ライフサイエンスコーパス: kidney cancer

1 ubstrate) as a potential target molecule for kidney cancer.

2 of Wilms' tumour, the most common paediatric kidney cancer.

3 rectomy is associated with increased risk of kidney cancer.

4 tegies directed against these rarer forms of kidney cancer.

5 gene for the hereditary type of chromophobe kidney cancer.

6 n sporadic and hereditary forms of papillary kidney cancer.

7 (RCC) is the most common and invasive adult kidney cancer.

8 VHL is the gene for clear cell kidney cancer.

9 nal cell carcinoma (ccRCC), a deadly form of kidney cancer.

10 role in the development or the inhibition of kidney cancer.

11 arcinomas (RCCs), the most prevalent form of kidney cancer.

12 ential therapeutic agents for BHD-associated kidney cancer.

13 uterine leiomyomas and an aggressive form of kidney cancer.

14 rgeted therapy in the management of advanced kidney cancer.

15 in a growing understanding of the biology of kidney cancer.

16 inactivated gene in Wilms tumor, a childhood kidney cancer.

17 tanding of the basic biology and genetics of kidney cancer.

18 s involved in the development of a pediatric kidney cancer.

19 three may participate in the development of kidney cancer.

20 by a paucity of orthotopic animal models of kidney cancer.

21 for the treatment of patients with advanced kidney cancer.

22 r counseling patients with various stages of kidney cancer.

23 ed targets for T-cell-based immunotherapy of kidney cancer.

24 is the most frequent genetic event in human kidney cancer.

25 d is inactivated in Wilms tumor, a pediatric kidney cancer.

26 of which leads to Wilms' tumor, a pediatric kidney cancer.

27 ostate cancer, hematologic malignancies, and kidney cancer.

28 ent of novel therapeutics for FLCN-deficient kidney cancer.

29 ts died, including 293 individuals (4.4%) of kidney cancer.

30 prognostic associations, including RUNX1 in kidney cancer.

31 carcinoma (ccRCC), the most frequent form of kidney cancer.

32 Wilms tumour is the most common childhood kidney cancer.

33 testing for detection of inherited forms of kidney cancer.

34 ristics with Wilms tumor, a common pediatric kidney cancer.

35 Wilms tumour is a childhood kidney cancer.

36 benefit to patients diagnosed with advanced kidney cancer.

37 rmamentarium in the fight against metastatic kidney cancer.

38 ratory disease, and lung, skin, bladder, and kidney cancers.

39 ted in a subset of sporadic type 1 papillary kidney cancers.

40 come for individuals with either prostate or kidney cancers.

41 au (VHL) cancer syndrome and the majority of kidney cancers.

42 mor suppressor gene is mutated in most human kidney cancers.

43 irmed in independent datasets for breast and kidney cancers.

44 oma, non-small cell lung cancer (NSCLC), and kidney cancers.

45 ost common treatment for patients with small kidney cancers.

46 l cell renal pelvis and ureter, and 22 other kidney cancers.

47 r cell kidney cancer (75%), type 1 papillary kidney cancer (10%), papillary type 2 kidney cancer (inc

48 tations of FBXW7 in prostate cancers (5.6%), kidney cancers (16.7%), and bladder cancers (18.8%).

49 leukemia (AML; SIR = 4.9) in Germany and for kidney cancer (2.3), AML (2.3) and nervous system cancer

50 mach cancer, 3.61 (95% CI, 1.33 to 9.79) for kidney cancer, 3.45 (95% CI, 1.09 to 10.9) for sarcoma,

51 .0001) and a greater than 2-fold increase of kidney cancer (4/45 vs 6/155; P = .004) over individuals

52 209314 due to uterine cancer; 421628 due to kidney cancer; 487518 due to liver cancer; 13927 due to

53 cancers (TFE3, TFEB, and MITF), chromophobe kidney cancer (5%), and oncocytoma (5%).

54 onfamilial kidney cancer includes clear cell kidney cancer (75%), type 1 papillary kidney cancer (10%

55 In kidney cancer, a spectrum of histological subtypes exist

56 difficult to treat, such as liver cancer and kidney cancer, among many others.

57 VHL inactivation/HIF activation may lead to kidney cancer and also indicate a mechanism by which red

58 renal carcinomas are the most common form of kidney cancer and frequently are linked to biallelic ina

59 cinoma (ccRCC) is the most common subtype of kidney cancer and has the highest propensity to manifest

60 Tumour sizes were smaller in kidney cancer and in situ colon cancers were more common

61 al cell carcinoma is the most common form of kidney cancer and is highly resistant to chemotherapy.

