ライフサイエンスコーパス: ccRCC

1 ccRCC cases are usually associated with mutations in von

2 ccRCC cells normally secrete low amounts of CXCL7; it wa

3 ccRCC harboring epigenetic silencing of NSD1 displayed a

4 ccRCC tumors exhibit substantial mutation heterogeneity.

5 Knockdown of SK1 in 786-0 ccRCC cells had no effect on cell proliferation.

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 ted our results on an independent set of 481 ccRCCs.

11 hich were further analyzed in a cohort of 98 ccRCC patients with 100 month follow-up.

12 ditional overexpression of CXCL7 accelerated ccRCC development.

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

14 survival for African Americans with advanced ccRCC has not changed.

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

16 histone mark as a root feature of aggressive ccRCC.

17 ption, genomic rearrangement, and aggressive ccRCCs.

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

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

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

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

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

23 mutated in clear cell renal cell carcinoma (ccRCC) and has been implicated in the control of multipl

24 ncer types, clear cell renal cell carcinoma (ccRCC) and prostate adenocarcinoma, by comparison with l

25 e growth of clear cell renal cell carcinoma (ccRCC) and stimulates MAP1LC3A (LC3A) and MAP1LC3B (LC3B

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

27 ETD2-mutant clear cell renal cell carcinoma (ccRCC) cells displayed impaired DNA damage signaling.

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

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

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

31 its role in clear cell renal cell carcinoma (ccRCC) has not been described previously.

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

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

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

35 d find that clear cell renal cell carcinoma (ccRCC) is among the highest for both scores.

36 Clear cell renal cell carcinoma (ccRCC) is an aggressive tumor with unpredictable behavio

37 Clear cell renal cell carcinoma (ccRCC) is characterized by inactivation of the von Hippe

38 Clear cell renal cell carcinoma (ccRCC) is characterized by loss of function of the von H

39 mportantly, clear-cell renal cell carcinoma (ccRCC) is frequently associated with monoallelic loss an

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

41 Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer and h

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

43 Human clear cell renal cell carcinoma (ccRCC) is therapy resistant; therefore, it is worthwhile

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

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

46 50 primary clear cell renal cell carcinoma (ccRCC) samples from The Cancer Genome Atlas (TCGA) revea

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

48 ted that in clear cell renal cell carcinoma (ccRCC) several chromatin remodeling enzymes are genetica

49 other hand, clear cell renal cell carcinoma (ccRCC) strongly deviated in terms of metabolic gene expr

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

51 ectivity to clear cell renal cell carcinoma (ccRCC) with common mutations.

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

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

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

55 Clear cell renal cell carcinoma (ccRCC), the most common form of kidney cancer, is charac

56 ll cases of clear cell renal cell carcinoma (ccRCC), the most frequent form of kidney cancer.

57 For clear cell renal cell carcinoma (ccRCC), three of the five commonly mutated genes encode

58 reported in clear cell renal cell carcinoma (ccRCC).

59 tients with clear cell renal cell carcinoma (ccRCC).

60 ciated with clear cell renal cell carcinoma (ccRCC).

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

62 , including clear-cell renal cell carcinoma (ccRCC).

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

64 of HIFs in clear cell renal cell carcinoma (ccRCC).

65 d inherited clear cell renal cell carcinoma (ccRCC).

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

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

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

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

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

71 tients with clear cell renal cell carcinoma (ccRCC); however, it is largely unknown how JARID1C dysfu

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

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

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

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

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

77 -deficient clear cell renal cell carcinomas (ccRCC), the most common form of kidney cancer, express t

78 Clear cell renal cell carcinomas (ccRCCs) are characterized by biallelic loss of the von H

79 Clear cell renal cell carcinomas (ccRCCs) display divergent clinical behaviours.

80 d sporadic clear cell renal cell carcinomas (ccRCCs) is believed to develop from cystic precursor les

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

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

83 ypes, including clear cell renal carcinomas (ccRCCs).

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

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

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

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

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

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

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

91 ccRCC hematogenous metastasis yet decreases ccRCC lymphatic metastases.

