ライフサイエンスコーパス: renal carcinoma

1 ce implicating a role for proline oxidase in renal carcinoma.

2 al tumor models and patients with metastatic renal carcinoma.

3 ligase complex with 'gatekeeper' function in renal carcinoma.

4 dual patients with organ-confined clear-cell renal carcinoma.

5 to that found in human hereditary papillary renal carcinoma.

6 uce complete regression of metastatic murine renal carcinoma.

7 ifferent mechanism than hereditary papillary renal carcinoma.

8 ithelial cells compatible with metastasis of renal carcinoma.

9 s, and their links to the risk of developing renal carcinoma.

10 h hereditary and sporadic forms of papillary renal carcinoma.

11 lymphomas and not previously described with renal carcinoma.

12 nephrectomy kidneys containing a coincident renal carcinoma.

13 genes and miRNAs not previously reported in renal carcinoma.

14 ating event in the development of clear-cell renal carcinoma.

15 thelia, which may promote the development of renal carcinoma.

16 carcinoma, and hereditary leiomyomatosis and renal carcinoma.

17 epithelial neoplasia, and invasive papillary renal carcinoma.

18 kinase inhibitor, in patients with advanced renal carcinoma.

19 stage disease, particularly with melanoma or renal carcinoma.

20 ence of Apc induces the rapid development of renal carcinoma.

21 tes an important role for Apc in suppressing renal carcinoma.

22 of sporadic hemangioblastomas and clear-cell renal carcinomas.

23 ression can contribute to the development of renal carcinomas.

24 ular endothelial growth factor by clear-cell renal carcinomas.

25 of shared albeit unidentified antigens among renal carcinomas.

26 f developing multiple independent clear cell renal carcinomas.

27 tion also is found in a majority of sporadic renal carcinomas.

28 aracterized by multiple, bilateral papillary renal carcinomas.

29 ng, skin, ovarian, pancreatic, prostate, and renal carcinomas.

30 e in HPRC and a subset of sporadic papillary renal carcinomas.

31 Met have been identified in human papillary renal carcinomas.

32 to the carcinogenetic process in breast and renal carcinomas.

33 tion to develop multiple bilateral papillary renal carcinomas.

34 n about cadherins in normal renal tissue and renal carcinomas.

35 milies and in a subset of sporadic papillary renal carcinomas.

36 activation of the MET protein and papillary renal carcinomas.

37 ndau disease and in most sporadic clear cell renal carcinomas.

38 bearing animals and patients with metastatic renal carcinomas.

39 ation, is also common in sporadic clear cell renal carcinomas.

40 ent of the malignant phenotype of clear cell renal carcinomas.

41 se-IX, which is over-expressed in clear-cell renal carcinomas.

42 nd is implicated in most sporadic clear cell renal carcinomas.

43 y defined a novel genetic locus nonpapillary renal carcinoma-1 (NRC-1) within chromosome 3p12, distin

44 lignant neoplasms: conventional (clear cell) renal carcinoma (11 of 11 cases), transitional cell carc

45 4)I-cG250 can identify accurately clear-cell renal carcinoma; a negative scan is highly predictive of

46 inhibits the growth of s.c. implanted human renal carcinoma A498 and human prostate carcinoma DU145

47 Human melanoma (A375), renal carcinoma (ACHN), and ovarian carcinoma (NIH-OVCAR

48 In a series of sporadic renal carcinomas, an acquired TRC8 mutation was identifi

49 By analysing 181 samples from 10 renal carcinoma and 11 colorectal cancers we demonstrate

50 for the hereditary form of type 1 papillary renal carcinoma and is mutated in a subset of sporadic t

51 In addition, pairs of human renal carcinoma and normal tissues showed a negative cor

52 that CoAA is a potential tumor suppressor in renal carcinoma and that CoAM is a counterbalancing spli

53 erfusion imaging in patients with metastatic renal carcinoma and to validate (62)Cu-ETS as a quantita

54 t p270 may be deficient in as many as 30% of renal carcinomas and 10% of breast carcinomas.

55 ally separated samples obtained from primary renal carcinomas and associated metastatic sites.

56 ) has been implicated in the pathogenesis of renal carcinomas and central nervous system hemangioblas

57 Visceral manifestations include renal carcinomas and cysts, pancreatic neuroendocrine tu

58 he MET gene which cause hereditary papillary renal carcinomas and for the search for additional mutat

59 ll lines and tumors, specifically clear cell renal carcinomas and hemangioblastomas.

