this enzyme genetical

47 We show here that BORIS is also expressed in multiple cancers and is thus itself a cancer-testis gene

48 The up-regulation of SRPK1 in multiple cancers and its ability to regulate multiple re

49 link PcG deregulation to the progression of multiple cancers and may have important implications for

50 ed gene-1 (AEG-1) expression is increased in multiple cancers and plays a central role in Ha-ras-medi

51 vated gene-1 (AEG-1) expression increases in multiple cancers and plays a crucial role in oncogenic t

52 cript are associated with increased risk for multiple cancers and the severity of a given cancer; how

53 t has been shown that ID1 is de-regulated in multiple cancers and up-regulation of ID1 is correlated

54 es from 109 patients with familial cancer or multiple cancers, and control blood samples from 475 hea

55 ted with markedly elevated lifetime risks of multiple cancers, and has been linked to an increased ri

56 g therapy with single-agent activity against multiple cancers, and have significant potential in comb

57 miR-26a was broadly reduced in multiple cancers, and overexpression of miR-26a signific

58 ling is one of the key oncogenic pathways in multiple cancers, and targeting this pathway is an attra

59 implicated as a drug resistance mechanism in multiple cancers, and the EGFR and Hedgehog pathways (Hh

60 Furthermore, PYCR1 is overexpressed in multiple cancers, and the PYCR1 knock-out suppresses tum

61 onine (K-to-M) mutations are associated with multiple cancers, and they function in a dominant fashio

62 afenib is a structurally unique inhibitor of multiple cancer-associated kinases, including KIT and pl

63 Cav1 regulates multiple cancer-associated processes.

64 ng cancer target whose inhibition may affect multiple cancer-associated signaling pathways and, moreo

65 ely involved in network modules that control multiple cancer-associated signalling pathways and cellu

66 identical retrogene NANOGP8 is expressed in multiple cancers, but generally not in normal tissues an

67 e reverse transcriptase that is expressed in multiple cancers, but not in the vast majority of normal

68 nhance T cell responses and show efficacy in multiple cancers, but the role of costimulatory molecule

69 of EGFR and subsequent pathway activation in multiple cancer cell backgrounds and may represent new t

70 ized compound (58) was a potent inhibitor of multiple cancer cell lines (IC50 <10 nM vs U251, HT1080,

71 ieve >/= 85% recovery of spiked cells across multiple cancer cell lines and 99.99% depletion of white

72 ion factor up-regulated on the mRNA level in multiple cancer cell lines and implicated recently in th

73 treatments caused loss of c-IAP1 and XIAP in multiple cancer cell lines and in tumor xenografts, but

74 of apoptotic priming is heterogeneous within multiple cancer cell lines and is not the result of expe

75 st cancer cell invasion and dissemination in multiple cancer cell lines and murine models of cancer m

76 Ser(9) (an inactivated form of GSK-3beta) in multiple cancer cell lines and primary human cancer samp

77 straightforward biochemical approaches from multiple cancer cell lines and subsequently characterize

78 However none are ubiquitous across multiple cancer cell lines and tissue types.

79 lta enhanced cisplatin-induced cell death in multiple cancer cell lines and, remarkably, enhanced the

80 n strength heterogeneity was observed across multiple cancer cell lines as well as isogenically, sugg

81 umor proliferation and inducing apoptosis on multiple cancer cell lines as well as xenograft models.

82 creased viability and increased apoptosis in multiple cancer cell lines but less so in normal fibrobl

83 RTVP-1 mRNA was induced in multiple cancer cell lines by adenovirus-mediated delive

84 the collagen alpha2(I) gene is methylated in multiple cancer cell lines correlating with loss of coll

85 reductase and deoxycytidine kinase (dCK) in multiple cancer cell lines depletes deoxycytidine tripho

86 In this study, we report that multiple cancer cell lines display degradation of ECM at

87 ch was effective in blocking the survival of multiple cancer cell lines in a low micromolar concentra

88 iphenylmethyl motif potently induce death of multiple cancer cell lines in culture.

89 n of mRTVP-1 or hRTVP-1 induced apoptosis in multiple cancer cell lines including prostate cancer cel

90 We show in multiple cancer cell lines of varying metastatic capabil

91 t-7 levels to suppress let-7 target genes in multiple cancer cell lines such as HMGA2 and MYC.

