ライフサイエンスコーパス: multiple cancer

1 efines the pathogenesis and vulnerability of multiple cancers.

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

3 nly germ cells with aberrant reactivation in multiple cancers.

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

5 l division and exerts oncogenic functions in multiple cancers.

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

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

8 tative immunogenic cancer/testis antigens in multiple cancers.

9 hways and a validated chemotherapy target in multiple cancers.

10 5 as an alternative cancer vaccine target in multiple cancers.

11 d with epithelial-mesenchymal program across multiple cancers.

12 ansferase 5 (PRMT5) has been associated with multiple cancers.

13 and persistent infection is associated with multiple cancers.

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

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

16 ed cellular regulators of MGMT expression in multiple cancers.

17 promoter mutations to aberrant expression in multiple cancers.

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

19 a source of broad therapeutic resistance in multiple cancers.

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

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

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

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

24 draining lymph nodes has been documented in multiple cancers.

25 vity at recommended levels to lower risks of multiple cancers.

26 rtant human pathogen that is associated with multiple cancers.

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

28 23-H1 is associated with aggressive forms of multiple cancers.

29 nd significantly reduced patient survival in multiple cancers.

30 ssociated with progression and metastasis of multiple cancers.

31 l-fate determination and is overexpressed in multiple cancers.

32 several biological processes associated with multiple cancers.

33 O) has altered the therapeutic landscape for multiple cancers.

34 ed as biomarkers and therapeutic targets for multiple cancers.

35 rations and abnormal expression of APE2 from multiple cancers.

36 therapy have revolutionized the treatment of multiple cancers.

37 apies have demonstrated clinical efficacy in multiple cancers.

38 ic dystrophy type 1, Alzheimer's disease and multiple cancers.

39 a nuclear import factor that is elevated in multiple cancers.

40 h increased metastasis and poor prognosis in multiple cancers.

41 anscriptional regulator CDK12, disrupt HR in multiple cancers.

42 ion factor implicated in the pathogenesis of multiple cancers.

43 of enhancers on transcriptional programs in multiple cancers.

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

45 sative agent of infectious mononucleosis and multiple cancers(5), utilizes a two-pronged approach to

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

47 Here, we report multiple-cancer analyses of APE2 genomic alterations and

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

49 Yet, lncRNA LINP1 is over-expressed in multiple cancers and confers resistance to ionizing radi

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

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

52 rvival and promotion of tumor progression in multiple cancers and is a known risk factor for metastas

53 e reader bromodomains, has shown promise for multiple cancers and neurodegenerative disease.

54 n at non-AUG start codons is associated with multiple cancers and neurodegenerative diseases.

55 isomerase (PDI) family, is overexpressed in multiple cancers and promotes angiogenesis to drive canc

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

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 We also found that multiple cancers are genetically correlated with non-can

63 e expression levels, and are associated with multiple cancer-associated biological processes and surv

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

65 Cav1 regulates multiple cancer-associated processes.

66 ) that plays a pivotal and versatile role in multiple cancer-associated processes.

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

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

69 of proliferation 1 (BOP1) is associated with multiple cancers but has not been implicated in CaP thus

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

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

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

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

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

75 inhibitors show robust cytotoxic effects in multiple cancer cell lines and induce cell-cycle arrest

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

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

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

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

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

81 We evaluated the durotactic potential of multiple cancer cell lines by employing substrate stiffn

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

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

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

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

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

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

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

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

90 In multiple cancer cell lines, EGFR activated phosphorylati

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

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

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

94 ited good antiproliferative activity against multiple cancer cell lines.

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

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

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

98 f mitochondrial oxidative phosphorylation in multiple cancer cell lines.

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

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

101 PRMT5 protein level and inhibited growth in multiple cancer cell lines.

102 ms that are recurrently heterogeneous within multiple cancer cell lines.

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

104 In multiple cancer cell populations, ONC201 synergized with

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

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

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

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

109 ls, whereas Ad.mda-7 down-regulates DICER in multiple cancer cells including glioblastoma multiforme

110 In multiple cancer cells, cell membrane-located GRP78 has b

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

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

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

114 hermore, using machine learning for studying multiple cancer cohorts together with a collection of mo

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

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

117 es and gene-sample biclusters underlying the multiple cancer datasets to learn the knowledge crossing

118 ug combinations that simultaneously suppress multiple cancer driver signaling pathways increase thera

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

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

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

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

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

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

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

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

127 us disease biomarkers, including markers for multiple cancer forms, cardiovascular diseases, or Alzhe

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

129 Remarkably, multiple cancer genes are under strong positive selectio

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

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

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

133 nflammation is an enabling characteristic of multiple cancer hallmarks.

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

135 nown to regulate cell growth and survival in multiple cancers; however, the role of CK2 in MB is curr

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

137 e variant include a strong family history or multiple cancers in a single patient, diagnosis of a hem

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

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

140 inhibitor with demonstrated activity across multiple cancers, in LGSOC.

141 we report two individuals from a family with multiple cancer incidences carrying a RPL9 missense vari

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

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

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

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

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

147 Netrin-1 and UNC5B are deregulated in multiple cancers, including colorectal, neuroblastoma, a

148 cytomegalovirus (HCMV) has been detected in multiple cancers, including glioblastoma, and its genome

149 alvular heart disease were also observed for multiple cancers, including haematological malignancies.