62 carcinoma (ccRCC) is the most common form of kidney cancer and is often linked to loss of chromosome

63 ssor protein (pVHL) is frequently mutated in kidney cancer and is part of the ubiquitin ligase comple

64 carcinoma (ccRCC) is the most common type of kidney cancer and it forms highly vascularized tumors.

65 mplete understanding of the genetic basis of kidney cancer and of the kidney cancer gene pathways and

66 riven clinical studies of mTOR inhibitors in kidney cancer and suggest that FDG-PET scans may have us

67 eptor coregulator involved in suppression of kidney cancer and suggests potentially significant new r

68 d the role of the VHL gene product (pVHL) in kidney cancer and the mammalian oxygen sensing pathway.

69 There was a positive association between kidney cancer and the very high and high serum exposure

70 M3 expression with respect to CD8 T cells in kidney cancer and validate it experimentally.

71 d new light on the molecular pathogenesis of kidney cancer and, perhaps more important, on how mammal

72 hylene, increases the incidence of liver and kidney cancers and leukemia in rats and mice.

73 to be mutated in gliomas, breast, prostate, kidney cancers and melanomas.

74 ancer, 6,386 with bladder cancer, 3,179 with kidney cancer, and 2,967 with head/neck cancer from five

75 omatic mutations in Wilms tumor, a pediatric kidney cancer, and by germline inactivation in osteopath

76 drug use disorders, chronic kidney disease, kidney cancer, and falls.

77 enopausal breast cancer, endometrial cancer, kidney cancer, and lung cancer in never smokers.

78 of in situ, but not invasive, breast cancer, kidney cancer, and melanoma.

79 in combination with VEGFR2 TKIs in resected kidney cancer; and as single agents or with VEGFR2 TKIs

80 ntly altered the ways in which patients with kidney cancer are managed.

81 The majority of kidney cancers are clear-cell carcinomas (ccRCC), charac

82 cells in kidney repair and the treatment of kidney cancers are discussed.

83 translating into new therapeutic targets for kidney cancer as well as for multiple conditions, such a

84 Wilms tumor is a pediatric kidney cancer associated with inactivation of the WT1 tu

85 of the human genome, encompassing a familial-kidney-cancer-associated breakpoint and a papilloma viru

86 w that RLIP76 is an important anticancer for kidney cancer because inhibition of RLIP76 function by a

87 wever, a similar conclusion was not made for kidney cancer because of a lack of research with individ

88 nables rapid urinalysis for the detection of kidney cancer biomarkers in artificial urine down to a c

89 enectomy does not appear to yield benefit in kidney cancer but maybe helpful in those with grossly id

90 eta2, and ARF) from 17 patients with primary kidney cancer by quantitative fluorogenic real-time PCR.

91 ession analysis of DUTT1 in lung, breast and kidney cancers, (c) identified tumour specific promoter

92 The analysis included 792 incident kidney cancer cases among 283,952 postmenopausal women.

93 med a case-control study in 2007-2010 of 122 kidney cancer cases and 640 population-based controls wi

94 entrations of 25(OH)D were measured from 775 kidney cancer cases and 775 age-, sex-, race-, and seaso

95 Here, we used sequencing data from 22 human kidney cancer cases to identify the activating mechanism

96 hat included 1,452 bladder cancer cases, 406 kidney cancer cases, and 2,434 controls.

97 agonist or knockdown with shRNA, reduces the kidney cancer cell invasion.

98 gative mutants reduced KIM-1 expression in a kidney cancer cell line (769-P) that expresses high basa

99 ed the Fhit deletion break points in a mouse kidney cancer cell line (RENCA).

100 rved in sporadic breast, brain, prostate and kidney cancer cell lines and in several primary tumours

101 ificant overexpression of galectin-1 in both kidney cancer cell lines and metastatic tissue specimens

102 In von Hippel-Lindau (VHL)-null kidney cancer cell lines, we reported previously that HI

103 Mutation and methylation were absent in 9 kidney cancer cell lines.

104 s evaluated using an in vitro model of human kidney cancer cells adapted to chronic oxidative stress.

105 ivity to Hsp90 was examined using 293T human kidney cancer cells stably expressing split Renilla luci

106 orafenib treatment and decreased survival of kidney cancer cells through inactivation of AKT and mTOR

107 indau tumor suppressor gene (VHL) sensitizes kidney cancer cells to the mTOR inhibitor CCI-779 in vit

108 ockdown decreased CXCR4 expression levels in kidney cancer cells, and restoration of CXCR4 expression

109 ular implantation of Caki-1 clear cell human kidney cancer cells, we examined tissue, serum, and urin

110 ) is a recently recognized form of inherited kidney cancer characterized by a predisposition to devel

111 Using a mouse xenograft model of kidney cancer, characterized by subcapsular implantation

112 oma (ccRCC) is the most common form of adult kidney cancer, characterized by the presence of inactiva

113 , we demonstrated that molecular profiles of kidney cancers closely correlated with their histologica

114 ave been identified which lead to hereditary kidney cancer conditions.

