ライフサイエンスコーパス: ccRCC

1 ccRCC harboring epigenetic silencing of NSD1 displayed a

2 ccRCC patients with VHL loss-of-function mutations displ

3 ccRCC preclinical models can be grouped into three broad

4 ccRCC shows a gene expression signature consistent with

5 - 7 [standard deviation]; 25 women) with 100 ccRCCs were evaluated.

6 ed their mRNA differential expressions in 19 ccRCCs and 10 GEO datasets.

7 The biomarker was validated in 19 ccRCCs and three public datasets.

8 datasets, together with a new dataset of 265 ccRCC gene expression profiles.

9 Results: Overall, 419 ccRCC tumor data sets from non-Hispanic white patients a

10 in ccRCC using bioinformatic analyses of 530 ccRCC patients from The Cancer Genome Atlas (TCGA) and T

11 CyTOF dataset, which profiled the TME in 73 ccRCC patients, revealed cell-type-specific SLAMF7 expre

12 on the metabolism and proliferation of 786O ccRCC cell line, suggesting the dispensable role of UQCR

13 Depletion of SFMBT1 abolished ccRCC cell proliferation in vitro and inhibited orthotop

14 e patients represent a challenge to adjuvant ccRCC drug development.

15 tors with antiangiogenic agents for advanced ccRCC.

16 ical activity in heavily pretreated advanced ccRCC patients.

17 These advanced ccRCC tumors were highly CD8(+) T cell infiltrated, with

18 lyzed 592 tumors from patients with advanced ccRCC enrolled in prospective clinical trials of treatme

19 ights into the therapeutic potential against ccRCC development by relieving metabolic stress.

20 histone mark as a root feature of aggressive ccRCC.

21 ion set of 125 white and 10 African American ccRCC patient tumors was identified from the publicly av

22 rphological differences between TFE3-RCC and ccRCC and contribute to a potential guideline for TFE3-R

23 significant differences between TFE3-RCC and ccRCC.

24 ential for the growth rate of VHL-associated ccRCC.

25 Herein we show using an autochthonous ccRCC model that Hif1a is essential for tumour formation

26 signatures that delineated four immune-based ccRCC subtypes characterized by distinct cellular pathwa

27 y occurring in Vhl mutant renal cells before ccRCC formation.

28 r that is capable of differentiating between ccRCC tumor and adjacent tissues.

29 pT4, node-positive) clear cell renal cancer (ccRCC) in the ASSURE trial (adjuvant sunitinib or sorafe

30 the pathogenesis of clear cell renal cancer (ccRCC); however, the molecular mechanisms underlying tra

31 metastatic clear cell renal cell carcinoma (ccRCC) after failure of antiangiogenic therapies, but it

32 IX-positive clear cell renal cell carcinoma (ccRCC) and colorectal cancer.

33 therapy in clear cell renal cell carcinoma (ccRCC) and other solid tumors.

34 focused on clear cell renal cell carcinoma (ccRCC) and utilized RNA sequencing and outcome data from

35 rofiling of clear cell renal cell carcinoma (ccRCC) by The Cancer Genome Atlas (TCGA) identified UQCR

36 rographs of clear cell renal cell carcinoma (ccRCC) cases from The Cancer Genome Atlas (TCGA).

37 rphology of clear cell renal cell carcinoma (ccRCC) cells results from a grade-dependent neutral lipi

38 features in clear cell renal cell carcinoma (ccRCC) confers a poor prognosis and is of unknown pathog

39 andscape of clear cell renal cell carcinoma (ccRCC) had been investigated extensively but its evoluti

40 Clear cell renal cell carcinoma (ccRCC) has been previously classified into putative disc

41 Although clear cell renal cell carcinoma (ccRCC) has been shown to result in widespread aberrant c

42 ng genes in clear cell renal cell carcinoma (ccRCC) has been uncovered through next-generation sequen

43 -associated clear cell renal cell carcinoma (ccRCC) has the potential to allow individualization of p

44 of sporadic clear cell renal cell carcinoma (ccRCC) have uncovered novel driver genes and pathways.