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

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

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

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

154 ubiquitous worldwide and is associated with multiple cancers, including nasopharyngeal carcinoma (NP

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

156 Dysregulation of MOF activity occurs in multiple cancers, including ovarian cancer, medulloblast

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

158 the resistance to PD-L1 blockade therapy in multiple cancers, including PCa.

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

160 ated MELK depletion impairs proliferation of multiple cancers, including triple-negative breast cance

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

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

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

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

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

166 rapies have extended patient survival across multiple cancer lineages, but there is a heated debate o

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

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

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

170 unity but protected against tumour growth in multiple cancer models.

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

172 ion and confers an elevated lifetime risk of multiple cancers notably colorectal and endometrial carc

173 suggest that levosimendan is active against multiple cancers, notably lymphoma, through the direct i

174 n volunteers, and show its ability to detect multiple cancers (pancreatic, cervical and lung) in pati

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

176 rved in extensive independent validations on multiple cancer patient datasets obtained from retrospec

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

178 They affect multiple cancer phenotypes by altering miRNA and mRNA ex

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

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

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

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

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

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

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

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

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

188 ial benefits and limitations of single-test, multiple cancer screens.

189 s a hub of an oncogenic network, integrating multiple cancer signaling pathways and serving as a pote

190 eRNAs are involved in multiple cancer signaling pathways through putatively re

191 Multiple cancer signalling networks take part in regulat

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

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

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

195 se mutations occur at a low frequency across multiple cancer subtypes, including breast, and are suff

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

197 dominant mutation associated with a familial multiple cancer syndrome in which carriers should underg

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

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

200 Even though the pathways are common to multiple cancers, the association of specific mRNAs with

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

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

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

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

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

206 biting consistent dysregulated expression in multiple cancer tissues.

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

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

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

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

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

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

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

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

215 ndeed, we find that citrin is upregulated in multiple cancer types and is essential for supplementing

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

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

218 ing cascades, continues to be pursued across multiple cancer types as a strategy for targeting the CS

219 al selectin ligands expressed on tissue from multiple cancer types at both primary and metastatic sit

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

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

222 Extensive analysis of multiple cancer types demonstrates significant upregulat

223 ation of such signatures that are present in multiple cancer types due to driver amplifications and d

224 Science probes over 1500 tumor samples from multiple cancer types for markers of a tumor microbiome

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

226 oma and lung cancer, meta-analyses that pool multiple cancer types have limitations to discern whethe

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

228 h SIRPalpha on phagocytes are active against multiple cancer types including T-cell lymphoma (TCL).

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

230 easily identify significant associations in multiple cancer types simultaneously.

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

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

233 as a synthetic lethal target in tumours from multiple cancer types with microsatellite instability.

234 existing expression-based biomarkers across multiple cancer types(2-6).

235 n global pharmacovigilance databases (across multiple cancer types) of encephalitis associated with c

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

237 MYC is a well-described BRD4 target gene in multiple cancer types, and prior work demonstrates that

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

239 folding subunit, have been identified across multiple cancer types, but the effects of the most commo

240 show that the G(s) pathway is upregulated in multiple cancer types, even those lacking known GNAS act

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

242 Multiple cancer types, including Ewing sarcoma tumors, a

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

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

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

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

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

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

249 In 11 out of 13 OGs shared among multiple cancer types, we found functional domains selec

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

251 terns for sex bias in immune features across multiple cancer types.

252 the tumor microenvironment conserved across multiple cancer types.

253 expression and decreased immune activity in multiple cancer types.

254 1 is related to aggressive tumor features in multiple cancer types.

255 RRES2) is transcriptionally downregulated in multiple cancer types.

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

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

258 ted with kataegic mutational patterns within multiple cancer types.

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

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

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

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

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

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

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

266 conditional diagnostics and therapeutics for multiple cancer types.

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

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

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

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

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

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

273 prognostic and therapeutic approaches across multiple cancer types.

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

275 universal biological mechanism shared among multiple cancer types.

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

277 immunotherapeutic targets for patients with multiple cancer types.

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

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

280 ns of clinical trials targeting autophagy in multiple cancer types.

281 f coronary artery disease and lower risk for multiple cancer types.

282 ortant biomarkers and therapeutic targets in multiple cancer types.

283 es elicited strong antitumor immunity across multiple cancer types.

284 e clinical outcomes has been observed across multiple cancer types.

285 1 levels associate with poor outcomes across multiple cancer types.

286 to increased inflammatory immune response in multiple cancer types.

287 pathway, a key signaling pathway involved in multiple cancer types.

288 ngements drive tumor growth and evolution in multiple cancer types.

289 loped to systematically analyze sQTLs across multiple cancer types.

290 to activate adenylate cyclase signalling in multiple cancer types.

291 ified as putative therapeutic targets across multiple cancer types.

292 umors display significantly less CNAs across multiple cancer types.

293 as activators of Hippo-pathway signaling in multiple cancer types.

294 oped to systematically analyze meQTLs across multiple cancer types.

295 s critically associated with tumor growth in multiple cancer types.

296 ocking antibodies are actively used to treat multiple cancer types; however, the underlying resistanc

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

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

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

300 eneity are defined and how these manifest in multiple cancers, with a focus on pancreatic ductal aden