115 Kidney cancer confined by the renal capsule can be surgi

116 The vast majority of work in kidney cancer deals with clear cell RCC, which is the mo

117 ities of three competing mortality outcomes: kidney cancer death, other cancer death, and noncancer d

118 Five-year probabilities of kidney cancer death, other cancer death, and noncancer d

119 nal and reproductive factors could influence kidney cancer development.

120 ), oral cavity/pharynx (difference = 2), and kidney cancers (difference = 2) and myeloma (difference

121 Wilms Tumor, the most common pediatric kidney cancer, evolves from the failure of terminal diff

122 carcinomas (ccRCC), the most common form of kidney cancer, express transcripts derived from the nove

123 Similar to other factors implicated in kidney cancer, FLCN has been shown to modulate activatio

124 for the treatment of patients with advanced kidney cancer, further genomic studies, such as whole ge

125 Positional cloning efforts for one kidney cancer gene are nearing completion.

126 he genetic basis of kidney cancer and of the kidney cancer gene pathways and, most importantly, to pr

127 Knowledge of these kidney cancer gene pathways has enabled new approaches i

128 ligase previously implicated as a hereditary kidney cancer gene, as required for US2-mediated MHC I u

129 come from the elucidation of the hereditary kidney cancer gene, TRC8, which functions partly to degr

130 ns and copy number alterations for important kidney cancer genes by the consistency between databases

131 s essential for an understanding of sporadic kidney cancer genetics.

132 ta suggest a major contribution of MARCKS to kidney cancer growth and provide an alternative therapeu

133 , bronchiectasis, myocardial infarction, and kidney cancer has been reported among young adults who w

134 Prognosis for patients with early stage kidney cancer has improved, but the treatment options fo

135 In the USA, the incidence of kidney cancer has increased 43% since 1973.

136 Study of the genes underlying kidney cancer has revealed that it is fundamentally a me

137 in-2 to patients with metastatic melanoma or kidney cancer have shown that immunological manipulation

138 as Hodgkin's disease, skin, lung, anal, and kidney cancers have been noted by some but not all autho

139 ey cancers, the management options for small kidney cancers have expanded and evolved.

140 ponse rates in hard-to-treat cancers such as kidney cancer, HER-2-positive breast cancer, head and ne

141 inked to an aggressive variant of hereditary kidney cancer (hereditary leiomyomatosis and renal cell

142 /neck (HR = 4.45; 95% CI, 2.56 to 7.73), and kidney cancers (HR = 5.33; 95% CI, 2.55 to 11.1).

143 was lower during kidney function intervals (kidney cancer: HR, 0.8; 95% CI, 0.7 to 0.8 and thyroid c

144 h increasing exposures for both cancers: for kidney cancer HRs for increasing exposure quartiles were

145 ly supported the conclusions that TCE causes kidney cancer in humans and that TCE may also cause live

146 n some clinical promise for the treatment of kidney cancer in humans, although the mechanisms respons

147 Embolization of kidney cancer in particular cases may be an alternative

148 ilarly elevated (approximately 4.5-fold) for kidney cancer in recipients with or without tBKVN, and i

149 against the use of these drugs for high-risk kidney cancer in the adjuvant setting and suggest that t

150 rtial nephrectomy among veterans treated for kidney cancer in the Veterans Health Administration (200

151 ts, and there are prior findings of elevated kidney cancer in this cohort.

152 tion (NIR) results in thermal destruction of kidney cancer in vitro and in vivo.

153 dult tea consumption and risk of bladder and kidney cancers in a population-based case-control study

154 Sporadic, nonfamilial kidney cancer includes clear cell kidney cancer (75%), t

155 illary kidney cancer (10%), papillary type 2 kidney cancer (including collecting duct and medullary R

156 Genomic studies identifying the genes for kidney cancer, including the VHL, MET, FLCN, fumarate hy

157 al features analogous to the growth of human kidney cancers, including a propensity for the formation

158 nhibitor used for the treatment of liver and kidney cancers, inhibits liver cyst growth in PC2-defect