45 that define clear cell renal cell carcinoma (ccRCC) initiation and progression are being increasingly

46 Clear-cell renal cell carcinoma (ccRCC) is a common aggressive urinary malignant tumor th

47 Clear cell renal cell carcinoma (ccRCC) is a gender-biased tumor.

48 Clear cell renal cell carcinoma (ccRCC) is highly heterogeneous and is the most lethal ca

49 Clear cell renal cell carcinoma (ccRCC) is histologically defined by its lipid and glycog

50 Clear cell renal cell carcinoma (ccRCC) is the most common renal cancer subtype, characte

51 Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer and it f

52 L-deficient clear-cell renal cell carcinoma (ccRCC) models.

53 les from 73 clear cell renal cell carcinoma (ccRCC) patients and five healthy controls.

54 ed in human clear cell renal cell carcinoma (ccRCC) samples, which was also verified in several indep

55 r causes of clear-cell renal cell carcinoma (ccRCC) that may originate from chronic inflammation.

56 rly true of clear cell renal cell carcinoma (ccRCC) where, although key mutations such as loss of VHL

57 c factor of clear cell renal cell carcinoma (ccRCC), as well as a factor in guiding treatment with an

58 In clear cell renal cell carcinoma (ccRCC), AXL expression is associated with antiangiogenic

59 of advanced clear cell renal cell carcinoma (ccRCC), but the drivers and resistors of the PD-1 respon

60 orm of RCC, clear cell renal cell carcinoma (ccRCC), inactivation of the von Hippel-Lindau tumor supp

61 alent type, clear cell renal cell carcinoma (ccRCC), is characterized by genetic mutations in factors

62 ppressor in clear cell renal cell carcinoma (ccRCC), primarily based on functional proliferation stud

63 rs, such as clear cell renal cell carcinoma (ccRCC), require exogenous glutamine for growth and exhib

64 ng event in clear cell renal cell carcinoma (ccRCC), the most common form of kidney cancer, and cause

65 Clear-cell renal cell carcinoma (ccRCC), the most common subtype of renal cancer, has a p

66 that drive clear cell renal cell carcinoma (ccRCC), we performed comprehensive genomic, epigenomic,

67 xpressed in clear cell renal cell carcinoma (ccRCC), where SLC2A3 expression is associated with patie

68 c driver in clear cell renal cell carcinoma (ccRCC).

69 eostasis in clear cell renal cell carcinoma (ccRCC).

70 mutated in clear cell renal cell carcinoma (ccRCC).

71 xpressed in clear cell renal cell carcinoma (ccRCC).

72 ated to the clear cell Renal Cell Carcinoma (ccRCC).

73 nagement of clear cell renal cell carcinoma (ccRCC).

74 ogenesis of clear cell renal cell carcinoma (ccRCC).

75 eatments in clear-cell renal cell carcinoma (ccRCC).

76 on, such as clear-cell renal cell carcinoma (ccRCC).

77 survival in clear cell renal cell carcinoma (ccRCC).

78 VHL-mutant clear cell renal cell carcinoma (ccRCC).

79 entified in clear cell renal cell carcinoma (ccRCC); however it is unclear if loss of SETD2 function

80 nome Atlas: clear cell renal cell carcinoma (ccRCC, also known as kidney renal clear cell carcinoma),

81 -house generated clear cell renal carcinoma (ccRCC) samples.

82 MLN4924 in human clear cell renal carcinoma (ccRCC).

83 han 90% of clear cell renal cell carcinomas (ccRCC) exhibit inactivation of the von Hippel-Lindau (pV

84 ajority of clear cell renal cell carcinomas (ccRCC), but genetic ablation of Vhl alone in mouse model

85 cribed for clear cell renal cell carcinomas (ccRCC), but they are less studied for other kidney cance

86 ajority of clear cell renal cell carcinomas (ccRCC), leading to accumulation of the HIF-1alpha and HI

87 Most clear cell renal cell carcinomas (ccRCCs) have inactivation of the von Hippel-Lindau tumor

88 ajority of clear cell renal cell carcinomas (ccRCCs), leading to inappropriate stabilization of hypox

89 pressor in clear cell renal cell carcinomas (ccRCCs).

90 Most clear cell renal carcinomas (ccRCCs) are initiated by somatic inactivation of the VHL

91 rise from dedifferentiation of carcinomatous ccRCCs and implicate specific genes in this process.

92 cohort to date) and 74 clear cell RCC cases (ccRCC, the most common RCC subtype) with matched gender

93 of pVHL is not sufficient, however, to cause ccRCC.