60 Met have been discovered in human papillary renal carcinomas and other cancers, while autocrine and

61 nervous system hemangioblastomas, clear cell renal carcinomas and pheochromocytomas.

62 ainly as a consequence of a biopsy or due to renal carcinomas and postinflammatory changes.

63 screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations

64 er tumorigenic cell lines, such as melanoma, renal carcinoma, and breast tumors, which were not engin

65 irt-Hogg-Dube syndrome, hereditary papillary renal carcinoma, and hereditary leiomyomatosis and renal

66 plays a causal role in hemangioblastoma and renal carcinoma, and raises the possibility that abnorma

67 ancer, non-small-cell lung cancer, melanoma, renal carcinoma, and squamous cell carcinoma, which were

68 umors, including VHL-associated and sporadic renal carcinomas, and it stimulates neoangiogenesis in g

69 Spinocerebellar hemangioblastomas, renal carcinomas, and pheochromocytomas typical of class

70 al hemangioblastomas, solid organ cysts, and renal carcinoma are common lesions; pheochromocytomas an

71 nts originally identified in human papillary renal carcinoma are oncogenic and thus are likely to pla

72 Inherited and sporadic clear cell renal carcinomas are characterized by inactivation of bo

73 Malignant papillary renal carcinomas are characterized by trisomy of chromos

74 Clear cell renal carcinomas are the most common form of kidney canc

75 opment of pneumothorax, pulmonary cysts, and renal carcinoma, arises from loss-of-function mutations

76 ion resulting from a t(X;17)(p11.2;q23) in a renal carcinoma arising in a 14-year-old boy.

77 t have been observed in hereditary papillary renal carcinomas as well as in other cancers.

78 even within specific stages, in bladder and renal carcinomas as well as low-grade gliomas.

79 ed in both sporadic and inherited clear cell renal carcinoma associated with VHL disease.

80 the common fragile site, FRA3B, a hereditary renal carcinoma-associated 3;8 translocation and the can

81 ree 5' untranslated exons centromeric to the renal carcinoma-associated 3p14.2 breakpoint, the remain

82 e were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors.

83 n a previous Env library screen on the human renal carcinoma Caki-1 cell line.

84 In clear cell renal carcinoma (CCRC), hypoxic signaling is constitutiv

85 using a set of in-house generated clear cell renal carcinoma (ccRCC) samples.

86 typical tumor-initiating event in clear cell renal carcinoma (ccRCC) that leads to the activation of

87 ase, congenital polycythaemia and clear cell renal carcinoma (ccRCC).

88 -tumor effect of MLN4924 in human clear cell renal carcinoma (ccRCC).

89 ubiquitin (Ub) ligases mutated in clear-cell renal carcinomas (ccRCC).

90 Most clear cell renal carcinomas (ccRCCs) are initiated by somatic inact

91 Clear cell renal carcinomas (ccRCCs) can display intratumor heterog

92 n diverse tumour types, including clear cell renal carcinomas (ccRCCs).

93 le of Hsp90 in HIF-1 alpha function, we used renal carcinoma cell (RCC) lines that lack functional VH

94 he cervical carcinoma cell line HeLa and the renal carcinoma cell line 786-O.

95 lectrophoretic protein patterns of the human renal carcinoma cell line ACHN were studied.

96 xpression of RASSF1A transcripts in KRC/Y, a renal carcinoma cell line containing a normal and expres

97 The most sensitive renal carcinoma cell line, A498, exhibited cell cycle ar

98 On the cellular level, A704 cells, a human renal carcinoma cell line, transfected with RanBPM exhib

99 tumor suppressor gene in a human clear cell renal carcinoma cell line, UOK 121, that contains a sile

100 n of downstream target genes and proteins in renal carcinoma cell lines and in a mouse xenograft mode

101 The promoter methylation status of three renal carcinoma cell lines was assessed with restriction

102 Complementation of VHL-defective clear cell renal carcinoma cell lines with wild-type VHL restored p

103 n human breast cancer cells (MDA-MB 231) and renal carcinoma cells (RCC-RS).

104 on of CD40 expressed on both mouse and human renal carcinoma cells (RCCs) triggers biological effects

105 promoting tumor formation by pVHL-defective renal carcinoma cells among the three HIFalpha paralogs.