92 We observed in multiple cancer cell lines that mutant TERT promoters ex

93 n of p31(comet) increased the sensitivity of multiple cancer cell lines to spindle poisons, including

94 nonlethally in G1-G1/S and S phase, whereas multiple cancer cell lines undergo G1-G1/S arrest and ce

95 expression, and AUC data, was performed with multiple cancer cell lines using specific siRNA knockdow

96 peutic activity of these derivatives against multiple cancer cell lines will provide clear structural

97 ARCN1 most significantly inhibited growth of multiple cancer cell lines without affecting normal cell

98 ded by weak mRNAs, exhibits activity against multiple cancer cell lines, and appears to have a prefer

99 d and dramatic maturation of procaspase-3 in multiple cancer cell lines, and powerfully induce caspas

100 In multiple cancer cell lines, EGFR activated phosphorylati

101 ibited the phosphorylation of Akt Ser-473 in multiple cancer cell lines, forced expression of myristo

102 with the spliceosome and is overexpressed in multiple cancer cell lines, our results suggest that C9O

103 fold of gemcitabine for growth inhibition of multiple cancer cell lines, while demonstrating little c

104 oliferative and cytotoxic activities against multiple cancer cell lines, with IC(50) values of 10-16

105 etabolism, and thymidine kinase activity, in multiple cancer cell lines.

106 AF4 is a promoter of CD133 transcription in multiple cancer cell lines.

107 nanomolar antiproliferative activity across multiple cancer cell lines.

108 potent antiproliferative activities against multiple cancer cell lines.

109 d with the degree of promoter methylation in multiple cancer cell lines.

110 activation of Stat3 by high cell density in multiple cancer cell lines.

111 n oncogenic RAS-driven human fibroblasts and multiple cancer cell lines.

112 etwork, and exert a cytotoxic effect against multiple cancer cell lines.

113 n level of DNAJB6a affected AKT signaling in multiple cancer cell lines.

114 f mitochondrial oxidative phosphorylation in multiple cancer cell lines.

115 ealed a p53-dependent induction of RPS27L in multiple cancer cell models.

116 gnaling and metabolic pathways that regulate multiple cancer cell phenotypes.

117 In multiple cancer cell populations, ONC201 synergized with

118 lel, miR-520f inhibited invasive behavior in multiple cancer cell systems and reduced metastasis in a

119 ult, simultaneous and sensitive detection of multiple cancer cell targets was achieved.

120 Decreased levels of Rad51 were observed in multiple cancer cell types during hypoxic exposure and w

121 +) channels (VGSCs) has been demonstrated in multiple cancer cell types where channel activity induce

122 phytoalexin, is known to induce apoptosis in multiple cancer cell types, but the underlying molecular

123 surface-associated active MT1-MMP enzyme in multiple cancer cell types, including breast carcinoma,

124 cells and the mislocalisation of PRH seen in multiple cancer cell types.

125 omotes tumor cell invasion and metastasis in multiple cancer cell types.

126 (CDDO-Me) effectively inhibits the growth of multiple cancer cell types.

127 inding protein 1 (And-1) that is elevated in multiple cancer cells and is essential for Gcn5 protein

128 applications in the sensitive monitoring of multiple cancer cells for biomedical research and medica

129 ity of HDACi was robustly enhanced by E1A in multiple cancer cells, but not in normal cells.

130 In multiple cancer cells, LCoR and KLF6 bind together on th

131 articles for the collection and detection of multiple cancer cells.

132 cruitment domain (ARC), a protein induced in multiple cancer cells.

133 For genes that are mutated in multiple cancer classes, mutations are usually similar i

134 s) displayed significant prognostic value in multiple cancer clinical data sets.

135 merging class of anti-tumor drugs, potent in multiple cancer contexts.

136 We apply this method to multiple cancer data sets, validating its accuracy by sh

137 The results on multiple cancer datasets show that our proposed method c

138 These molecular alterations include multiple cancer-driving mutations, gene fusions, amplifi

139 therapeutic approach to simultaneously stop multiple cancer-driving pathways in HCC.

