ライフサイエンスコーパス: multiple tumor

1 ) and 45 were "redundant" (distributed among multiple tumors).

2 e in tumor size in a subset of patients with multiple tumors.

3 Statins inhibit the growth of multiple tumors.

4 ation, and its expression is misregulated in multiple tumors.

5 ci recurrently affected by LOH events across multiple tumors.

6 ied in the characterization and treatment of multiple tumors.

7 tion seem to contribute to the occurrence of multiple tumors.

8 r very large CFS gene that is inactivated in multiple tumors.

9 elta11/delta11)Chk2-/- female mice developed multiple tumors.

10 activity and exhibits aberrant expression in multiple tumors.

11 among Atp2a2(+/-) mice, and many animals had multiple tumors.

12 , we identified several sequence variants in multiple tumors.

13 t was recurrently somatically inactivated in multiple tumors.

14 -Lindau disease (VHL) are at risk to develop multiple tumors.

15 cally reduce cell invasion and metastasis in multiple tumors.

16 er tumor size (1.09; 1.02-1.16), presence of multiple tumors (1.70; 1.43-2.02), lymph node metastasis

17 transplant patients were more likely to have multiple tumors (78% vs 28%, P < 0.001).Overall (OS) and

18 90)Y treatment of mNET if the study included multiple tumor and microsphere types.

19 Multiple tumor and surgical factors are associated with

20 d an effective approach for the treatment of multiple tumors and anticipate that the molecules disclo

21 ly analyzed their differential regulation in multiple tumors and found severe deregulation in liver,

22 aling 30 transcripts with high expression in multiple tumors and little or no expression in the norma

23 ydrogenase-2 mutations has been described in multiple tumors and more recently in chondrosarcomas.

24 Predictors of dropout include multiple tumors and tumors with a diameter >3 cm.

25 ; P < .001), among patients with N1 disease, multiple tumors and vascular invasion, either alone or t

26 pha-fetoprotein level greater than 20 ng/mL, multiple tumors, and ALBI grade 2 or 3 were associated w

27 ridine (FdUrd, floxuridine) have activity in multiple tumors, and both agents undergo intracellular p

28 ammed death ligand 1 (PD-L1) is expressed by multiple tumors, and its interaction with PD-1 resulted

29 as many Gadd45a-null than wild-type mice had multiple tumors, and three times as many had multiple ma

30 effective vaccine formulation would deliver multiple tumor antigens in a fashion that potently stimu

31 pansion of functional T cells that recognize multiple tumor antigens, including HPV16 E7, and these T

32 onses include multiple T cell clones against multiple tumor antigens.

33 more than 5 cm, and (c) patients with either multiple tumors, any more than 5 cm, or tumor with major

34 Multiple tumors are a hallmark of neurofibromatosis type

35 ns recurring at the same genomic site across multiple tumors are actually passenger events, recurring

36 Multiple tumors arising in the same mouse had distinct X

37 crease; P < 0.05) and more likely to develop multiple tumors, as 20% of the beta-pol(+/-) animals die

38 of CD4 T cell activity to promote priming to multiple tumor-associated Ags.

39 tumor cells serve as the superior source of multiple tumor-associated antigens (TAAs) to pulse dendr

40 e nullizygous for ARF, p53, and Mdm2 develop multiple tumors at a frequency greater than those observ

41 Multiple tumor-bearing mice were evaluated with 68Ga-DOT

42 Fair skin type, multiple tumors before retransplantation, treatment with

43 Simultaneous detection of multiple tumor biomarkers in body fluids could facilitat

44 ions of differential DNA copy number between multiple tumor biopsies that correlated with altered exp

45 Multiple tumor burden in Ovca1 heterozygotes that were a

46 strate that cyclin D1 action is conserved in multiple tumor cell backgrounds, inhibiting AR-dependent

47 Chronic cadmium exposure produced multiple tumor cell characteristics in HPDE cells and CC

48 6 kinase (RSK) family has been implicated in multiple tumor cell functions, the full understanding of

49 on of proliferation and cytotoxicity against multiple tumor cell lines and found to be potent and eff

50 an improved ability to reduce the growth of multiple tumor cell lines and to inhibit ligand-induced