92 t higher SK1 and S1P levels in VHL-defective ccRCC could induce invasion in an autocrine manner and a

93 e protein encoded by the VHL gene)-deficient ccRCC cells, FBP1 restrains cell proliferation, glycolys

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

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

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

97 pecific VHL deletion in mice fails to elicit ccRCC-specific metabolic phenotypes and tumour formation

98 In established ccRCC, HIF1alpha has been implicated as a renal tumor su

99 Subcutaneous CAIX-expressing ccRCC xenografts were visualized by optical imaging with

100 wed clear delineation of the CAIX-expressing ccRCC xenografts, and image contrast improved with time.

101 model to develop a five-CpG-based assay for ccRCC prognosis that can be used with formalin-fixed par

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

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

104 S727 is an independent prognostic factor for ccRCC.

105 KIM-1 is a suggested susceptibility gene for ccRCC and ectodomain shedding of this molecule may be a

106 rget PML degradation and mTOR inhibition for ccRCC treatment.

107 nhibitor TGX221 as a selective inhibitor for ccRCC with both VHL and SETD2 mutations.

108 which is associated with poor prognosis for ccRCC patients.

109 a novel inhibitor with high selectivity for ccRCC with VHL and SETD2 mutations.

110 ched for compounds with high selectivity for ccRCC with VHL and/or SETD2 mutations.

111 identified a potential targeted therapy for ccRCC and other VHL-related disease in patients carrying

112 a practical and reliable prognostic tool for ccRCC that can add prognostic value to the staging syste

113 y 2.7-fold higher in solid tumor tissue from ccRCC patients, and this was associated with less surviv

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

115 Human ccRCC tumours clustering with cell lines display clinica

116 roduce kidney tumours that approximate human ccRCC.

117 eterodimer of HIF-2alpha-HIF-1beta) in human ccRCC cells and suppressed tumorigenesis in 56% (10 out

118 ltifocal carcinomas, closely mimicking human ccRCC.

119 ore, VIM tumours more closely simulate human ccRCC.

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

121 ions and suggest that AA may be an important ccRCC carcinogen in Romania, a finding with major public

122 In ccRCC the biallelic inactivation of the VHL gene leads t

123 ET activation by growth arrest-specific 6 in ccRCC and identify AXL as a therapeutic target driving t

124 y suppressed to safeguard the genome, and in ccRCC cells, JARID1C inactivation led to the unrestraine

125 To test the role of BAP1 in ccRCC development, we generated mice deficient for eithe

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

127 catenin inhibitors to rescue ciliogenesis in ccRCC.

128 s, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tumor xenografts.

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

130 define a novel pathway of PML degradation in ccRCC that involves SCP downregulation, revealing contri

131 ithin a region that is frequently deleted in ccRCC on chromosome 3p: SETD2, BAP1, and PBRM1.

132 eterozygosity, hallmarked by VHL deletion in ccRCC, may uniquely shape tumor metabolism.

133 SETD2 depletion in ccRCC cells revealed aberrant and reduced nucleosome com

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

135 g HIF2alpha as a pivotal oncogenic driver in ccRCC.

136 se no other gene is mutated as frequently in ccRCC and VHL mutations are truncal, VHL inactivation is

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

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

139 , we hypothesized that the stabilized HIF in ccRCC cells will be associated with increased SK1 expres

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

141 ssociated with microsatellite instability in ccRCC.

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

143 ked homologs whose deficiency is involved in ccRCC progression.

144 ts use for exposing metabolic liabilities in ccRCC, whose emergent metabolic network enforces outstan

145 FBP1 protein explains its ubiquitous loss in ccRCC, distinguishing FBP1 from previously identified tu

146 Few data are available concerning LOX in ccRCC.

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

148 miR-126 is a promising prognostic marker in ccRCC that can distinguish between clear cell and papill

149 odifying gene silenced by DNA methylation in ccRCC.

150 rophage migration inhibitory factor (MIF) in ccRCC as an autocrine-signaling molecule with elevated e

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

152 Amongst the genes most frequently mutated in ccRCC, we identified SETD2 inactivation as a potent enha

153 clei in uninvolved vs 70% positive nuclei in ccRCC) and reduced by ~60% in metastases (90% positive i

154 duces the inflammatory responses observed in ccRCC.