94 d re-expressed these mutants in Caki2 cells (ccRCC cells with the loss of function mutation in PBRM1)

95 enic pairs of clear cell renal cancer cells (ccRCC), with or without VHL, upon the deprivation of ind

96 ngly, clear cell renal cell carcinoma cells (ccRCC) have a dysregulated lipid-mediated checkpoint due

97 cal nephrectomy for histologically confirmed ccRCC and fell into 1 of the following high-risk groups:

98 by which AR can either increase or decrease ccRCC metastasis at different sites and may help us to d

99 ccRCC hematogenous metastasis yet decreases ccRCC lymphatic metastases.

100 reprogramming and survival of VHL-deficient ccRCC cells.

101 FTO expression is increased in VHL-deficient ccRCC tumors compared to normal adjacent tissue.

102 Furthermore, in 14q-deleted ccRCC patients with complete (uncensored) survival data,

103 on, and the adverse prognosis of 14q-deleted ccRCC patients.

104 were of higher grade and stage in different ccRCC datasets.

105 most reliable parameters for differentiating ccRCC from other RCC subtypes are aorta-based corrected

106 When differentiating ccRCC from other RCC subtypes, a cut-off AV of 86-89 HU,

107 serves as a potential therapeutic avenue for ccRCC.

108 ial biomarker for use in early detection for ccRCC, and provides a better understanding of carcinogen

109 ol of fatty acid metabolism as essential for ccRCC tumorigenesis.

110 testing CDK4/6 inhibitors as treatments for ccRCC, alone and in combination with HIF-2alpha inhibito

111 s, but its activity on brain metastases from ccRCC remains unknown, because these patients were exclu

112 atients with untreated brain metastases from ccRCC.

113 odels are built to distinguish TFE3-RCC from ccRCC.

114 r rational treatment selection stemming from ccRCC pathobiology.

115 ative groups with high-risk patients who had ccRCC histology and pT3, pT4, or node-positive disease a

116 type of RCC (ccRCC) and analysis of in-house ccRCC cell lines suggested a post-transcriptional contro

117 Human ccRCC tumours clustering with cell lines display clinica

118 and cell viability of 786-O and Caki-1 human ccRCC cell lines.

119 roduce kidney tumours that approximate human ccRCC.

120 man and Drosophila) and across diverse human ccRCC cell lines in culture and xenografts.

121 and ERK1/2 activation were observed in human ccRCC tumors.

122 th altered immune microenvironments in human ccRCC.

123 ltifocal carcinomas, closely mimicking human ccRCC.

124 While correlative studies of human ccRCC and functional studies using human ccRCC cell line

125 ore, VIM tumours more closely simulate human ccRCC.

126 man ccRCC and functional studies using human ccRCC cell lines have implicated HIF-1alpha as an inhibi

127 Here we identified ccRCC lines whose ability to proliferate in vitro and in

128 es reveal an oncogenic role of HIF-1alpha in ccRCC initiation and suggest that alterations in the bal

129 The loss of 5hmC in ccRCC was not due to mutational or transcriptional inact

130 the therapeutic potential of high-dose AA in ccRCC.

131 and chromosomal copy number abnormalities in ccRCC, including chromosome 3p loss, provides a mechanis

132 derlying mechanism for high mTOR activity in ccRCC cells.

133 etabolism may be a new therapeutic avenue in ccRCC.

134 The change in ccRCC volume between two time points and apparent diffus

135 chnique can be utilized to follow changes in ccRCC metabolism in vivo Further development of these pa

136 minantly PBRM1 mutations, are most common in ccRCC.

137 LOY as a highly recurrent genetic defect in ccRCC that leads to downregulation of hitherto unsuspect

138 HIF1alpha is not a target of 14q deletion in ccRCC and that it is not a tumor-suppressor in this mali

139 escribe the mechanism of lipid deposition in ccRCC by identifying the rate-limiting component of mito

140 as predicted to have antisurvival effects in ccRCC, primarily through Th2 immune- and NRF2-dependent

141 tworks associated with survival endpoints in ccRCC were identified, and master regulators of the tran

142 F1A mRNA and HIF1alpha protein expression in ccRCC (R = 0.02), reflecting the primarily post-translat

143 creased HIF-2alpha target gene expression in ccRCC cells and expression was restored upon forced HIF-

144 in most cell types, high PHD3 expression in ccRCC cells maintains elevated HIF-2alpha expression and

145 elation of PHD3 and HIF2A mRNA expression in ccRCC tumors was detected.

146 and were an independent prognostic factor in ccRCC.