51 ipase C gamma, and focal adhesion kinase, in multiple tumor cell lines in a pattern correlating to th

52 Investigations using multiple tumor cell lines in the orthotopic model sugges

53 Transfection of HDAC5 inhibited growth of multiple tumor cell lines including U2OS osteogenic sarc

54 t cooperate with Pumilio to target E2F3, and multiple tumor cell lines shorten the 3' end of the E2F3

55 nctional validation using siRNA knockdown in multiple tumor cell lines showed that C13orf34, MAD2L1,

56 ion and increased cytotoxic activity against multiple tumor cell lines when maintained at low cytokin

57 xhibited potent in vitro cytotoxicity toward multiple tumor cell lines with a mean GI50 of 100 nM.

58 of cancer cell types, de-stabilized EGFR in multiple tumor cell lines.

59 irmed by reciprocal coimmunoprecipitation in multiple tumor cell lines.

60 feration in non-tumorigenic cells but not in multiple tumor cell lines.

61 potencies at low nanomolar concentrations in multiple tumor cell lines.

62 MDA-7/IL-24 protein in inducing apoptosis in multiple tumor cell lines.

63 Lapatinib and obatoclax killed multiple tumor cell types, and cells lacking phosphatase

64 ed mechanism that promotes MET expression in multiple tumor cell types.

65 utational tools to separate contributions of multiple tumor clones and assorted stromal and infiltrat

66 0% of the beta-pol(+/-) animals died bearing multiple tumors compared with only 5% of the beta-pol(+/

67 rated in diagnostic samples and persisted in multiple tumor compartments over time, except in patient

68 bled these durable improvements by targeting multiple tumor compartments to (i) increase intratumoral

69 fied known drivers of melanoma and predicted multiple tumor dependencies.

70 k, intraperitoneally injected ID8 cells form multiple tumor deposits and ascites that resemble human

71 function of the p53 pathway is preserved in multiple tumor-derived cell lines expressing wild-type p

72 Multiple tumor-derived KDM2B mutations impaired the func

73 Multiple tumors displayed similarities in abrogated gene

74 ons have VHL disease and are at high risk of multiple tumors (e.g., CNS hemangioblastomas, pheochromo

75 es defines subgroups with high MYC levels in multiple tumor entities and identifies novel targets for

76 licable cancer vaccines, which could combine multiple tumor epitopes defined by CD8(+) CTLs, as well

77 strongly correlates with NRF2 activation in multiple tumor expression datasets.

78 enotype had a greater tendency toward having multiple tumor foci and demonstrated significantly short

79 ation results in progressive transduction of multiple tumor foci in the liver, without evidence of sp

80 to target gene- and virus-based therapies to multiple tumor foci located within an organ, such as the

81 81% of the Rint-1 heterozygotes succumbed to multiple tumor formation with haploinsufficiency during

82 NF2 cause neurofibromatosis type 2 (NF2), a multiple tumor forming disease of the nervous system.

83 sed metastases in an individual, we analyzed multiple tumors from men with disseminated prostate canc

84 is improving, so are the demands to analyze multiple tumor genomes simultaneously growing.

85 , revealed a molecular subtype field effect; multiple tumors had different mutations that deregulated

86 P < .001), tumor size (HR, 1.50; P < .001), multiple tumors (HR, 1.58; P < .001), cirrhosis (HR, 1.5

87 lonal heterogeneity and antigen selection in multiple tumors, implicating B-cell receptor-mediated an

88 The occurrence of multiple tumors in an organ heralds a rapidly fatal cour

89 d persistence of targeted neoepitopes across multiple tumors in single LS patients has not been rigor

90 s, ovary, testis, and neuronal tissues, with multiple tumors in some fish.

91 disorder characterized by the development of multiple tumors in the central nervous system, most nota

92 cancer syndrome, characterized primarily by multiple tumors in the parathyroid glands, endocrine pan

93 demonstrated different clonality patterns in multiple tumors in the same organ in each individual pat

94 durable clinical responses in patients with multiple tumor indications.

95 shaped the transcriptional landscape across multiple tumor-infiltrating immune cell types.

