ライフサイエンスコーパス: human cancer

1 dult stem cell homeostasis and is altered in human cancer.

2 ing ARF is the most commonly deleted gene in human cancer.

3 genes, several of which are dysregulated in human cancer.

4 oinformatics analyses of SFRP1 expression in human cancer.

5 r rationale for its frequent inactivation in human cancer.

6 cesses that contribute to the development of human cancer.

7 MAPK) signaling or genetic alteration across human cancer.

8 ptor tyrosine kinase is a driver oncogene in human cancer.

9 ferent clinical applications in all types of human cancer.

10 ighlighting novel opportunities for treating human cancer.

11 ing pathway, which is causally implicated in human cancer.

12 hastic model of LINE-1 (L1) transposition in human cancer.

13 est burdens of structural aberrations across human cancer.

14 of SNPs that control transcript isoforms in human cancer.

15 applied what I learned in tumor virology to human cancer.

16 tions that most resemble those that occur in human cancer.

17 p53, is the most frequently mutated gene in human cancer.

18 Misregulation of Wnt signaling is common in human cancer.

19 ajor process that drives genome evolution in human cancer.

20 studies, particularly in genomic studies of human cancer.

21 ne synthesis, is frequently overexpressed in human cancer.

22 olyomavirus (MCPyV), the first PyV linked to human cancer.

23 d to the testis but anomalously activated in human cancer.

24 pment, and homeostasis, and are disrupted in human cancers.

25 ome-wide copy-number alterations in multiple human cancers.

26 of the role of mtDNA genetics in relation to human cancers.

27 enomically and proteomically altered in many human cancers.

28 genes, is highly expressed in a majority of human cancers.

29 vel diagnostic and therapeutic biomarkers of human cancers.

30 t warrants further study in Parkin-deficient human cancers.

31 h pathway signaling is implicated in several human cancers.

32 irus that is the causative agent of multiple human cancers.

33 vement of CAR-T cell-based immunotherapy for human cancers.

34 sphatase whose activity is inhibited in most human cancers.

35 hy TP53 is the most commonly mutated gene in human cancers.

36 bclonal heterogeneity characteristic of many human cancers.

37 he functional impact of somatic mutations in human cancers.

38 ation along with patient survival in various human cancers.

39 oncogenic RAS mutations are often unique to human cancers.

40 rate recovery of the evolutionary history of human cancers.

41 the treatment landscape for a wide range of human cancers.

42 ) can mediate complete regression of certain human cancers.

43 ith poor prognosis in patients with multiple human cancers.

44 Specific CTCF binding events occur in human cancers.

45 ytic proteins as causative in high incidence human cancers.

46 3 is the most frequently mutated gene across human cancers.

47 e-scale mutation-rate variations observed in human cancers.

48 t impact on the formation and progression of human cancers.

49 sylation has also been identified in several human cancers.

50 agents was conserved across yeast, mice and human cancers.

51 of the gene encoding p27, CDKN1B, is rare in human cancers.

52 f indels across 2,575 whole genome sequenced human cancers.

53 ent tumor suppressor and commonly mutated in human cancers.

54 rotransposon overexpression is a hallmark of human cancers.

55 screens for synthetic lethal drug targets in human cancers.

56 1 expression is significantly upregulated in human cancers.

57 ible prognostic and diagnostic biomarkers in human cancers.

58 f the most frequent molecular alterations in human cancers.

59 ficacious immunotherapy for the treatment of human cancers.

60 in this pathway have been implicated in many human cancers.

61 stics of senescent T cells and their role in human cancers.

62 recurrent genetic alterations drives several human cancers.

63 ase signaling is implicated in many types of human cancers.

64 induce durable responses in a wide range of human cancers.

65 nt transformation and has been implicated in human cancers.

66 s are the most commonly mutated oncogenes in human cancers.

67 red to be an important therapeutic target in human cancers.

68 class switch events were observed in diverse human cancers.

69 implicated in the pathology of a variety of human cancers.

70 7p13.1, a hotspot of monoallelic deletion in human cancers.

71 gnaling, is constitutively active in ~70% of human cancers.

72 jor oncogenes with a high occurrence rate in human cancers.

73 infiltration and patient survival in diverse human cancers.

74 new therapeutic agents that target ERBB3 in human cancers.

75 or p53 is somatically mutated in half of all human cancers.

76 the CD44-mediated effects on ferroptosis in human cancers.

77 f the PI3K pathway is a common alteration in human cancers.

78 of the most frequently inactivated genes in human cancers.

79 derestimates mitotic dysfunction in advanced human cancers.