147 confirms the upregulation of these genes in ccRCC samples compared to adjacent normal tissue.

148 one 3 lysine 36 trimethylation (H3K36me3) in ccRCC.

149 to further examine the role of HIF1alpha in ccRCC using bioinformatic analyses of 530 ccRCC patients

150 IF-2alpha expression is particularly high in ccRCC and is associated with increased ccRCC growth and

151 d Nedd8-conjugating enzyme E2 were higher in ccRCC tissues and RCC cancer cells than in normal.

152 ll gene-specific signatures was increased in ccRCC compared with pRCC and chRCC, and expression of se

153 uld be relevant for clinical intervention in ccRCC.

154 liferation, anti-migration, anti-invasion in ccRCC cells.

155 ked homologs whose deficiency is involved in ccRCC progression.

156 Few data are available concerning LOX in ccRCC.

157 hich occur in a mutually exclusive manner in ccRCC and define biologically distinct subsets of ccRCC.

158 odifying gene silenced by DNA methylation in ccRCC.

159 PDZK1 overexpression and knockdown models in ccRCC cell lines, we demonstrated that PDZK1 inhibited c

160 Truncal mutations in ccRCC, including those in VHL, SET2, PBRM1 and BAP1, may

161 duces the inflammatory responses observed in ccRCC.

162 To evaluate DFS and overall survival (OS) in ccRCC high-risk patients randomized to sunitinib or sora

163 P-1 activation and poor clinical outcomes in ccRCC.

164 ce that neddylation pathway is overactive in ccRCC and that MLN4924 induces dose-dependent anti-proli

165 ound that endogenous LOX is overexpressed in ccRCC, is involved in a positive-regulative loop with HI

166 is a hallmark of the methylator phenotype in ccRCC, implying a convergence toward loss of function of

167 ation and promoting STAT5 phosphorylation in ccRCC cells.

168 seem to modulate immune cell populations in ccRCC tumours.

169 and immunotherapeutic biomarker potential in ccRCC.

170 d CapZ, is an indicator of poor prognosis in ccRCC.

171 targeting a RUNX1-transcriptional program in ccRCC.

172 breadth of important unanswered questions in ccRCC research far exceeds the accessibility of model sy

173 ive mechanism of lipid storage regulation in ccRCC cells, opening novel translational outcomes.

174 To evaluate its role in ccRCC resistance to RTKi, we established and characteriz

175 nctionally relevant, as deletion of RUNX1 in ccRCC cell lines reduced tumor cell growth and viability

176 blished the importance of RUNX1 and RUNX2 in ccRCC.

177 e gene of HERV-E as expressed selectively in ccRCC tumors, as distinct from normal kidney tissues or

178 d therapeutic inhibition of AXL signaling in ccRCC tumor xenografts reduced tumor vessel density and

179 ce for a pathogenic role of V2R signaling in ccRCC, and suggest that inhibitors of the AVP-V2R pathwa

180 The 36-kDa AnxA3 silencing in ccRCC cells increased lipid storage induced by adipogeni

181 in the canonical pathway, PHD3 silencing in ccRCC cells leads to down-regulation of HIF-2alpha prote

182 lterations influence alternative splicing in ccRCC.

183 owth, angiogenesis, and metastatic spread in ccRCC.

184 a significant increment of lipid storage in ccRCC cells that had a low 36-kDa AnxA3 expression and 3

185 ct as negative regulator of lipid storage in ccRCC cells.

186 approaches for new therapeutic strategies in ccRCC.

187 nt cytotoxic endoplasmic reticulum stress in ccRCC.

188 as identified as a novel tumor suppressor in ccRCC by negating SHP-1 activity.

189 5hmC is associated with reduced survival in ccRCC and provide a preclinical rationale for exploring

190 signature correlated with poorer survival in ccRCC, pRCC and chRCC.

191 o identify additional therapeutic targets in ccRCC downstream of VHL loss besides hypoxia-inducible f

192 ultures, we performed, for the first time in ccRCC, a detailed study of endogenous LOX and also inves

193 requently altered in many cancers, including ccRCC.

194 gh in ccRCC and is associated with increased ccRCC growth and aggressiveness.