96 If a cancer patient develops multiple tumors, it is sometimes impossible to determine

97 Coronin 1C is overexpressed in multiple tumors, leading to the widely held view that th

98 e, and tissue-sparing assays relevant across multiple tumor lineages in the Clinical Laboratory Impro

99 icting shorter OS included large tumor size, multiple tumors, lymph node metastasis, and vascular inv

100 The overexpression of Aurora kinases in multiple tumors makes these kinases appealing targets fo

101 ion images yields high resolution 3D maps of multiple tumor microenvironment components and biomarker

102 ing a microfluidic device design that mimics multiple tumor microenvironmental cues concurrently with

103 nd CD8(+) T cells are kinetically induced in multiple tumor microenvironments in mice and humans.

104 rently immunosuppressive, and irradiation of multiple tumors might optimize systemic effects of radio

105 Using multiple tumor models and diverse donor-host combination

106 est and compare their results with those for multiple tumor models and tumor types using RTCGD.

107 LGK974 is potent and efficacious in multiple tumor models at well-tolerated doses in vivo, i

108 tically impaired angiogenesis by engineering multiple tumor models deprived of endoglin, a co-recepto

109 (89)Zr-5B1 localized to multiple tumor models representing diseases with undetec

110 nucleolin aptamer inhibited tumor growth in multiple tumor models without measurable toxicity, was c

111 ficantly boosted the efficacy of PTX@HSST on multiple tumor models, including lung metastatic tumors

112 of IGF-IR, which shows antitumor activity in multiple tumor models, including sarcoma.

113 In multiple tumor models, intravenous peptibody injection c

114 d decreased angiogenesis and tumor burden in multiple tumor models.

115 nabling larger zones of tumor destruction in multiple tumor models.

116 rrelated with enhanced invasive potential in multiple tumor models.

117 systemic tumor-specific T cell responses in multiple tumor models.

118 astasis in two genetic mouse backgrounds and multiple tumor models.

119 ystems that is associated with resistance in multiple tumor models: lymphoma, lung and colon.

120 man cancer have established the existence of multiple tumor modifiers that influence parameters of ca

121 Multiple tumors more often occurred in patients with SDH

122 tumors (n = 1121, 64%) were more common than multiple tumors (n = 624, 36%).

123 , tumor necrosis factor ligands that bind to multiple tumor necrosis factor receptor and have been re

124 arize key microbiota alterations observed in multiple tumor niches, their association with clinical s

125 ach tumor were sufficiently distinctive that multiple tumor nodules from the same patient could usual

126 a single tumor and microvascular invasion or multiple tumors, none more than 5 cm, and (c) patients w

127 ications-and individual genes are mutated in multiple tumors, notably TCF3, NOTCH1, MYD88, and BRAF.

128 ectrum of neoplasms, usually presenting with multiple tumors of different histological types and dyin

129 TSC is characterized by multiple tumors of the brain, kidney, heart, and skin.

130 sis, an autosomal dominant predisposition to multiple tumors of the skin appendages.

131 the sample, and the ctDNA may originate from multiple tumors or clones.

132 nt of ER status, especially in patients with multiple tumors or for tumors that are difficult to biop

133 mor; less frequently had a pancreatic tumor, multiple tumors, or developed a new lesion postoperative

134 umor progression, with patches, plaques, and multiple tumors over the body (up to 3 cm; Fig 1).

135 rosis/cirrhosis of the host liver (P =.001), multiple tumors (P =.007), and tumor size greater than 5

136 Profiling multiple tumors per patient enabled by the CMT model all

137 The reported multiple tumor phenotype of carriers is not easily recon

138 This multiple tumor phenotype was not previously observed wit

139 Fbx4(+/-) and Fbx4(-/-) mice succumb to multiple tumor phenotypes, including lymphomas, histiocy

140 Although ostensibly induced by multiple tumor-produced cytokines (tumorkines), their fu

141 cancer, at least in part, through modulating multiple tumor-promoting autocrine/paracrine factors.

142 Expression and secretion of multiple tumor-promoting cytokines or chemokines in the

143 Our results suggest that Id-1 regulates multiple tumor-promoting pathways in glioblastoma and th

144 that these cells are activated to signal via multiple tumor-promoting reparatory, trophic, angiogenic

145 ation of lesions observed across a cohort of multiple tumors provides statistically significant evide

146 inhibition of growth of liver metastases of multiple tumors regardless of their TLR5 status.