106 LT-1 was evaluated using H2O2-treated UOK262 renal carcinoma cells and a paraquat-induced oxidative s

107 neered stable transfectants from RenCa mouse renal carcinoma cells and SW620 human colon carcinoma ce

108 unction we subjected mRNA from VHL defective renal carcinoma cells and transfectants re-expressing a

109 pVHL-defective renal carcinoma cells exhibit increased NF-kappaB activi

110 oxia, insulin-like growth factor (IGF)-I, or renal carcinoma cells expressing constitutively high bas

111 sion inhibited metastatic growth of colon or renal carcinoma cells in liver but not lung.

112 monstrate that SK1 is overexpressed in 786-0 renal carcinoma cells lacking functional VHL, with conco

113 Renal carcinoma cells lacking wild-type pVHL were found

114 oduction of the 18-kDa VHL gene product into renal carcinoma cells lacking wild-type VHL protein led

115 f wildtype, but not mutant, pVHL into VHL-/- renal carcinoma cells partially corrected this defect.

116 ctor (HIF)-2alpha in VHL-positive clear cell renal carcinoma cells phenocopied loss of VHL with respe

117 ive stress in chemotherapeutic resistance in renal carcinoma cells potentially through epigenetic mec

118 r ability to inhibit the viability of VHL-/- renal carcinoma cells preferentially compared with isoge

119 In contrast, in renal carcinoma cells that constitutively express HIF-1a

120 We show in von Hippel-Lindau (VHL)-defective renal carcinoma cells that express constitutively high l

121 When reintroduced into renal carcinoma cells that lack a wild-type VHL allele,

122 ctor (VEGF) and GLUT1 when reintroduced into renal carcinoma cells that lack a wild-type VHL allele.

123 cultured and ex vivo freshly isolated human-renal carcinoma cells to drug-induced cell death in xeno

124 nlike conventional BALB/c mice that rejected renal carcinoma cells transfected with the influenza vir

125 VHL-negative renal carcinoma cells underwent apoptosis following chem

126 VHL-negative 786-O renal carcinoma cells underwent apoptosis following UV i

127 irradiation on VHL-negative and VHL-positive renal carcinoma cells was examined.

128 olony forming efficiency of Eker rat-derived renal carcinoma cells was significantly reduced followin

129 Expression of wild-type VHL in renal carcinoma cells with inactivated endogenous VHL re

130 r complex III of the ETC, in patient-derived renal carcinoma cells with mutations in fumarate hydrata

131 ype 2B mutants when reintroduced into VHL-/- renal carcinoma cells with respect to HIF regulation.

132 n extracellular fibronectin matrix by VHL-/- renal carcinoma cells, as determined by immunofluorescen

133 ersely, in checkpoint-deficient VHL-negative renal carcinoma cells, inhibition of miR-28-5p function

134 r displayed enhanced activity against VHL-/- renal carcinoma cells, suggesting that in some cases hit

135 In UOK-145 papillary renal carcinoma cells, which endogenously express PSF-TF

136 itize TRAIL-mediated apoptosis in a panel of renal carcinoma cells.

137 s but critically dependent on Hif-2 alpha in renal carcinoma cells.

138 c from mitochondria, and apoptosis in 786-0 renal carcinoma cells.

139 expression of endogenous MDR1 mRNA in human renal carcinoma cells.

140 , was grossly defective compared with VHL+/+ renal carcinoma cells.

141 nversely correlated to miR-141 expression in renal carcinoma cells.

142 reductive carboxylation in SkMel5 and 786-O renal carcinoma cells.

143 izes tuberin protein levels in VHL-deficient renal carcinoma cells.

144 f extracellular-regulated kinase (ERK)1/2 in renal carcinoma cells.

145 selectively target VHL-deficient clear cell renal carcinoma cells.

146 sion and HIF-2alpha-regulated VEGF levels in renal carcinoma cells.

147 and PAI-1 are overproduced by pVHL-defective renal carcinoma cells.

148 reen, we now identify TRC8 (translocation in renal carcinoma, chromosome 8 gene), an ER-resident E3 l

149 f a 56-year-old male patient with clear cell renal carcinoma confirmed on a histopathological examina

150 93 cells heterologously expressing TRPC4 and renal carcinoma-derived A-498 cells endogenously express

151 and long-term survival of UOK-145 papillary renal carcinoma-derived cells, which endogenously expres

152 ollowing Wnt3a stimulation in both renal and renal carcinoma-derived cells.

