ライフサイエンスコーパス: human cancer

1 ryotypes, recapitulating a common feature of human cancer.

2 with clinical importance in the treatment of human cancer.

3 ors and other strategies in the treatment of human cancer.

4 p the most frequently mutated gene family in human cancer.

5 Loss of cell-cycle control is a hallmark of human cancer.

6 unction and targeted therapies for mutp53 in human cancer.

7 d cell-autonomous role for E2F activators in human cancer.

8 lity could help to improve immunotherapy for human cancer.

9 major implications for PDX-based modeling of human cancer.

10 nce genetic mechanism for PP2A inhibition in human cancer.

11 tumor-suppressor function in mouse models of human cancer.

12 e accurate preclinical models of this lethal human cancer.

13 and metabolism, and is often deregulated in human cancer.

14 , EphA2 is a relevant therapeutic target for human cancer.

15 y serve as a potential therapeutic target in human cancer.

16 tate cancer but perhaps also more broadly in human cancer.

17 the most frequently mutated gene product in human cancer.

18 ed TP53 as the most commonly mutated gene in human cancer.

19 comprehensive compendium of mouse models of human cancer.

20 gene therapy is a potential strategy to cure human cancer.

21 -CD47 checkpoint could be useful in treating human cancer.

22 loring targets and trends in the genetics of human cancer.

23 ome that is frequently mutated or deleted in human cancer.

24 ding protein 2 (MSI2) has important roles in human cancer.

25 veal the mutagenic processes responsible for human cancer.

26 sceptibility loci for several major forms of human cancer.

27 RNA (lncRNA) that is widely overexpressed in human cancer.

28 ion was developed for the early diagnosis of human cancer.

29 p53 is the most frequently mutated gene in human cancer.

30 ation of their expression is associated with human cancer.

31 n exclusively in testis and a broad range of human cancers.

32 at is mutated and inactivated in 50% of all human cancers.

33 -cell sequencing data sets from a variety of human cancers.

34 better understand and target these cells in human cancers.

35 RB loss to differentially reprogram E2F1 in human cancers.

36 edicine offers unique advantages in treating human cancers.

37 arget and a prognostic marker for metastatic human cancers.

38 ectively mutated in approximately 20% of all human cancers.

39 s implicated in tumor progression of various human cancers.

40 n asymmetry, which is frequently observed in human cancers.

41 ns in the cohesin complex in a wide range of human cancers.

42 gregation has been associated with different human cancers.

43 nd its expression is dysregulated in several human cancers.

44 oncoding RNA that is widely overexpressed in human cancers.

45 , the most frequently mutated Ras isoform in human cancers.

46 of metastasis and therapeutic resistance in human cancers.

47 tion of FOXP1-SHQ1 and PTEN loss observed in human cancers.

48 HIV/AIDS, and is an etiologic agent for some human cancers.

49 further study of these abnormalities across human cancers.

50 vival, and their mutants occur frequently in human cancers.

51 tion mutations of FBXW2 are found in various human cancers.

52 as biomarker for diagnosis and prognosis of human cancers.

53 DD45B confers poor clinical outcomes in most human cancers.

54 tein synthesis and is hyperactivated in many human cancers.

55 Genomic rearrangements are a hallmark of human cancers.

56 EBV) infection is causally linked to several human cancers.

57 and are the mutations most commonly seen in human cancers.

58 proteins harbor recurrent mutations in most human cancers.

59 n the development and progression of several human cancers.

60 ls with mTORC1 activation, a common event in human cancers.

61 volving the PI3K pathway occur frequently in human cancers.

62 being widely used to treat various types of human cancers.

63 relevant to metastatic progression in solid human cancers.

64 pressive effect of the pathway in Ras-driven human cancers.

65 with aggressive clinical features of several human cancers.

66 ked to the genome stability and a variety of human cancers.

67 and with increasing disease stage in primary human cancers.

68 tes with pro-inflammatory gene expression in human cancers.

69 ribute to the development and progression of human cancers.

70 sponsible for two-thirds of the mutations in human cancers.

71 pathway, are an underlying cause of >70% of human cancers.

72 high genome instability across many frequent human cancers.

73 xpression signature consistent with multiple human cancers.

74 acquired biallelic mutations are frequent in human cancers.

75 aration, and is frequently over-expressed in human cancers.

76 c target that is mutated in up to a third of human cancers.

77 tumor suppressor p53 occur in a majority of human cancers.

78 herapeutic for the treatment of a variety of human cancers.

79 blockade to enhance therapeutic efficacy for human cancers.

80 of Ras are involved in approximately 30% of human cancers.