147 For PCCA, multiple tumors (relative risk [RR] = 3.5; 95% confidenc

148 By coupling the split dCas12a design to multiple tumor-relevant promoters, we provide a proof of

149 oid mediators, eliminated micrometastases in multiple tumor-resection models, resulting in long-term

150 tation read counts as input and can leverage multiple tumor samples accurately and efficiently.

151 pulation bulk sequencing data collected from multiple tumor samples from a patient.

152 clone-specific CNAs and WGDs jointly across multiple tumor samples from the same patient.

153 ed in the hundreds, and many were present in multiple tumor sections, implying clonal distribution.

154 DNA specimens from multiple tumor sites and normal tissue controls were obt

155 DNA was extracted from normal tissue and multiple tumor sites in patients with PSCP.

156 However, seven out of 12 animals developed multiple tumors, some with metastases.

157 Multiple tumor specific ceramide and sphingomyelin speci

158 h expression levels that distinguish between multiple tumor subclasses, normal and tumor tissues, and

159 mor heterogeneity can drive the evolution of multiple tumor subclones harboring unique resistance mec

160 isons of (1) tumor versus normal tissue, (2) multiple tumor subtypes and (3) survival times.

161 anscriptomic modules abnormally expressed in multiple tumors, such that the genes in a module were li

162 g different human tissues and upregulated in multiple tumors, suggesting that c-Drosha plays a unique

163 ment-damaged tissues, inducing production of multiple tumor-supporting secreted factors.

164 ally imposed damage, are thought to activate multiple tumor suppressive pathways, particularly apopto

165 The progression of nevi is restrained by multiple tumor-suppressive mechanisms.

166 Multiple tumor-suppressive miRNAs were downregulated coo

167 of the INK4 molecules, p16, is also known as multiple tumor suppressor and has been found to be mutat

168 ARF has multiple tumor suppressor functions, some of which are m

169 g prostate, indicate that there are probably multiple tumor suppressor genes (TSGs) present in this r

170 including prostate, indicate that there are multiple tumor suppressor genes (TSGs) present within th

171 While multiple tumor suppressor genes are likely to reside on

172 These results suggest that multiple tumor suppressor genes are located on five dist

173 LOH analysis suggests that multiple tumor suppressor genes play a role in the devel

174 as remained obscure, one possibility is that multiple tumor suppressor genes residing on this chromos

175 hin the 6q21 region, and loss of function of multiple tumor suppressor genes within 6q21 may be a cri

176 tic status of NB by epigenetic repression of multiple tumor suppressor genes.

177 l adhesion and modulation of the activity of multiple tumor suppressor genes.

178 wild-type in KS and PEL, down-regulation of multiple tumor suppressor miRNAs provides a novel, alter

179 c function by way of epigenetic silencing of multiple tumor suppressor miRNAs.

180 Senescence stimuli activate multiple tumor suppressor pathways to initiate cycle arr

181 tead genetic data point to a contribution of multiple tumor suppressor pathways, including p53, Rb/IN

182 this protein, and propose that by disrupting multiple tumor suppressor pathways, SKI functions as a m

183 eading to the cytoplasmic mislocalization of multiple tumor suppressor proteins.

184 or p16(INK4a) (hereafter p16) functions as a multiple tumor suppressor.

185 These studies suggest that multiple tumor suppressor/oncogene pathways coordinately

186 tional intratumor heterogeneity was seen for multiple tumor-suppressor genes converging on loss of fu

187 gions permits the simultaneous repression of multiple tumor suppressors by broadly decreasing the res

188 SCLC in which CGRP(CreER) was used to ablate multiple tumor suppressors in PNECs that were simultaneo

189 recognition event is implicated in silencing multiple tumor suppressors.

190 Schwannomatosis is a multiple tumor syndrome in which patients develop benign

191 the setting of nonhereditary and hereditary multiple tumor syndromes continues to expand.

192 anding of the molecular pathogenesis of GIST multiple tumor syndromes, we can refine our screening pr

193 tions to our knowledge about hereditary GIST multiple tumor syndromes.

194 nocarriers selectively delivered melittin to multiple tumor targets, including endothelial and cancer

195 y mature and exhibited enhanced ADCC against multiple tumor targets.