140 y, chemical or genetic Pin1 ablation blocked multiple cancer-driving pathways simultaneously in HCC c

141 ctive targeted drugs to simultaneously block multiple cancer-driving pathways.

142 CC, and promotes tumorigenesis by activating multiple cancer-driving pathways.

143 bits HCC by directly targeting Pin1 to block multiple cancer-driving pathways.

144 family of tyrosine kinases is deregulated in multiple cancers either through amplification, overexpre

145 progression that is aberrantly regulated in multiple cancers, especially in breast cancers.

146 a set of positive and negative controls for multiple cancers for which pathway information was avail

147 od to infer a graph model for the markers of multiple cancers from a large population of CGH data.

148 Our results support the hypothesis that multiple cancer genes are targeted by regional chromosom

149 Remarkably, multiple cancer genes are under strong positive selectio

150 prostate cancer genes and appears to disrupt multiple cancer genes coordinately.

151 in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously

152 are by identifying targetable alterations in multiple cancer genes, little is known about how physici

153 f them have been implicated in cancer (often multiple cancers) genesis in past studies, which also su

154 ng approach is developed for the analysis of multiple cancer genomic datasets.

155 nflammation is an enabling characteristic of multiple cancer hallmarks.

156 o reason that CIN enables the acquisition of multiple cancer hallmarks; however, there is a growing b

157 s linked to enhanced metastatic potential in multiple cancers; however, the role of RhoC GTPase in Ca

158 n implicated in the growth and metastasis of multiple cancers; however, while their involvement in ca

159 llelic inactivation of NF2 is known to cause multiple cancers in both humans and mice.

160 EBV is linked to the development of multiple cancers in both lymphoid and epithelial cells,

161 on chromosome 10 (Pten) are associated with multiple cancers in humans, including T cell malignancie

162 thods to predict core cancer genes shared by multiple cancers in the hope of elucidating common cance

163 eat promise to augment immunotherapy against multiple cancers including metastatic melanoma, in which

164 preventive and chemotherapeutic activity for multiple cancers including pancreatic cancer; however, t

165 been used in treatment or chemoprevention of multiple cancers including prostate cancer.

166 tolerated and has therapeutic potential for multiple cancers, including breast cancer, where its eff

167 are in clinical trials for the treatment of multiple cancers, including breast cancer.

168 phase protein, which is also up-regulated in multiple cancers, including breast, lung, and pancreas.

169 es causally associated with benign warts and multiple cancers, including cervical and head-and-neck c

170 disposition syndrome that increases risk for multiple cancers, including colon, endometrial, and ovar

171 have unique anticancer properties and target multiple cancers, including colon, pancreatic, breast, p

172 and silencing of PTEN have been observed in multiple cancers, including follicular thyroid carcinoma

173 ifunctional protein that is overexpressed in multiple cancers, including hepatocellular carcinoma (HC

174 main containing 1 (SND1) is overexpressed in multiple cancers, including hepatocellular carcinoma (HC

175 proteins in the malignant transformation of multiple cancers, including lung adenocarcinoma, cholang

176 nsformation and metastasis, is a hallmark of multiple cancers, including mammary, prostate, and lung

177 pulation and is linked to the development of multiple cancers, including nasopharyngeal carcinoma.

178 loci encoding miR-204 are frequently lost in multiple cancers, including ovarian cancers, pediatric r

179 PCR superfamily) and promote angiogenesis in multiple cancers, including pancreatic cancer.

180 The oncogene DJ-1 has been associated with multiple cancers, including prostate cancer, where it ca

181 ator of transcription 3 (STAT3) is linked to multiple cancers, including pulmonary adenocarcinoma.

182 RT) gene promoter occur at high frequency in multiple cancers, including urothelial cancer (UC), but

183 sis, the purpose of its somatic silencing in multiple cancers is largely unknown.

184 al PRMT5 as a potential vulnerability across multiple cancer lineages augmented by a common "passenge

185 mixing, as exemplified by the coexistence of multiple cancer lineages harboring distinct ERG fusions

186 ong the most frequent genomic aberrations in multiple cancer lineages including ovarian and breast ca

187 unction and downregulates CCN1 expression in multiple cancer lineages, resulting in a profound inhibi

188 is able to predict clinical outcomes across multiple cancer lineages.