80 rough a transcriptome sequencing analysis of human cancers.

81 s has produced treatment advances in various human cancers.

82 that Pten-NOLC1 gene fusion is a driver for human cancers.

83 ed genes overlap with recurrent mutations in human cancers.

84 tion as a potential therapeutic modality for human cancers.

85 y therapeutics are being leveraged to target human cancers.

86 ad to chromosomal instability, a hallmark of human cancers.

87 ago, mutations in KRAS exist in ~30% of all human cancers.

88 that is frequently overexpressed in various human cancers.

89 RK signaling axis is frequently activated in human cancers.

90 on worldwide and is associated with numerous human cancers.

91 ific kinase, is also frequently activated in human cancers.

92 as been shown to be overexpressed in several human cancers.

93 -wide CTCF binding patterns across different human cancers.

94 nd UBR5 genes were coamplified in MYC-driven human cancers.

95 mination and mutagenesis in driving multiple human cancers.

96 ow mutations in these proteins contribute to human cancers(20,21).

97 coupled early tumor ischemia/reperfusion to human cancer ablation.

98 Moreover, ALOX12 missense mutations from human cancers abrogate its ability to oxygenate polyunsa

99 Most human cancers acquire mutations causing defects in the p

100 We conclude that loss of MCPH1 is common in human cancer and is likely to be a cause of CA.

101 omplexes (also called BAF complexes) in both human cancer and neurological disorders, suggesting new

102 Importantly, human cancer and other disease mutations map to nearly e

103 etwork is one of the most frequent events in human cancer and serves to disconnect the control of cel

104 understanding of humoral immune responses in human cancer and suggest that tumour-infiltrating B cell

105 Proof-of-concept studies on human cancers and cardiovascular diseases further showca

106 oss-of-function mutations in SPRED1 occur in human cancers and cause the developmental disorder, Legi

107 gram is associated with poor survival across human cancers and demonstrates chemoresistance in mice.

108 ARID1A mutations occur in human cancers and drive cancer development.

109 t that OGA is upregulated in a wide range of human cancers and drives aerobic glycolysis and tumor gr

110 have found that it is overexpressed in many human cancers and functions as an oncogene.

111 -Myc) is a common feature in the majority of human cancers and has been linked to oncogenic malignanc

112 demethylation enzyme TET2 is associated with human cancers and has been linked to stem cell traits in

113 nic event, occurring in approximately 25% of human cancers and has no effective treatment.

114 gene fusions have been identified in various human cancers and identifying the essential components o

115 ndeed, MYC is overexpressed in up to ~50% of human cancers and is considered a highly validated antic

116 PKM2 is expressed in many human cancers and is regulated by complex mechanisms tha

117 dification pathways are also misregulated in human cancers and may be ideal targets of cancer therapy

118 Further, using a pan-cancer analysis of human cancers and multiple mouse models of tumour progre

119 HP2) is an attractive therapeutic target for human cancers and other human diseases.

120 As ILC2s and T cells co-exist in human cancers and share stimulatory and inhibitory pathw

121 have started to emerge in the development of human cancers and viral infections, but their relevance

122 The Ras GTPases are frequently mutated in human cancer, and, although the Raf kinases are essentia

123 me NOX4, which is upregulated by CAF in many human cancers, and compared this with TGFbeta1 inhibitio

124 ppressors that are frequently inactivated in human cancers, and FOXO3 is the second most replicated g

125 hosphatase PP2A subunits occur in a range of human cancers, and partial loss of PP2A function contrib

126 y may be underrepresented in a wide range of human cancers, and several of these genes warrant furthe

127 Further, MEILB2-BRME1 is activated in many human cancers, and somatically expressed MEILB2-BRME1 im

128 lterations in this pathway are found in most human cancers, and specific cyclin-dependent kinase Cdk4

129 his motif are found at low frequency in some human cancers, and substitution of Y80 by a phosphomimet

130 gene is the most frequently mutated gene in human cancers, and the majority of TP53 mutations are mi

131 telomerase are found in the vast majority of human cancers, and we have recently begun to understand

132 However, the causes of CA in human cancer are unclear.

133 frequent genetic alterations across multiple human cancers are mutations in TP53 and the activation o

134 utic strategies for treating the devastating human cancers associated with this new tumorigenic virus

135 (ctDNA) allows tracking of the evolution of human cancers at high resolution, overcoming many limita

136 red by both mutation and allelic deletion in human cancer, but the functional implications of such al

137 e 10) levels are frequently found reduced in human cancers, but how PTEN is down-regulated is not ful

138 s are frequent drivers of multiple different human cancers, but the development of therapeutic strate

139 inib appears to be a promising treatment for human cancer cachexia due to its selective inhibition of

140 gests that other genes frequently mutated in human cancer can be immunogenic, thus offering a rapid w

141 TPMs, accounted for how approximately 90% of human cancers can aberrantly activate telomerase.

142 Indeed, domain disruptions in human cancers can lead to misregulation of gene expressi

143 s expressed in tumor macrophages in over 200 human cancer cases and inversely correlated with prolong

144 uch as nucleotides and are indispensable for human cancer cell growth.