196 h have defective TGF-beta signaling, develop multiple tumors that are phenotypically similar to those

197 mach, whereas 100% of the +/- mice developed multiple tumors that were a mixture of adenomas, squamou

198 The patient subsequently developed multiple tumors throughout the body with similar histopa

199 WNT pathways are aberrantly regulated in multiple tumor types (albeit in a context-dependent mann

200 in the miR-106b family are overexpressed in multiple tumor types and are correlated with the express

201 er511 phosphorylation and VEGF production in multiple tumor types and correlates with poor clinical o

202 xidoreductase 1 (NQO1) is highly enriched in multiple tumor types and has emerged as a promising targ

203 putative TAA demonstrating overexpression in multiple tumor types and low or absent expression in ess

204 nectin splice variant, which is expressed by multiple tumor types and on neovasculature, are likewise

205 The high expression across multiple tumor types and restricted expression in normal

206 Overexpression of Bcl-2 is seen in multiple tumor types and targeting Bcl-2 may provide the

207 ve demonstrated the overexpression of Ran in multiple tumor types and that its expression is correlat

208 ts with altered APA isoform abundance across multiple tumor types are controlled by NMD.

209 s a candidate tumor suppressor implicated in multiple tumor types based on mutations or homozygous de

210 tter signature separates primary samples for multiple tumor types from The Cancer Genome Atlas into l

211 Unblinded clinical trials in multiple tumor types have shown that the assay will be u

212 nhibit the growth of cell lines derived from multiple tumor types in vitro, and tumor models in vivo.

213 role of tumor progression was described for multiple tumor types including breast, prostate, and hep

214 ene at 3p14.2, have been found frequently in multiple tumor types including non-small cell lung cance

215 t EGR1 is regulated by microRNA (miR)-183 in multiple tumor types including synovial sarcoma, rhabdom

216 regulator of oncogenic signaling pathways in multiple tumor types is the unique isomerase Pin1.

217 tein CD276/B7-H3 is broadly overexpressed by multiple tumor types on both cancer cells and tumor-infi

218 assification of human PNETs and suggest that multiple tumor types or variants can be generated from a

219 ene signature with prognostic ability across multiple tumor types remains lacking.

220 Cross-examination of EYA4 expression across multiple tumor types suggests a cell-type-specific tumor

221 the prevalence of VEGFA high-level gains in multiple tumor types suggests indications for clinical t

222 ion profiles of adenocarcinoma metastases of multiple tumor types to unmatched primary adenocarcinoma

223 In multiple tumor types, activation of the transcription fa

224 t that clonal heterogeneity is common across multiple tumor types, and discuss the potential clinical

225 ted by measuring HER2 expression profiles on multiple tumor types, and on normal and diseased heart t

226 g throughout all stages of carcinogenesis in multiple tumor types, and prior to tumor formation.

227 In blood and multiple tumor types, autotaxin produces LPA from lysoph

228 Somatic mutations of PIK3R1 are observed in multiple tumor types, but the tumorigenic activity of th

229 R), is implicated in promoting metastasis in multiple tumor types, including both sarcomas and carcin

230 orchestrate tumor-promoting inflammation in multiple tumor types, including breast cancer.

231 ted at 3pl4.2, have been found frequently in multiple tumor types, including head and neck squamous c

232 Loss of LINC00261 was observed in multiple tumor types, including liver, breast, and gastr

233 We evaluated the utility of CIBERSORTx in multiple tumor types, including melanoma, where single-c

234 Lsm1 is over-expressed in multiple tumor types, including over 80% of pancreatic t

235 player in the MAPK pathway, are described in multiple tumor types, including subsets of melanoma, non

236 ed in vitro migration of CFPs in response to multiple tumor types, indicating broad biological signif

237 For multiple tumor types, loss of RB function is associated

238 dual breast tumor molecular subtypes, across multiple tumor types, or after gene expression was norma

239 rapidly altered the treatment landscape for multiple tumor types, providing unprecedented survival i

240 A3B is also overexpressed in multiple tumor types, such as carcinomas of the bladder,

241 simultaneously overcoming drug resistance in multiple tumor types, thereby positioning this compound

242 Plk1 has been shown to be overexpressed in multiple tumor types, thus attracting high interest to i

243 portance of the loop domain was confirmed in multiple tumor types, two in vivo models of senescence,

244 rable and demonstrated antitumor activity in multiple tumor types, warranting further evaluation.