195 A higher AR expression increases ccRCC hematogenous metastasis yet decreases ccRCC lympha

196 at the increased accumulation of lipids into ccRCC cells correlated with a decrease of the 36/33 isof

197 pendent expression profiling of intratumoral ccRCC regions demonstrated that average intertumoral het

198 atous and sarcomatoid elements were in known ccRCC genes including von Hippel-Lindau tumor suppressor

199 the effect of EZH2 on outcomes in localized ccRCC is unclear, and molecular biomarkers are not curre

200 improves patient stratification in localized ccRCC, which supports further integration of lncRNAs in

201 on in an independent cohort of 167 localized ccRCCs.

202 c lncRNAs in a training set of 351 localized ccRCCs from The Cancer Genome Atlas and validated lncRNA

203 Although many ccRCC patients initially respond to antiangiogenic thera

204 died 5 patients with localized or metastatic ccRCC in a microdosing regimen, after the administration

205 patients had locally advanced or metastatic ccRCC that had progressed during one or more prior regim

206 point inhibitors in patients with metastatic ccRCC.

207 recently characterized epigenetic modulating ccRCC tumor-suppressor with a marked impact on survival,

208 roteomic characterization of treatment-naive ccRCC and paired normal adjacent tissue samples.

209 d drug Tolvaptan, could be utilized as novel ccRCC therapeutics.

210 remodelling factor PBRM1 (mutated in 40% of ccRCC) rescues VHL-induced replication stress, maintaini

211 orts a large-scale proteogenomic analysis of ccRCC to discern the functional impact of genomic altera

212 a activities can affect different aspects of ccRCC biology and disease aggressiveness.

213 or is nearly universal; thus, the biology of ccRCC is characterized by activation of hypoxia-relevant

214 from these defects enable categorization of ccRCC into clinically and therapeutically relevant subty

215 f VHL loss of function in the development of ccRCC via inflammation remains poorly understood.

216 somatic mutation rate and gene expression of ccRCC tumors from white and African American patients.

217 ologic AA treatment led to reduced growth of ccRCC in vitro and reduced tumor growth in vivo, with in

218 ke significantly delayed xenograft growth of ccRCC.

219 A hallmark of ccRCC is genetic loss-of-function of VHL (von Hippel-Lin

220 stromal cells; however, the vast majority of ccRCC tumors tend to be Pfn1-positive selectively in str

221 ution patterns in the clinical management of ccRCC.

222 of UQCRH in the Warburg effect metabolism of ccRCC have not been characterized.

223 nhibited cell proliferation and migration of ccRCC via targeting SHP-1.

224 Using an in vitro model of ccRCC primary cell cultures, we performed, for the first

225 In multivariate models of ccRCC patients treated with ICB (n = 189), loss-of-funct

226 few (including some often used as models of ccRCC) resemble pRCC, and none resemble chRCC.

227 nxA3 isoforms in lipid storage modulation of ccRCC cells.

228 The evolution patterns of ccRCC have great inter-patient heterogeneities, with del

229 ing in mediating the angiogenic potential of ccRCC cells and support the combination of AXL inhibitor

230 ing in promoting the angiogenic potential of ccRCC cells through the regulation of the plasminogen re

231 age, tumor weight and size, and prognosis of ccRCC patients.

232 hese data suggest that during progression of ccRCC, a decline in H3K36me3 is observed in distant meta

233 r role in the development and progression of ccRCC.

234 opportunities that exploit this property of ccRCC.

235 tumor cell aggressiveness in the setting of ccRCC.

236 dothelial cells in the clinical specimens of ccRCC.

237 In contrast to previous studies of ccRCC, in pRCC, driver gene mutations and most arm-level

238 and define biologically distinct subsets of ccRCC.

239 We successfully found two subtypes of ccRCC using five genomics datasets for Kidney Renal Clea

240 We identify three prognostic subtypes of ccRCC with distinct clonal architectures and immune infi

241 nvelope peptides presented on the surface of ccRCC cells, offering potentially useful tumor-restricte

242 low UQCRH expression and shorter survival of ccRCC patients through in silico analysis and identified

243 bitors are now approved for the treatment of ccRCC, and a HIF2alpha inhibitor has advanced to phase 3

244 shows promise for PT2977 in the treatment of ccRCC.

245 p with HIF-1alpha, and has a major action on ccRCC progression through cellular adhesion, migration,

246 While we focus on ccRCC, this methodology may be employed to predict opioi

247 an tumors with BAP1 mutations, we focused on ccRCC-specific edges associated with tumors that exhibit

248 ing that the androgen receptor (AR)-positive ccRCC may prefer to metastasize to lung rather than to l

249 eral other yet-to-be-characterized potential ccRCC tumor-suppressors.