145 ns in uracil pattern upon drug treatments in human cancer cell line models derived from HCT116.

146 ine synthesis, and inhibited tumor growth in human cancer cell line xenografts.

147 tumour spheroids formed from two established human cancer cell lines (HCT116 and CAL27) to single and

148 which has promising activity against several human cancer cell lines and inhibits tumor cell migratio

149 Gene expression profiling of 165 pairs of human cancer cell lines and their Cas9-expressing deriva

150 Human cancer cell lines are frequently used as model sys

151 s showed improved activity against mouse and human cancer cell lines defective in O-linked glycosylat

152 Multifaceted characterizations of human cancer cell lines hold huge treasures for cancer r

153 HepG2 is one of the most widely used human cancer cell lines in biomedical research and one o

154 e of determining the metastatic potential of human cancer cell lines in mouse xenografts at scale.

155 The new compounds were screened in the 60 human cancer cell lines of the NCI drug screen and showe

156 gainst A549, DU 145, HeLa, HCT 116, and MCF7 human cancer cell lines provide insights into the impact

157 ity assays against a representative panel of human cancer cell lines revealed that polyamines L1a and

158 On average, the sensitivity of human cancer cell lines to DNMDP is correlated with PDE3

159 s of E3 ligase components across hundreds of human cancer cell lines(3-5), we identify CR8-a cyclin-d

160 these observations, Akt3 up-regulates p53 in human cancer cell lines, and the expression of Akt3 posi

161 25-fold increased cytotoxicity against five human cancer cell lines, and up to 70-fold less toxicity

162 growth inhibitory activities against various human cancer cell lines, including A549, Caco-2, and SF2

163 cytotoxic and target-mediated selectivity on human cancer cell lines.

164 ts proliferation, migration, and invasion in human cancer cell lines.

165 itochondrial membrane dissipation by DOX, in human cancer cell lines.

166 and celery that inhibits growth of fungi and human cancer cell lines.

167 nd evaluation of their activity against five human cancer cell lines.

168 on in lal(-/-) Tregs and Bregs, and improves human cancer cell rejection.

169 ion in the lal(-/-) lymph nodes and improves human cancer cell rejection.

170 completely inhibited ADO production in both human cancer cells and CD8(+) T cells.

171 ybrid nucleosomes that are known to exist in human cancer cells and contain H3 histone variants CENP-

172 orylation can also be found in ERK-activated human cancer cells and contribute to tumorigenesis.

173 or-type kappa (PTPRK), as a Wnt inhibitor in human cancer cells and in the Spemann organizer of Xenop

174 Importantly, PTEN null human cancer cells and in vivo murine models are sensiti

175 analyze cell cycles in deep lineage trees of human cancer cells and mouse embryonic stem cells and de

176 e degradation of stalled RFs in KB2P1.21 and human cancer cells by recruiting the base excision repai

177 Acute knockdown of DHX33 in multiple human cancer cells caused decreased Bcl-2 protein level,

178 eports showed that the knockdown of RBM10 in human cancer cells enhances the growth of mouse tumor xe

179 DNA damage, and apoptosis were increased in human cancer cells following depletion of the B-family D

180 ocompromised zebrafish that robustly engraft human cancer cells for in excess of 28 d.

181 rtly after the discovery of RAS mutations in human cancer cells nearly 40 years ago.