189 ET is implicated in the malignant process of multiple cancers, making disruption of this interaction

190 of genes with rare somatic mutations across multiple cancers; many of these genes have additional ev

191 s progression-free survival of patients with multiple cancers; more than 30 clinical trials are under

192 Older Tak1DeltaHEP mice developed multiple cancer nodules characterized by increased expre

193 As our capacity to produce such data for multiple cancers of the same type is improving, so are t

194 he retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulat

195 zed those loci that carried the signature in multiple cancer patients.

196 gy, oligopolyposis, young, colon/breast, and multiple cancer) prior to analysis.

197 gration, comparison, and cross-validation of multiple cancer profiling studies.

198 luation, cross-validation, and comparison of multiple cancer profiling studies.

199 ontinuum model is most likely to apply where multiple, cancer-promoting mutations have relatively sma

200 offers access and the capability to analyze multiple cancer proteomic datasets generated through the

201 dence studies of retrospective cohorts using multiple cancer registries are feasible.

202 Our results indicate that linkage with multiple cancer registries can be a sensitive method for

203 Each construct consists of multiple cancer-related antigens displayed on a single p

204 Because it is an oncoprotein associated with multiple cancer-related diseases, as well as a potential

205 n, accompanied by induction in expression of multiple cancer-related genes.

206 Monensin suppresses multiple cancer-related pathways including Elk1/SRF, AP1

207 suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell

208 EAPII interacts with multiple cancer-related proteins, but its biological sig

209 ression of this particular isoform activates multiple cancer-related transcription factor reporters,

210 e proposed that this SNP might contribute to multiple cancer risk and variability in drug response.

211 Lynch syndrome poses multiple cancer risks, yet attention has focused on scre

212 Recurrent CNA (RCNA) occurs in multiple cancer samples across the same chromosomal regi

213 Finally, multiple cancer-specific motifs have been identified.

214 itical that consideration be given to use of multiple cancer stem-like cell markers and suitable proc

215 there was strong evidence for linkage in the multiple-cancer subgroup (p = 0.00007).

216 ential model built on the gene expression of multiple cancer subtypes to devise an EMT metric that ch

217 Risk of multiple cancer surgeries was 33.7% for patients undergo

218 ction of EBV is linked to the development of multiple cancers that have distinct patterns of expressi

219 d from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 c

220 thway has been proposed for the treatment of multiple cancers, the effect of c-Met inhibition in HCC

221 nse to programmed death 1 (PD-1) blockade in multiple cancers, the majority of patients still fail to

222 s among the most commonly methylated loci in multiple cancers, the retinoic acid-induced tumor suppre

223 nd associated with poor clinical outcomes in multiple cancers, these results have implications for ot

224 transcription factor that is deregulated in multiple cancers through loss of heterozygosity (LOH) an

225 creased MEG3 expression has been reported in multiple cancer tissues.

226 biting consistent dysregulated expression in multiple cancer tissues.

227 to jointly analyze expression profiles from multiple cancers to identify miRNA-gene interactions tha

228 to develop a method that can jointly analyze multiple cancers to study miRNA-gene interactions withou

229 and infected patients should have access to multiple cancer treatments with close monitoring while r

230 and levels of Akt phosphorylation at S473 in multiple cancer types (P<0.0001).

231 observed between CNA and gene expression in multiple cancer types and biological milestones achieved

232 XO-dependent E2F1 transcriptional program in multiple cancer types and by the association of a reduce

233 somatic copy-number aberration regions from multiple cancer types and could be used to pinpoint new

234 CARM1 overexpression has been reported in multiple cancer types and has been shown to modulate onc

235 se elements are significantly mutated across multiple cancer types and have mutation densities simila

236 serpin family members are similarly lost in multiple cancer types and hold tumor suppressor function

237 athway is implicated in the tumorigenesis of multiple cancer types and its deregulation is associated

238 of the commonalities and differences between multiple cancer types and potential therapies.

239 Genome Atlas patient transcriptomics data of multiple cancer types and single-cell RNA-seq data of lu

240 A target and biological relationships across multiple cancer types by integrating web-based analysis

241 A tropism for multiple cancer types combined with an exquisite tumor s

242 Extensive analysis of multiple cancer types demonstrates significant upregulat

243 nucleotide polymorphisms (SNPs) at 5p15 and multiple cancer types have been reported.

