ライフサイエンスコーパス: multiple tumor

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

2 ci recurrently affected by LOH events across multiple tumors.

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

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

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

6 activity and exhibits aberrant expression in multiple tumors.

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

8 , we identified several sequence variants in multiple tumors.

9 nt Wilms' tumor had histologic maturation of multiple tumors.

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

11 cally reduce cell invasion and metastasis in multiple tumors.

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

13 Statins inhibit the growth of multiple tumors.

14 t was recurrently somatically inactivated in multiple tumors.

15 ation, and its expression is misregulated 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 ly analyzed their differential regulation in multiple tumors and found severe deregulation in liver,

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

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

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

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

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

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

27 , disease-free interval less than 12 months, multiple tumors, and extrahepatic disease were independe

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 Multiple tumors arising in the same mouse had distinct X

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

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

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

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

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

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

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

43 Multiple tumor burden in Ovca1 heterozygotes that were a

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

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

46 6 kinase (RSK) family has been implicated in multiple tumor cell functions, the full understanding of

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

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

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

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

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

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

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

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

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

56 irmed by reciprocal coimmunoprecipitation in multiple tumor cell lines.

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

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

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

60 promote spontaneous pulmonary metastasis of multiple tumor cell types in both the chick embryo and s

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

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

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

64 0% of the beta-pol(+/-) animals died bearing multiple tumors compared with only 5% of the beta-pol(+/

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

66 In four of four cases, multiple tumors demonstrated the same pattern of X-chrom

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

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

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

70 site locus FRA3B, is homozygously deleted in multiple tumor-derived cell lines.

71 Multiple tumor-derived KDM2B mutations impaired the func

72 In three of nine patients, multiple tumors displayed the same pattern of loss of he

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

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

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

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

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

78 , 8p LOH was seen in some but not all of the multiple tumor foci examined.

79 ression, findings that were possible because multiple tumor foci from each lesion were individually m

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

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

82 81% of the Rint-1 heterozygotes succumbed to multiple tumor formation with haploinsufficiency during

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

84 of a delivery vector, including targeting of multiple tumors from a distant inoculation site, selecti

85 s in ETs from different MEN1 patients and in multiple tumors from individual MEN1 patients.

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

87 Examination of multiple tumors from the same patient revealed that some

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

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

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

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

92 All 5 had multiple tumors in addition to vestibular schwannoma, an

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

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

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

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

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

98 durable clinical responses in patients with multiple tumor indications.

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

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

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

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

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

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

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

111 In multiple tumor models, intravenous peptibody injection c

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

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

114 rrelated with enhanced invasive potential in multiple tumor models.

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

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

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

118 Multiple tumors more often occurred in patients with SDH

119 Somatic mutations in PTEN occur in multiple tumors, most markedly glioblastomas.

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

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

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

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

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

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

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

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

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

129 of 55 years (OR = 4.1, 95% CI 2.1-8.0) with multiple tumors (OR = 9.5, 95% CI 4.4-20.6), with a dist

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

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

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

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

134 This multiple tumor phenotype was not previously observed wit

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

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

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

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

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

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

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

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

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

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

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

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

147 cus on the X chromosome was evaluated in the multiple tumor sites.

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

149 Multiple tumor specific ceramide and sphingomyelin speci

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

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

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

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

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

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

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

157 Multiple tumor-suppressive miRNAs were downregulated coo

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

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

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

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

162 ss studies have suggested the involvement of multiple tumor suppressor genes (TSGs), but few detailed

163 While multiple tumor suppressor genes are likely to reside on

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

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

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

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

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

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

170 tumors and is believed to be the location of multiple tumor suppressor genes.

171 crete locations, suggesting the existence of multiple tumor suppressor loci in 6q that may contribute

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

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

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

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

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

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

178 a specific role for Id2 as an antagonist of multiple tumor suppressor proteins.

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

180 ic cyclin D-dependent kinase inhibitor and a multiple tumor suppressor.

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

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

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

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

185 romosome 17q, which supports the notion that multiple tumor suppressors may reside on chromosome 17 i

186 recognition event is implicated in silencing multiple tumor suppressors.

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

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

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

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

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

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

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

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

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

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

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

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

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

200 ired for spontaneous pulmonary metastasis of multiple tumor types even though it was not necessary fo

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

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

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

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

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

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

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

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

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

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

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

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

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

214 In multiple tumor types, activation of the transcription fa

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

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

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

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

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

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

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

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

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

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

225 B is required for HLA class 11 expression in multiple tumor types, the RB-defective non-small cell lu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 istone H3 lysine methylation deregulation in multiple tumor types.

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

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

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

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

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

246 sociated with favorable clinical outcomes in multiple tumor types.

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

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

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

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

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

252 ically useful classification from samples of multiple tumor types.

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

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

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

256 been associated with favorable prognosis in multiple tumor types.

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

258 1 (PD-L1) have shown remarkable activity in multiple tumor types.

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

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

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

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

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

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

265 3B is broadly responsible for mutagenesis in multiple tumor types.

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

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

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

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

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

271 Multiple tumors were available from four patients, and i

272 Short disease-free interval or multiple tumors were nevertheless associated with a 5-ye

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

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

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

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

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

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

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