153 Moreover, two renal carcinoma-derived mutant p53 proteins were deficie

154 inactivation is observed in most clear cell renal carcinoma, driving the malignant phenotype.

155 Progression to renal carcinoma, fatal bleeding from the liver hemangiom

156 the VHL tumor suppressor gene in clear cell renal carcinoma for potential clinical benefit and may h

157 lso tested the effects of cimetidine against renal carcinoma, for which it was not predicted to be ef

158 2C mutant, retained the ability to suppress renal carcinoma growth in vivo.

159 ed in VHL disease and in sporadic clear-cell renal carcinomas, has recently been shown to have as a f

160 than sporadic RCCs, that some TSC-associated renal carcinomas have a different immunophenotype than s

161 The gene defect for hereditary papillary renal carcinoma (HPRC) has recently been mapped to chrom

162 Hereditary papillary renal carcinoma (HPRC) is a newly recognized inherited d

163 Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of

164 Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bil

165 n the Met gene in human hereditary papillary renal carcinoma (HPRC), were expressed in NIH3T3 cells.

166 response that would restrict development of renal carcinoma in vivo.

167 ies represent only a small proportion of the renal carcinomas in this collection of ESRD tumors.

168 An identical system can be identified in renal carcinomas, in which, after nuclear transmigration

169 Renal carcinoma is a common and aggressive malignancy wh

170 tion of sorafenib and interferon in advanced renal carcinoma is greater than expected with either int

171 y which expression of IGF-1R is increased in renal carcinoma is not known.

172 We have confirmed that renal carcinoma is sometimes part of MCUL, as part of th

173 A distinctive subset of renal carcinomas is associated with Xp11.2 translocation

174 inoma, a hereditary form of type 2 papillary renal carcinoma, is caused by inactivation of a Krebs cy

175 However, unlike most renal carcinomas, it also focally expressed melanocytic

176 itochondria have been observed in clear cell renal carcinomas known to have frequent VHL alterations.

177 Two malignant (adrenal and renal carcinoma) lesions and one precancerous (pancreati

178 angioblastomas, retinal angiomas, clear-cell renal carcinoma, neuroendocrine tumors and cysts of the

179 histopathologically classified as clear-cell renal carcinoma or otherwise.

180 Late-stage clear cell renal carcinoma poses a formidable clinical challenge du

181 y of MET mutations in noninherited papillary renal carcinomas (PRC) suggests that noninherited PRC ma

182 roteins expressed differentially between two renal carcinoma proteomes.

183 ajority of patients with sporadic clear cell renal carcinoma (RCC).

184 Murine renal carcinoma (Renca) cells were constitutively resist

185 Human prostate cancer (PC3) and murine renal carcinoma (RENCA) cells were irradiated with a 1,0

186 male nude mice and orthotopically implanted renal carcinoma (RENCA) tumors in BALB/c mice, in terms

187 n of wild type VHL transgene into clear cell renal carcinoma restored low level expression of STRA13.

188 rmethylation was most frequent in breast and renal carcinoma, showing aberrant methylation in 30 and

189 G250 ((124)I-cG250) PET predicts clear-cell renal carcinoma, the most common and aggressive renal tu

190 found in the majority of sporadic clear cell renal carcinoma, the most common malignant neoplasm of t

191 cases and pT1b in one case (five clear cell renal carcinoma, two chromophobe type, and one lipoma).

192 ns in the MET gene associated with papillary renal carcinoma type 1.

193 distinct from two other causes of inherited renal carcinoma, von Hippel-Lindau disease (VHL) and the

194 Growth of subcutaneous implants of RENCA renal carcinoma was also inhibited by the combination of

195 Renal carcinoma was observed with an earliest onset of 4

196 ty-three patients with metastatic clear-cell renal carcinoma were treated with bevacizumab 10 mg/kg i

197 us system, pheochromocytomas, and clear cell renal carcinoma, which result from somatic inactivation

198 ible patients had metastatic or unresectable renal carcinoma with a clear-cell component, no prior sy

199 has shown the potential to target clear cell renal carcinoma with high sensitivity and specificity.

200 romoting activity by Ror2 within a subset of renal carcinomas, with significant implications for unra