244 Thus, in multiple cancer types in which ABT-737 is incapable of c

245 TET1ALT is aberrantly activated in multiple cancer types including breast, uterine and glio

246 ystematic collection and curation of TSGs in multiple cancer types is critically important for furthe

247 Successful treatment of multiple cancer types requires early detection and ident

248 ) and HER2 (ErbB2) drives the progression of multiple cancer types through complex mechanisms that ar

249 s that could improve patient survival across multiple cancer types where nucleoside analogues are use

250 They also represent multiple cancer types, and include both recurrent and no

251 WAC, which were identified by our screens in multiple cancer types, as new tumor suppressor genes in

252 ase inhibitor p16(INK4A) are associated with multiple cancer types, but are more commonly found in me

253 methylation (H3K36me3) is frequently lost in multiple cancer types, identifying it as an important th

254 and TRAIL induced significant cell death in multiple cancer types, including renal, prostate, and lu

255 Multiple cancer types, including up to 83% of glioblasto

256 ding partner PBF have been widely studied in multiple cancer types, particularly thyroid and colorect

257 Here we show that across multiple cancer types, responses (as evaluated by Respon

258 prognostic factor for favorable survival in multiple cancer types, such as colorectal and endometria

259 have identified common FFL regulators across multiple cancer types, such as known FFLs consisting of

260 the expression of PKC isozymes is altered in multiple cancer types, the causal relationship between s

261 is associated with metastatic progression in multiple cancer types, yet the role of CD24 in this proc

262 , functional, and mechanistic involvement in multiple cancer types.

263 1 is related to aggressive tumor features in multiple cancer types.

264 or gene with its expression downregulated in multiple cancer types.

265 prognostic and therapeutic approaches across multiple cancer types.

266 been linked to favorable clinical outcome in multiple cancer types.

267 RRES2) is transcriptionally downregulated in multiple cancer types.

268 universal biological mechanism shared among multiple cancer types.

269 and repression, has increased expression in multiple cancer types.

270 or, an oncogene or a metastasis regulator in multiple cancer types.

271 FRvIII, are important therapeutic targets in multiple cancer types.

272 identify novel drugs and drug targets across multiple cancer types.

273 ges and is associated with poor prognosis in multiple cancer types.

274 H3 proteins, induces apoptotic cell death in multiple cancer types.

275 ting an expanded role for galpha subunits in multiple cancer types.

276 on data as a basis for the classification of multiple cancer types.

277 ty of tissues and are often overexpressed in multiple cancer types.

278 struct the evolutionary relationship between multiple cancer types.

279 rged as contributing to cancer metastasis in multiple cancer types.

280 le in both tumor growth and dissemination in multiple cancer types.

281 se (MT1-MMP) exerts its enhanced activity in multiple cancer types.

282 n shown to function as a tumor suppressor in multiple cancer types.

283 ted with kataegic mutational patterns within multiple cancer types.

284 e for development as a novel therapeutic for multiple cancer types.

285 ntification of critical molecular targets of multiple cancer types.

286 ate the use of HA as a delivery platform for multiple cancer types.

287 in a large panel of cancer cell lines across multiple cancer types.

288 for drug development as it is upregulated in multiple cancer types.

289 recruiting patients, using a range of OVs in multiple cancer types.

290 mechanism to activate cancer driver genes in multiple cancer types.

291 matic analysis of ARE-mRNA expression across multiple cancer types.

292 ations are detected in known cancer genes in multiple cancer types.

293 e previously unreported non-pairwise MEGS in multiple cancer types.

294 S protein associated with the progression of multiple cancer types.

295 nally activated by MYC and is upregulated in multiple cancer types.

296 omising clinical benefit in the treatment of multiple cancer types.

297 , race, cancer type (acute myeloid leukemia, multiple cancers v acute lymphoblastic leukemia), and th

298 ta indicate that endothelial L1 orchestrates multiple cancer vessel functions and represents a potent

299 in PTEN, PHTS also causes increased risks of multiple cancers via dysregulation of the PI3K and MAPK

300 thus may serve as a therapeutic strategy in multiple cancers where ASS1 is downregulated.