81 hway, which is frequently found defective in human cancers.

82 suggest that our data may have relevance to human cancers.

83 suppressor proteins and is overexpressed in human cancers.

84 is one of the most commonly mutated genes in human cancers.

85 AS oncogenes have been implicated in >30% of human cancers, all representing high unmet medical need.

86 rovirus group HERV-K (HML-2) is seen in many human cancers, although the identities of the individual

87 plored the prevalence of parainflammation in human cancer and determined its relationship to certain

88 nal framework to study personal regulomes in human cancer and epigenetic therapy.

89 proto-oncogenes are among the most common in human cancer and frequently occur in acute myeloid leuke

90 pleural mesothelioma (MPM) is an aggressive human cancer and miRNAs can play a key role for this dis

91 S is the most frequently mutated oncogene in human cancer and plays a central, although poorly unders

92 hip between the levels of MTA1 and DNMT3a in human cancer and that high levels of MTA1 in combination

93 drogenase 1 (IDH1) gene occur in a number of human cancers and confer a neomorphic enzyme activity th

94 nctions that are co-opted or abated to drive human cancers and developmental disorders.

95 are observed frequently in most intractable human cancers and establish dependency for tumor mainten

96 gression in aggressive preclinical models of human cancers and induced cell killing in leukemia cells

97 PIM1 is overexpressed in many human cancers and is a promising target for drug develop

98 2 (PRC2) that is highly expressed in diverse human cancers and is associated with a poor prognosis.

99 ession signature that is present in numerous human cancers and is associated with poor survival.

100 ortantly, OTUD1 is lost in multiple types of human cancers and loss of OTUD1 increases metastasis in

101 tion of RNA-DNA hybrids is linked to various human cancers and neurodegenerative disorders, our study

102 r organoids are a robust model of individual human cancers and present a unique platform for patient-

103 It was recurrently mutated in advanced human cancers and significantly co-occurred with RAS or

104 at PARK2 expression is frequently reduced in human cancers and that this alteration leads to dysregul

105 mutations are the oncogenic drivers of many human cancers and yet there are still no approved Ras-ta

106 p53 is the most frequently mutated gene in human cancer, and over half of human cancers contain p53

107 Genomic instability is a hallmark of human cancer, and results in widespread somatic copy num

108 or (FR) is highly expressed in many types of human cancers, and it has been actively studied for deve

109 is repeatedly overexpressed in a variety of human cancers, and it has been implicated in all major h

110 that PARK2 is altered in over a third of all human cancers, and its depletion results in enhanced pho

111 correlated with EMT and shorter survival in human cancers, and PAQR11 was found to be essential for

112 Metabolic deregulation is a hallmark of human cancers, and the glycolytic and glutamine metaboli

113 The devastating diseases of human cancer are mimicked in basic and translational can

114 Approximately 15% of human cancers are MTAP(-/-).

115 Its mutants, present in about 30% of human cancers, are major drivers of oncogenesis and rend

116 ng, which is inactivated in both obesity and human cancers, as a key target of SET1B/COMPASS.

117 These data indicate that human cancer-associated genetic alterations in the FEN1

118 ions of protein and immunoassaying a type of human cancer biomarker.

119 GMP, common in many human cancers but of uncertain origin, served as an inte

120 ty to kinase inhibitors used widely to treat human cancer, but effective patient stratification based

121 G2 gene encoding SA2 is often inactivated in human cancer, but not in in a manner associated with ane

122 ule that drives progression of many types of human cancer, but the basis for its actions remains obsc

123 response kinase ATM is frequently mutated in human cancer, but the significance of these events to ch

124 or suppressor or as an oncogene in different human cancers, but direct evidence for its role in tumor

125 q25 locus, which is known to be amplified in human cancers, but its role in tumorigenesis remains und

126 yl isothiocyanate (PEITC) can reduce risk of human cancers, but possible epigenetic mechanisms of the

127 ng DNA strands were reported in yeast and in human cancers, but the causes of these differences remai

128 ) folds of POT1 have been identified in many human cancers, but the mechanism underlying how hPOT1 mu

129 expressed as cancer/testis antigens (CTA) in human cancers, but the tolerance status of MGCA has not

130 utated tumours represent a large fraction of human cancers, but the vast majority remains refractory

131 tions are found in a significant fraction of human cancers, but therapeutic inhibition of PI3K has on

132 Oncogenic gene fusions drive many human cancers, but tools to more quickly unravel their f

133 tory activities and potent cytotoxicities in human cancer cell cultures and reduced lethality in an a

134 e inhibitory data and cytotoxicity data from human cancer cell cultures establish that modification o