159 Kidney cancer is a devastating disease; however, biologi

160 Kidney cancer is associated with renal vein or inferior

161 Evidence for kidney cancer is built mostly on retrospective data, whi

162 Although the role of oxidative stress in kidney cancer is known, the chemotherapeutic response of

163 Kidney cancer is not a single disease; it is made up of

164 Kidney cancer is not a single disease; it is made up of

165 Incidence of kidney cancer is on the rise, and a better understanding

166 Early-stage kidney cancer is treated with a radical nephrectomy, but

167 l carcinoma (ccRCC), the most common form of kidney cancer, is characterized by elevated glycogen lev

168 cell carcinoma (RCC), the most common human kidney cancer, is frequently infiltrated with tumor-asso

169 inoma (ccRCC), the most common type of adult kidney cancer, is often associated with genomic copy num

170 enal cell carcinoma, the most common form of kidney cancer, is usually linked to inactivation of the

171 ncer Cell, Sourbier and colleagues show that kidney cancers lacking fumarate hydratase display increa

172 1 (WT1) gene in humans can lead to childhood kidney cancer, life-threatening glomerular nephropathy a

173 ent to account for the differential risks of kidney cancer linked to VHL mutations.

174 older with a pathologically confirmed small kidney cancer (<4 cm) diagnosed between January 1, 2001,

175 improved among whites but not among blacks, kidney cancer mortality rates increased in all race and

176 models were built for prostate, bladder, and kidney cancer mortality, controlling for categorized uro

177 gist density on local prostate, bladder, and kidney cancer mortality.

178 ysed DUTT1 for mutations in lung, breast and kidney cancers, no inactivating mutations were detected

179 Wilms' tumor (WT), a childhood kidney cancer, occurs both sporadically and, less freque

180 r signaling, are initially effective against kidney cancer (or renal cell carcinoma, RCC); however, d

181 Kidney cancer [or renal cell carcinoma (RCC)] is known a

182 Kidney cancer, or renal cell carcinoma (RCC), is a disea

183 n D is inversely associated with the risk of kidney cancer overall or with renal cell carcinoma speci

184 errant chromatin regulation is a key step in kidney cancer pathogenesis.

185 Because responses were observed in kidney cancer patients in the phase I trials, we perform

186 so predict clinical outcome in both lung and kidney cancer patients, with lower levels predicting sig

187 ages at diagnosis of oral cavity/pharynx and kidney cancers, possibly reflecting accelerated cancer p

188 of the University of California Los Angeles Kidney Cancer Program.

189 we investigated the role of this molecule in kidney cancer progression and metastasis.

190 ression constitute a new strategy to control kidney cancer progression.

191 with most data in patients with a history of kidney cancer, prostate cancer, urothelial cancer, and s

192 treatment for many patients with early-stage kidney cancer, recent clinical trial data, which demonst

193 In conclusion, unlike other hereditary kidney cancer-related genes (i.e., VHL and MET), which a

194 However, the role of galectin-1 in kidney cancer remains elusive.

195 h the prognosis for patients with metastatic kidney cancer remains poor, a number of promising immuno

196 DF/HCC Kidney Cancer SPORE P50 CA101942-01, Kidney Cancer Research Network of Canada, Canadian Insti

197 The Trust Family Fund for Kidney Cancer Research.

198 be significant contributions to the field of kidney cancer research.

199 T cells in many tumors, except in brain and kidney cancers, resembled those for peripheral blood cel

200 well as with breast, colon, endometrial, and kidney cancer (respective hazard ratios of 1.24, 1.35, 1

201 Kidney cancer risk also was increased in liver recipient

202 ysterectomy were at a significantly elevated kidney cancer risk in both NIH-AARP (hazard ratio = 1.28

203 Among kidney recipients, kidney cancer risk was elevated (SIR, 6.66 [95% CI, 6.12

204 intervals relating reproductive factors and kidney cancer risk were computed by Cox regression.

205 Hispanic recipients had larger increases in kidney cancer risk with transplantation (SIRs: 8.96 in b

206 g 25(OH)D were significantly associated with kidney cancer risk.

207 ation between tea consumption and bladder or kidney cancer risk.

208 ower using both simulated and real datasets (kidney cancer RNA-seq dataset).

209 ity cohort mitochondrial DNA haplogroups and kidney cancer RNA-seq datasets).