155 Loss of this key organelle in ccRCC is caused by loss of VHL and associated with incre

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

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

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

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

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

161 ation and promoting STAT5 phosphorylation in ccRCC cells.

162 and immunotherapeutic biomarker potential in ccRCC.

163 tin landscape and transcriptional program in ccRCC or other cancers is not understood.

164 n stream products of VHL, SETD2, and PTEN in ccRCC cells with VHL and SETD2 mutations.

165 tic and epigenetic alterations that recur in ccRCC and discuss the mechanisms through which these eve

166 els of ATG7 and beclin 1 are also reduced in ccRCC tumors.

167 identified in spatially separated regions in ccRCC, indicative of intratumour heterogeneity.

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

169 tes that autophagy has an anticancer role in ccRCC tumorigenesis, and suggests that constitutive auto

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

171 or the disease-associated effects of SNPs in ccRCC.

172 n 2 (NPTX2) is overexpressed specifically in ccRCC primary tumors and metastases, and that it contrib

173 lterations influence alternative splicing in ccRCC.

174 owth, angiogenesis, and metastatic spread in ccRCC.

175 approaches for new therapeutic strategies in ccRCC.

176 nt cytotoxic endoplasmic reticulum stress in ccRCC.

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

178 alidate HIF2alpha as a therapeutic target in ccRCC, reveal variable sensitivity to HIF2alpha antagoni

179 We validate HIF-2 as a target in ccRCC, show that some ccRCCs are HIF-2 independent, and

180 We found that in ccRCC, but not in prostate adenocarcinoma, flux balance

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

182 requently altered in many cancers, including ccRCC.

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

184 Our data further indicate that FBP1 inhibits ccRCC progression through two distinct mechanisms.

185 These discoveries provide insight into ccRCC development and set the foundation for the first m

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

187 decreases in chromatin accessibility at key ccRCC-linked genes, including PBRM1, SETD2 and MLL2.

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

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

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

191 on in an independent cohort of 167 localized ccRCCs.

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

193 in ADC values in patients with high and low ccRCC grades was observed.

194 ion in normal kidney, primary and metastatic ccRCC, and RCC subtypes.

195 essed in two independent cohorts: metastatic ccRCC (n=71) and the Cancer Genome Atlas Kidney Renal Cl

196 inactivation of AXL signaling in metastatic ccRCC cells reversed the invasive and metastatic phenoty

197 ion of AXL receptor expression in metastatic ccRCC.

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

199 r cell RCC (ccRCC), in particular metastatic ccRCC.

200 Moreover, ccRCC patients harboring JARID1C mutations exhibited abe

201 Unexpectedly, some VHL-mutant ccRCCs were resistant to PT2399.

202 SETD2 aberrations and that H3K36me3-negative ccRCCs display elevated DNA damage in vivo.

203 d a novel chimera, the CTSC-RAB38, in 20% of ccRCC samples.

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

205 au (VHL) mutations that occur in over 90% of ccRCC tumours.

206 reduce both the invasion and angiogenesis of ccRCC and therefore improve the survival rate of patient

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

208 ntial racial differences in tumor biology of ccRCC.

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

210 may be an early event in the development of ccRCC.

211 nes that explained the partial divergence of ccRCC metabolism correlated with loss of von Hippel-Lind

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

213 ion not only inhibited malignant features of ccRCC, including proliferation, migration, invasion, tum

214 erexpression signifies an aggressive form of ccRCC in the cancer genome atlas (TCGA) database.

215 y be an initiating event in the formation of ccRCC.

216 ic datasets, we characterize three groups of ccRCC tumors: T cell enriched, heterogeneously infiltrat

217 L7 antibodies strongly reduced the growth of ccRCC tumors in nude mice.

218 ke significantly delayed xenograft growth of ccRCC.

219 A hallmark of ccRCC is loss of the primary cilium.

220 We observe that the immunogenicity of ccRCC tumors cannot be explained by mutation load or neo

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

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

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

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

225 s were associated with worsened prognosis of ccRCC.

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

227 To understand the progression of ccRCC, we generated a novel mouse Vhlh conditional knock

228 ential for the initiation and progression of ccRCC.