135 Compounds 16b and 17b are the most potent in human cancer cell cultures with MGM GI50 values of 0.063

136 -induced translation stress, and analysis of human cancer cell line data from Project Achilles furthe

137 Experiments involving a human cancer cell line panel and mouse xenografts reveal

138 ound that it was broadly upregulated in many human cancer cell lines and cancers, including most nota

139 pounds, which were tested against aggressive human cancer cell lines and for protein synthesis inhibi

140 itotic entosis occurs constitutively in some human cancer cell lines and mitotic index correlates wit

141 Finally, our data generated from both human cancer cell lines and mouse xenograft model showed

142 apy-resistant high-mesenchymal cell state in human cancer cell lines and organoids and show that it d

143 e further supported by consistent results in human cancer cell lines and primary samples of human hae

144 potent anti-proliferative activities against human cancer cell lines by inhibiting tubulin polymeriza

145 inhibited the growth of multiple RAS-mutant human cancer cell lines of diverse tissue origin by bloc

146 Biological investigation of 2-5 on human cancer cell lines showed enhancement of antiprolif

147 together with recently reported evidence in human cancer cell lines that ETAA1 activates ATR kinase

148 sed a genome-scale shRNA viability screen in human cancer cell lines to systematically identify genes

149 mal mouse intestinal epithelia and adenomas, human cancer cell lines with or without drug treatments,

150 IHSF115 is cytotoxic for a variety of human cancer cell lines, multiple myeloma lines consiste

151 By profiling the response of over 120 human cancer cell lines, we derived an expression-based

152 to study genome-wide chromatin structure in human cancer cell lines, yet numerous technical challeng

153 ts from large-scale chemical screening using human cancer cell lines.

154 termined at a ratio 1:6 (named PRP) using 24 human cancer cell lines.

155 oss-of-function screens performed in diverse human cancer cell lines.

156 We also measured expression by 15 human cancer cell lines.

157 tificial liposomes and cytotoxic activity on human cancer cell lines.

158 depletion of GGPP, in a variety of different human cancer cell lines.

159 Here, constricted migration of two human cancer cell types and primary mesenchymal stem cel

160 Human cancer cells (breast MCF7, breast-to-lung metastat

161 man DEAD-box RNA helicases in two permissive human cancer cells (HeLa and A549), one semi-permissive

162 be adapted to study the interactions between human cancer cells and a humanized bone microenvironment

163 icromolar antiproliferative activity towards human cancer cells and are active in vivo.

164 Here, the application of PINEM on whole human cancer cells and membrane vesicles isolated from t

165 Here, using human cancer cells and patient-derived xenografts in mic

166 down-regulation alters cell proliferation in human cancer cells by inducing both apoptosis and cell c

167 Impaired DDR in SALL4-deficient human cancer cells can be rescued by the restored expres

168 rome fibroblasts or by depletion of BLM from human cancer cells confirms a role for Sgs1/BLM in suppr

169 dated SF3B1 as a CYCLOPS gene and found that human cancer cells harboring partial SF3B1 copy-loss lac

170 ingly suppresses the growth of both, fly and human cancer cells harbouring oncogenic Ras mutations.

171 astasis to the bone rely on the injection of human cancer cells into the mouse skeleton.

172 MYXV tropism for human cancer cells is largely mediated by intracellular

173 We found that different mouse and human cancer cells produced greater levels of p40 than p

174 knockdown or LDHA Y10F rescue expression in human cancer cells resulted in decreased tumour metastas

175 The upregulation of HP1alpha in human cancer cells suppressed open chromatin, glycolysis

176 or partially permissive for the majority of human cancer cells that harbor defects in antiviral sign

177 Herein we show in a diverse array of human cancer cells that IMP2 overexpression stimulates a

178 Furthermore, TLS affords human cancer cells the ability to counteract chemotherap

179 l transition (EMT) markers were performed on human cancer cells treated with PRP.

180 hows promising antiproliferative activity on human cancer cells, endorsing their further exploration

181 ssed in Fbxo4 knockout cells, tissues and in human cancer cells, harbouring inactivating Fbxo4 mutati

182 rms various sizes of cytoplasmic clusters in human cancer cells, independent of protein expression le

183 that activation of NRF2, in either mouse or human cancer cells, leads to increased dependency on exo

184 impressive activities against drug resistant human cancer cells, making them desirable for potential

185 When exposed to human cancer cells, NK cell expanded ex vivo in the pres

186 In human cancer cells, we found that changes in the maximum

187 fy host factors relevant for MYXV tropism in human cancer cells, we performed a small interfering RNA

188 s chalcone derivatives inhibit the growth of human cancer cells.