182 inhibitor and show that CD80 is expressed by human cancer cells originating from both solid epithelia

183 ession cloning approach to identify genes in human cancer cells that are able to complement the loss

184 nt findings (Tsabar et al.) demonstrate that human cancer cells that evade the cell cycle blockage no

185 In human cancer cells that harbor mutant KRAS and WT p53 (p

186 rms and performed experiments with suspended human cancer cells to characterize the performance of th

187 Using Drosophila neuroblasts and human cancer cells to study mitotic spindle assembly in

188 ell, an interpretable deep learning model of human cancer cells trained on the responses of 1,235 tum

189 d antiproliferative activity toward cultured human cancer cells, a favorable in vivo pharmacokinetic

190 In cocultures with primary human cancer cells, actively migrating monocyte-derived

191 Here, we report that, in human cancer cells, BRD4S forms nuclear puncta that poss

192 r differences in DeltaPsim in unsynchronized human cancer cells, cells synchronized in G1, S, and G2,

193 In human cancer cells, depletion of miR181ab1 impaired prol

194 In both C. elegans and human cancer cells, ether-lipid synthesis protects again

195 ct to induce high cytotoxicity in a range of human cancer cells, including T98g (glioma multiforme),

196 Whereas this complex was highly cytotoxic in human cancer cells, it showed low toxicity in hemolysis

197 exhibits cytotoxic activity against various human cancer cells, killing SW48 colon cancer cells in p

198 ve G-quadruplex ligand that, when studied in human cancer cells, proved to be able to stabilize both

199 tural studies of p53 assemblies derived from human cancer cells.

200 crease in aneuploidy in checkpoint-deficient human cancer cells.

201 lex structures and increase R loop levels in human cancer cells.

202 ty to trigger DNA damage in rapidly dividing human cancer cells.

203 LRPPRC acted as an inhibitor of autophagy in human cancer cells.

204 ave demonstrated a dual targeting of GLS2 in human cancer cells.

205 sly increase R-loop levels within minutes in human cancer cells.

206 rogate the cytotoxic effects of cisplatin on human cancer cells.

207 stem in regulating the migration of amoeboid human cancer cells.

208 tive in three different models of hypoxia in human cancers compared to the parental cytotoxic agent a

209 A large fraction of human cancers contain genetic alterations within the Mit

210 ted and localized to the nucleus in multiple human cancers, correlating with treatment resistance and

211 PH1 deep gene deletions are seen in 5-15% of human cancers, depending on the anatomic site of the tum

212 Genetic alterations commonly found in human cancers (e.g. mutations in KRAS or loss of PTEN) h

213 may therefore have a more important role in human cancer etiology than previously thought.

214 Immunohistochemical staining of human cancers for endogenous APCN showed elevated expres

215 Overexpression of D-type cyclins in human cancer frequently occurs as a result of protein st

216 urrent somatic single point mutations in the human cancer genome.

217 g between recurrent and rare variants in the human cancer genome.

218 signature was detected in a subset of 5,876 human cancer genomes from two independent cohorts, predo

219 sis and are enriched at mutation hotspots in human cancer genomes, implicating them in disease etiolo

220 Human cancers harbor substantial genetic, epigenetic, an

221 We speculate that human cancers harboring these mTOR mutations, such as AT

222 on of tumor suppressors for the treatment of human cancer has been a long sought, yet elusive, strate

223 Mouse models of human cancer have transformed our ability to link geneti

224 mplications of ERBB2 alternative splicing in human cancers have not been explored.

225 hich are mutated in approximately 24% of all human cancers, have earned a well-deserved reputation as

226 mmunity, and shortened host survival in many human cancer histologies and in murine cancer models.

227 sferases, are frequently mutated in multiple human cancers; however, the molecular basis of how these

228 rns of substitution mutational signatures in human cancer; (iii) information on false-positive discov

229 Unlike other human cancers, in which all primary tumors arise de novo

230 d as a highly mutated driver in a variety of human cancers including breast cancer.

231 ase 5B) is frequently upregulated in various human cancers including prostate cancer.

232 Despite its importance in human cancers, including colorectal cancers (CRC), oncog

233 s mutated at a high frequency only in select human cancers, including malignant mesothelioma and meni

234 o play a detrimental role in many metastatic human cancers, including melanoma and other nonmelanoma

235 are correlated with prognosis in a range of human cancers, including neuroblastoma, cervical, brain,

236 A-to-I editing levels are high in several human cancers, including thyroid cancer, but ADAR1 edita

237 subunit of PI3K and is frequently mutated in human cancers, including ~30% of colorectal cancer.

238 or mutations occurring with low frequency in human cancers is an ongoing endeavor.

239 -2 family of proteins, whose upregulation in human cancers is associated with high tumor grade, poor

240 roteins, whose upregulation when observed in human cancers is associated with high tumor grade, poor

241 this, we analyzed TERT expression across 10 human cancer lines using single-molecule RNA fluorescent

242 up-regulated on the cell surface of several human cancers, making it a promising therapeutic target

243 To assess human cancer metabolism, here we report a method to coll

244 tation signature similar to aging-associated human cancer mutation signatures.

245 Further, in 33 human cancers (n = 9502) MYC and TWIST1 predict poor sur

246 unities for TNBC and other highly aggressive human cancers of epithelial origin.