245 By analyzing 6,456 genomes from multiple tumor types, we constructed a map of oncogenic

246 ons between mRNA processing and neoplasia in multiple tumor types, with diagnostic potential.

247 pe, several cellular pathways are mutated in multiple tumor types-transcriptional regulation of diffe

248 ith worse survival outcomes in patients with multiple tumor types.

249 e of carboxyl terminal fragments of MUC16 in multiple tumor types.

250 including PD-1 and PD-L1 inhibitors, across multiple tumor types.

251 ow that INCR1 controls IFNgamma signaling in multiple tumor types.

252 3B is broadly responsible for mutagenesis in multiple tumor types.

253 in tumorigenesis, being highly expressed in multiple tumor types.

254 unction as tumor suppressors or oncogenes in multiple tumor types.

255 factor-A (VEGF-A), has clinical activity in multiple tumor types.

256 antly inhibited local and systemic growth of multiple tumor types.

257 (EGFR) antibody cetuximab is efficacious in multiple tumor types.

258 affirms that the IDO pathway is activated in multiple tumor types.

259 istone H3 lysine methylation deregulation in multiple tumor types.

260 n is associated with advanced disease across multiple tumor types.

261 ET is an important protein for metastasis in multiple tumor types.

262 ng in the c-Met pathway has been observed in multiple tumor types.

263 of which is universally linked to MT1-MMP in multiple tumor types.

264 hase II clinical trials for the treatment of multiple tumor types.

265 sociated with favorable clinical outcomes in multiple tumor types.

266 in cancer and are frequently inactivated in multiple tumor types.

267 cogenic signals elevate expression of Id2 in multiple tumor types.

268 have been implicated as growth regulators in multiple tumor types.

269 ght impose limitations in its application to multiple tumor types.

270 ing technology has been used to characterize multiple tumor types.

271 it may serve as an effective therapy against multiple tumor types.

272 ically useful classification from samples of multiple tumor types.

273 region of frequent loss of heterozygosity in multiple tumor types.

274 is thus a very strong candidate involved in multiple tumor types.

275 l lines, suggesting an important function in multiple tumor types.

276 re rapidly becoming the standard of care for multiple tumor types.

277 8(+) compared to CD4(+) T cell states within multiple tumor types.

278 ith DNA methylation at TSSs was confirmed in multiple tumor types.

279 nce of debris via macrophage phagocytosis in multiple tumor types.

280 been associated with favorable prognosis in multiple tumor types.

281 ent and is associated with poor prognosis in multiple tumor types.

282 1 (PD-L1) have shown remarkable activity in multiple tumor types.

283 d patient survival and poor prognosis across multiple tumor types.

284 mplicated in the progression and survival of multiple tumor types.

285 ative prognostic marker, is overexpressed in multiple tumor types.

286 regulation in cancer cell lines derived from multiple tumor types.

287 Loss of 14-3-3sigma has been observed in multiple tumor types; however, the mechanisms by which 1

288 Selecting a target expressed in multiple-tumor types and that is required for tumor grow

289 tinct staging system for ICC that focuses on multiple tumors, vascular invasion, and lymph node metas

290 s; a Canadian woman with polyposis, CRC, and multiple tumors was reported to be heterozygous for the

291 Six of the genes that were mutated in multiple tumors were assessed in up to 88 additional HNS

292 Multiple tumors were available from four patients, and i

293 ed of 18 participants; six participants with multiple tumors were included in both arms.

294 Multiple tumors were present in 27.3% of HCC patients an

295 Mice bearing multiple tumors were treated with rCE-expressing HB1.F3.

296 the NH(2)-terminal domain (NTD) occurred in multiple tumors, whereas those in the ligand binding dom

297 expression profiling of miRNAs and genes in multiple tumors with sufficiently large sample size.

298 ependent efficacy, and tumor accumulation in multiple tumor xenograft models.

299 AZD7762 was also a radiation sensitizer in multiple tumor xenograft models.

300 L-Cys and CSSC pool suppresses the growth of multiple tumors, yet is very well tolerated for prolonge