189 natural genetic and epigenetic diversity of human cancer cells.

190 e can support the growth of various types of human cancer cells.

191 of calcitonin and each of its precursors in human cancer cells.

192 ring resistance to cisplatin and olaparib in human cancer cells.

193 er exogenous DNA damage and spontaneously in human cancer cells.

194 ools to study the properties of the BRCA1 in human cancer cells.

195 ee example separations: live and dead yeast; human cancer cells/red blood cells; and rodent fibroblas

196 ly dividing cells, including the majority of human cancers, cells bypass this growth limit through te

197 es have been published about mouse models of human cancer, collating information and data for a speci

198 tated gene in human cancer, and over half of human cancers contain p53 mutations.

199 RNA-binding protein whose overexpression in human cancer correlates with aggressive disease, drug re

200 mone calcitonin is intimately connected with human cancer development and proliferation.

201 xpression of MCM8 may play critical roles in human cancer development.

202 stic insights into driver events relevant to human cancer development.

203 signaling pathway plays an important role in human cancer development.

204 both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern.

205 ers based on increased expression in primary human cancers, facilitation of tumor growth in murine xe

206 Interrogation of human cancer gene expression data revealed that high TNC

207 complementing the sequencing-based census of human cancer genes.

208 mary leukemia/lymphoma and gastric cancer by human cancer genome sequencing efforts, suggesting both

209 About a third of all human cancers harbor mutations in one of the K-, N-, or

210 te the development of targeted therapies for human cancer harboring mutp53.

211 tional responsiveness and cellular growth in human cancers harboring activating mutations in MAPK sig

212 cer, recent discoveries indicate a subset of human cancers harboring amplifications in mTORC2-specifi

213 Elucidation of the mutational landscape of human cancer has progressed rapidly and been accompanied

214 ntum leap in our knowledge of mutagenesis in human cancers has resulted, stimulating a flurry of rese

215 A1), one of the most upregulated oncogene in human cancer, has an important role in gene expression,

216 sidered as a potential therapeutic target in human cancer, has been known to regulate many biological

217 Large-scale genomic analyses of human cancers have cataloged somatic point mutations tho

218 osphatase 2A (PP2A) function in a variety of human cancers have stimulated drug discovery efforts aim

219 ve results in vitro that are not relevant to human cancer hazard).

220 tivation of Ras signalling occurs in 30% of human cancers; however, activated Ras alone is not suffi

221 ions in migration and/or invasion of several human cancers; however, the role of MLK3 in colorectal c

222 We applied this concept to human cancer, hypothesizing that oncogenic mutations cou

223 led the genomic landscape of common forms of human cancer in unprecedented detail.

224 contribute to the pathogenesis of different human cancers in different geographic areas.

225 tion of the immunogenic targets expressed by human cancers in vivo.

226 Pin1 is prevalently overexpressed in human cancers including 70% of HCC, and promotes tumori

227 amplicon) is frequently observed in numerous human cancers including GBM.

228 mation has been associated with a variety of human cancers including prostate cancer.

229 core challenge in the clinical management of human cancer, including in urothelial carcinoma of the b

230 an important tool for treatment of advanced human cancers, including bladder cancer.

231 n PIK3CA are frequently found in a number of human cancers, including breast cancer, altering cellula

232 s been implicated in the etiology of various human cancers, including breast cancer.

233 y to interrogate the molecular landscapes of human cancers, including childhood brain tumors.

234 library targeting genes commonly mutated in human cancers into the brains of conditional-Cas9 mice r

235 etic and epigenetic heterogeneity underlying human cancers into therapeutic strategies is an ongoing

236 ich PP2A function is recurrently affected in human cancer, involving haploinsufficiency of PPP2R4, a

237 eep understanding of the immune landscape in human cancer is essential for guiding the development of

238 isms of how ALT maintains telomere length in human cancer is poorly understood.

239 Tyrosine-kinase inhibitor (TKI) therapy for human cancers is not curative, and relapse occurs owing

240 o catalog the genomic events associated with human cancer, it remains difficult to interpret and extr

241 gulation of the FOXO genes are infrequent in human cancers, it remains unclear how these tumour suppr

242 show that ecDNA was found in nearly half of human cancers; its frequency varied by tumour type, but

243 remodeling complex are frequently mutated in human cancers leading to epigenetic dependencies that ar

244 at measuring the levels of cyclin D3-CDK6 in human cancers might help to identify tumour subsets that

245 e in tumour cells in a variety of murine and human cancer models.