247 ighly regulated process that is perturbed in human cancers, often through activation of the PI3K/mTOR

248 maps CHD4 mutations that are associated with human cancer or the intellectual disability disorder Sif

249 bility, they can accelerate the evolution of human cancers or lead to the development of genetically

250 ss tumors, but they are often inactivated in human cancers overexpressing inhibitory proteins.

251 Compared with healthy controls, human cancer patients were also found to have higher lev

252 n repertoire sequencing studies conducted on human cancer patients, with a focus on studies of the T-

253 lecules similar to escape mechanisms seen in human cancer patients.

254 platinum-based drugs on plasma S1P levels in human cancer patients.

255 eveal mechanisms whereby myeloid cells drive human cancer progression by thwarting protective immunit

256 ecular, cellular and biophysical features of human cancer progression.

257 ever, the frequency of domain disruptions in human cancers remains unclear.

258 MYC is deregulated in > 50% of human cancers, rendering it an attractive drug target.

259 Analysis of patient datasets across human cancers revealed distinct inflammatory TME phenoty

260 Analysis of human cancers reveals similar transcriptional changes in

261 case studies of large curated datasets from human cancer RNA-Seq, where we identify novel putative b

262 Pten-NOLC1 fusion is present in primary human cancer samples and cancer cell lines from differen

263 sistent with these results, we observed that human cancer samples with deficient B12/FA uptake demons

264 analyses from datasets of commonly occurring human cancers show that higher levels of ZNF281 correlat

265 otein stability and consistent with this, in human cancer specimens, low nuclear BARD1 protein strong

266 Similar experiments were then carried out in human cancer spheroids that provide a realistic tumor mo

267 functions as oncogenic driver in a range of human cancers such as neuroblastoma.

268 The expression pattern of DeltaNp63 in human cancer suggests dynamic regulation of this isoform

269 ch TP53, the most frequently mutated gene in human cancer, suppresses tumorigenesis remain unclear.

270 gh TP53 is the most commonly mutated gene in human cancers, the p53-dependent transcriptional program

271 ins, as well as MS imaging of N-glycans from human cancer tissue sections.

272 d by higher human FcRn (hFcRn) expression in human cancer tissue that provides the mechanistic basis

273 Eight out of ten different human cancer tissue types screened for hFcRn expression

274 substrate utilization in purine synthesis in human cancer tissues should be considered when targeting

275 and TWIST1 generally appear to cooperate in human cancer to elicit a cytokinome that enables metasta

276 o chromosome ends and is upregulated in most human cancers to enable limitless proliferation.

277 mbined with other chemotherapeutic agents in human cancer trials.

278 ll receptor (TCR) recognized and killed most human cancer types via the monomorphic MHC class I-relat

279 dentifies overexpression of hFcRn in several human cancer types with mechanistic data suggesting hFcR

280 lysis of purified Tregs sorted from multiple human cancer types, we identified a conserved Treg immun

281 e delineated outstanding genomic zones in 17 human cancer types.

282 d with negative patient outcomes in multiple human cancer types.

283 pair whole-genome datasets from 42 different human cancer types.

284 rug target classification for nine different human cancer types.

285 e and 45 truncating RNF43 mutations found in human cancers using a combination of cell-based reporter

286 miR-200c were significantly elevated in all human cancer versus all control blood samples.

287 As the first discovered human cancer virus, Epstein-Barr virus (EBV) causes Burk

288 trosome loss-which has not been described in human cancer-was associated with PCa progression.

289 of FOXO1 has been reported in many types of human cancer, we sought to investigate whether restorati

290 well-known oncoprotein overexpressed in most human cancers, we show that FBXL16 stabilizes C-MYC by a

291 Mutations of the cohesin complex in human cancer were first discovered ~10 years ago.

292 Fascin is also highly up-regulated in human cancers, where it increases invasive cell behavior

293 l the repertoire of mutational signatures in human cancers while others are either novel or composite

294 naling, and cytotoxic T cell infiltration in human cancers, while a FBXO44-immune gene signature corr

295 es linked to localized gene amplification in human cancers with acquired drug resistance or oncogene

296 Human cancers with activating RAS mutations are typicall

297 ors might be novel tools in the treatment of human cancers with deregulated FKBP51.

298 argeting of ligand-dependent Hh signaling in human cancers with somatic mutations in both TP53 and RB

299 quamous cell carcinomas, are the most common human cancers worldwide.

300 Mutant Ras proteins are important drivers of human cancers, yet no approved drugs act directly on thi