250 Thus, we aimed to predict ccRCC recurrence risk using lncRNA expression.

251 s active in patients with heavily pretreated ccRCC, validating direct HIF-2alpha antagonism for the t

252 Analysis of 576 primary ccRCC samples demonstrated that loss of 5hmC was strongl

253 within spatially distinct regions of primary ccRCC tumors.

254 GF) expression) from 9 patients with primary ccRCC.

255 also verified in several independent public ccRCC data sets.

256 t is lost in the majority of clear cell RCC (ccRCC) cases.

257 ing VHL, a common initiating clear cell RCC (ccRCC) genetic lesion, and PBRM1 and BAP1 which are earl

258 Clear cell RCC (ccRCC) showed more intense contrast enhancement than oth

259 s derived from patients with clear cell RCC (ccRCC) who exhibited primary resistance to VEGFRi and qu

260 ological subtypes, including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromophobe RCC (chRCC)

261 n human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes.

262 R expression and activity in clear cell RCC (ccRCC).

263 CREB1 protein in the clear cell type of RCC (ccRCC) and analysis of in-house ccRCC cell lines suggest

264 rgized with pazopanib and axitinib to reduce ccRCC patient-derived xenograft growth and vessel densit

265 investigations showed that MCPIP1 regulated ccRCC cell motility, lung metastasis, and mesenchymal ph

266 is and identified KMRC2 as a highly relevant ccRCC cell line that displays hypermethylation-induced U

267 erations shows that most cell lines resemble ccRCC, a few (including some often used as models of ccR

268 odels of acquired or intrinsically resistant ccRCC.

269 reduced the growth of a pazopanib-resistant ccRCC patient-derived xenograft.

270 rapeutic intervention in sunitinib-resistant ccRCC as well as a predictive marker for RTKi response i

271 In this respect, ccRCC might differ from other solid tumors like esophage

272 juvant treatment for patients with high-risk ccRCC.

273 with localized completely resected high-risk ccRCC.

274 t monotherapy in participants with high-risk ccRCC.

275 n this population of patients with high-risk ccRCC.

276 Since ccRCC tumors with PBRM1 mutations respond to targeted th

277 HIF-2alpha inhibitors are effective in some ccRCC cases, but both de novo and acquired resistance ha

278 ng multi-platform genomic data for subtyping ccRCC with the goal of assisting diagnosis, personalized

279 and anti-VEGF-C compounds to better suppress ccRCC progression.The incidence of renal cell carcinoma

280 Furthermore, PET imaging confirmed that ccRCC tumors exhibited increased tumoral uptake of (18)F

281 We show here that ccRCC xenograft tumors under the renal capsule exhibit e

282 Log-rank test showed that ccRCC patients with low levels of CA9 promoter methylati

283 ignals from multiple pathways, including the ccRCC-initiating VHL-HIF2A pathway.

284 y then result in differential impacts on the ccRCC metastatic destinations of VHL-wt ccRCC cells unde

285 nt of a novel therapy to better suppress the ccRCC progression under different oxygenization conditio

286 Here we identify three ccRCC epigenetic clusters, including a clear cell CpG is

287 sights into the molecular drivers underlying ccRCC ontogeny and progression.

288 ould help us in diagnosing and understanding ccRCC.

289 inhibition in HIF-2alpha-dependent VHL(-/-) ccRCC cells and not antagonistic with HIF-2alpha inhibit

290 the increased CDK4/6 requirement of VHL(-/-) ccRCC cells.

291 bolic abnormalities recently associated with ccRCC, it can now be viewed as a metabolic disease.

292 Sixty-three patients with ccRCC were evaluable for overall survival (median, 28.9

293 and Participants: Overall, 438 patients with ccRCC were identified through The Cancer Genome Atlas (T

294 of PET to identify and manage patients with ccRCC who are likely to respond to glutaminase inhibitor

295 success of mTOR inhibition in patients with ccRCC.

296 ntagonism for the treatment of patients with ccRCC.

297 tion and improved survival for patients with ccRCC.

298 PECT tracer for the imaging of patients with ccRCC.

299 the ccRCC metastatic destinations of VHL-wt ccRCC cells under different oxygen conditions.

300 ith VHL to modulate the metastasis of VHL-wt ccRCC via an oxygen-dependent manner.

301 anisms of AR roles in VHL wild-type (VHL-wt) ccRCC, remain unclear.