246 bset of HPV are the causative agents of many human cancers, most notably cervical cancer.

247 nts has improved patient outcomes in several human cancers, no such advance has been achieved in musc

248 cal imaging can visualize characteristics of human cancer noninvasively.

249 ection of differentially expressed miRNAs in human cancers obtained from microarray data.

250 rcomas seem to represent the best example in human cancers of the concept of epithelial-mesenchymal t

251 are aberrantly activated in a wide range of human cancers, often endowing tumors with aggressive pro

252 ver, this has not been well-characterized in human cancer patients.

253 yme for vitamin D, is often overexpressed in human cancers, potentially neutralizing the antitumor ef

254 nesis, is detectable in a yeast model of the human cancer predisposition disorder, Bloom's syndrome.

255 tance of YEATS domain-containing proteins in human cancer remains largely unknown.

256 s and nasal polyposis, but their function in human cancer remains unclear.

257 ing module, but its functional importance in human cancer remains unknown.

258 a comprehensive picture of miRNA editing in human cancers remains largely unexplored.

259 protein, or RNA) were examined across 11,219 human cancers representing 32 major types.

260 l death 1 (PD-1) antibody in mouse models of human cancer results in inhibition of tumor growth at do

261 Basal cell carcinoma (BCC), the most common human cancer, results from aberrant activation of the He

262 In this work, a mutation analysis of human cancer revealed subtle but impactful copy number g

263 eneration RNA sequencing (RNA-Seq) data from human cancer samples reveled thousands of uncharacterize

264 their incidence and striking similarities to human cancers, sharing similar clinical and pathologic f

265 as a critical lncRNA widely overexpressed in human cancers.Significance: These findings expand knowle

266 2O, a ubiquitin ligase overexpressed in some human cancers, specifically triggers the ubiquitination

267 FEN1 mutations have been detected in human cancer specimens and have been suggested to cause

268 n KPC mice of different ages and analysis of human cancer specimens revealed that RET expression is u

269 lecular regulation is validated in mouse and human cancer specimens.

270 rognosis and patient outcome in a variety of human cancer subtypes.

271 uman populations and is associated with many human cancers, such as nasopharyngeal carcinoma (NPC), H

272 presented by the frequent CDKN2A deletion in human cancer that, through inactivation of p14ARF, activ

273 p53 tumor suppressor and is elevated in many human cancers that retain wild-type p53.

274 role of DNA methyltransferase 3a (DNMT3a) in human cancer, the nature of its upstream regulator(s) an

275 nd are clinically linked to various types of human cancer; they are therefore being pursued as attrac

276 T), is overexpressed in approximately 90% of human cancers to maintain telomere length for cell immor

277 However, co-expression analysis using human cancer transcriptomic data is confounded by somati

278 ast, MAGE-F1 is highly amplified in multiple human cancer types and amplified tumors have increased m

279 compendium of 2218 primary tumours across 12 human cancer types and systematically screen for homozyg

280 Carcinomas constitute over 80% of all human cancer types with no effective therapy for metasta

281 WWOX gene deletions occur in a variety of human cancer types, and reduced Wwox protein expression

282 Analyzing 12 human cancer types, we find that, for most, highly aneup

283 and are orthologously methylated across most human cancer types.

284 ient survival in breast cancer and six other human cancer types.

285 helial cell cannibalism that is prevalent in human cancer, typically triggered by loss of matrix adhe

286 A complete understanding of human cancer variants requires new methods to systematic

287 s, for example, is frequently inactivated in human cancers via multiple mechanisms such as mutation.

288 e the development and progression of various human cancers via their gain of new functions (GOF) thro

289 Additionally, Amigo2 expression in human cancers was higher in liver metastatic lesions tha

290 in S100A4 is expressed at elevated levels in human cancers, where it has been linked to increased inv

291 on of ZEB1 has been reported in a variety of human cancers, where it is generally believed to foster

292 Protein kinases are frequently mutated in human cancers, which leads to altered signaling pathways

293 The genetic dependencies of human cancers widely vary.

294 Finally, human cancers with activating mutations in the MAPK casc

295 igand PD-L1, have been approved for treating human cancers with durable clinical benefit.

296 Here, we analyze data on human cancers with somatic mutations in two of the major

297 Chromosomal aberrations are a hallmark of human cancers, with complex cytogenetic rearrangements l

298 AF) complexes contribute to more than 20% of human cancers, with driving roles first identified in ma

299 ATC is one of the most aggressive human cancers, with rapid growth, tumor invasion, and de

300 ted in the pathogenesis of 10% to 15% of all human cancers worldwide.