229 r role in the development and progression of ccRCC.

230 opportunities that exploit this property of ccRCC.

231 M-seq permits the temporal resolution of ccRCC evolution and refines mutational signatures occurr

232 e in silico methods, can predict the risk of ccRCC associated with VHL missense mutations with high s

233 symphony to generate predictions for risk of ccRCC for all possible VHL missense mutations and presen

234 The risk of ccRCC in VHL disease is linked to the degree of destabil

235 haracterizations of the genetic signature of ccRCC have revealed several factors correlated with tumo

236 markers might improve risk stratification of ccRCC.

237 and define biologically distinct subsets of ccRCC.

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

239 classifier predicts the overall survival of ccRCC patients (hazard ratio=2.96-4.82; P=3.9 x 10(-6)-2

240 s as a pertinent target for the treatment of ccRCC.

241 hibiting cell motility and tumourigenesis of ccRCC cells with VHL and SETD2 mutations.

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

243 Microarray analysis of 769-P ccRCC-derived cells where HAVCR/KIM-1 levels have been u

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

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

246 al tubular epithelial cells, the presumptive ccRCC cell of origin, thereby inhibiting a potential War

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

248 argeting these genes may selectively prevent ccRCC growth.

249 osis in VHL-deficient cell lines and primary ccRCC tumor cells, but not in VHL-restored counterparts.

250 i were reduced an average of ~20% in primary ccRCC (90% positive nuclei in uninvolved vs 70% positive

251 within spatially distinct regions of primary ccRCC tumors.

252 down-regulated in metastatic versus primary ccRCC.

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

254 ostic significance of miR-126 in 264 primary ccRCCs.

255 l ITH is virtually identical between primary ccRCCs of the lowest stage and advanced, metastatic tumo

256 t SPOP serves as a regulatory hub to promote ccRCC tumorigenesis.

257 also verified in several independent public ccRCC data sets.

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

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

260 nificantly down-regulated in clear cell RCC (ccRCC), in particular metastatic ccRCC.

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

262 restores tumorigenesis in VHL-reconstituted ccRCC cells.

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

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

265 imple and atypical renal cysts that resemble ccRCC precursor lesions is greatly accelerated by the co

266 odels of acquired or intrinsically resistant ccRCC.

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

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

269 juvant treatment for patients with high-risk ccRCC.

270 with localized completely resected high-risk ccRCC.

271 t monotherapy in participants with high-risk ccRCC.

272 e HIF-2 as a target in ccRCC, show that some ccRCCs are HIF-2 independent, and set the stage for biom

273 utated tumors and rare in previously studied ccRCCs.

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

275 chitecture and evolutionary histories of ten ccRCCs.

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

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

278 ic diversity has given rise to the idea that ccRCC should actually be considered as a series of molec

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

280 The ccRCCs exhibited the highest miR-126 expression, and pap

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

282 contributions of HIF1alpha and HIF2alpha to ccRCC initiation in the context of Vhl deficiency.

283 , revealing contributions of this pathway to ccRCC progression and offering a mechanistic rationale f

284 away from H3K36me3 sites in SETD2 wild-type ccRCCs relative to tumours with bi-allelic SETD2 aberrat

285 Renal cell carcinoma of clear-cell type (ccRCC) is an enigmatic tumor type, characterized by freq

286 nal cell carcinoma (RCC) of clear-cell type (ccRCC), the most common type, begins with an intragenic

287 e results show that the processes underlying ccRCC tumorigenesis may vary in different populations an

288 ould help us in diagnosing and understanding ccRCC.

289 The clear cell variant (ccRCC) is the most common and aggressive subtype of this

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

291 creased genomic rearrangements compared with ccRCC patients with tumors endowed with other genetic le

292 ion level of autophagy genes correlates with ccRCC progression.

293 lecular target for therapy for patients with ccRCC diagnosed with or at risk of developing metastatic

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

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

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

297 e survival of African American patients with ccRCC, even in the targeted therapy era.

298 in white and African American patients with ccRCC.

299 rgins or metastatic lesions in patients with ccRCC.

300 ntagonism for the treatment of patients with ccRCC.