210 idual cancers, but both were associated with kidney cancer (RR, 1.8; 95% CI, 1.3-2.5; and RR, 1.9; 95

211 ay strong tissue specificity (such as VHL in kidney cancer samples and GATA3 in breast cancer samples

212 ophageal, gastric, cervical, pancreatic, and kidney cancers, showed that reintroduction of FHIT resul

213 breast cancer (SIR = 1.6, 95% CI: 1.0, 2.4), kidney cancer (SIR = 3.9, 95% CI: 2.2, 6.3), and melanom

214 titutes of Health, National Cancer Institute Kidney Cancer Specialized Program of Research Excellence

215 No difference was noted in kidney cancer-specific survival (HR, 0.82; 95% CI, 0.19-

216 MAIN OUTCOME MEASURES: Overall and kidney cancer-specific survival.

217 try body mass index is associated with worse kidney cancer-specific survival.

218 DF/HCC Kidney Cancer SPORE P50 CA101942-01, Kidney Cancer Resea

219 Collecting duct carcinoma (CDC) is a kidney cancer subtype that is thought to arise from prin

220 nderstand the molecular distinctions between kidney cancer subtypes, we analyzed exome, transcriptome

221 lays a unique transcriptomic signature among kidney cancer subtypes, with a putative cell of origin i

222 easingly utilized in patients with localized kidney cancer, such as nephron-sparing and minimally inv

223 reported adverse events, or patient-reported kidney cancer symptoms.

224 ries have come from research into hereditary kidney cancer syndromes and the genetic mutations respon

225 Hereditary kidney cancer syndromes offer valuable insight into the

226 New hereditary kidney cancer syndromes, like familial oncocytoma and th

227 view the current knowledge of the hereditary kidney cancer syndromes, the genes that cause them, new

228 We also evaluated the algorithm on lung and kidney cancer TCGA datasets with high dimensionality, ag

229 ted transcription (MiT) family translocation kidney cancers (TFE3, TFEB, and MITF), chromophobe kidne

230 We present two mouse models of kidney cancer that recapitulate the genomic alterations

231 Strikingly, in kidney cancer, the pseudogene expression subtypes not on

232 the reader with the known heritable forms of kidney cancer, the recent advances in the field and thei

233 wnward size and stage migration of localized kidney cancers, the management options for small kidney

234 In contrast, for kidney cancer, there was no association with tea use.

235 e of 10.5 per Sv (10 cases) was observed for kidney cancer; this may have resulted from chance, inter

236 er valuable insight into the pathogenesis of kidney cancer through identification of the underlying g

237 gulation in liver, breast, lung, ovarian and kidney cancers, thus proving our GBA hypothesis.

238 dicare beneficiaries with clinical stage T1a kidney cancer treated with partial or radical nephrectom

239 c PRCC, and patients are often excluded from kidney cancer trials.

240 f renal tumors, suggesting its major role in kidney cancer tumorigenesis.

241 e missense mutations result in a low risk of kidney cancer (type 2A VHL disease) while others result

242 t Award); The Trust Family Research Fund for Kidney Cancer; US National Institutes of Health, Nationa

243 ts (SEER) database to evaluate the impact of kidney cancer versus competing causes of death in patien

244 Of these cancer sites, only kidney cancer was included in the IARC 2002 report, alth

245 The risk of kidney cancer was increased most of all cancers after ki

246 Kidney cancer was the cause of death for 37 patients (1.

247 7138 Medicare beneficiaries with early-stage kidney cancer, we identified 1925 patients (27.0%) treat

248 presentation of 608 patients with hereditary kidney cancer were 39.3 years and 37 years, respectively

249 ong the Texas-Mexico border, and clusters of kidney cancer were observed in North and South Dakota an

250 Case studies of colon, gastric, and kidney cancers were also implemented, and the top 5 dise

251 ues, approximately 40-90% of these pediatric kidney cancers were hypermethylated in four of the genes

252 antial hope for those patients with advanced kidney cancer, where before the outlook was often bleak.

253 nce of mTOR mutations observed in clear cell kidney cancer, where VHL loss and HIF activation is path

254 k of cancer or of individual cancers, except kidney cancer, which has been associated with hypertensi

255 mong Medicare beneficiaries with early-stage kidney cancer who were candidates for either surgery, tr

256 iology of the various histologic subtypes of kidney cancer will be reviewed, as these subtle yet impo

257 tumor suppressor implicated in the pediatric kidney cancer Wilms tumor and in mesenchymal differentia

258 carcinoma (pRCC) is an important subtype of kidney cancer with a problematic pathological classifica

259 tation are predisposed to develop aggressive kidney cancer with few treatment options and poor therap

260 bladder cancer, and 8% to 14% reduction for kidney cancer with increasing urologist density) relativ

261 from the distal nephron compared with other kidney cancers with more proximal origins.

262 s are histologically and genetically diverse kidney cancers with variable prognoses, and their optimu

263 irculating 25-hydroxyvitamin D (25(OH)D) and kidney cancer within a large, nested case-control study