ライフサイエンスコーパス: RCC

1 RCC is considered to be an immunogenic tumour but is kno

2 RCCs accelerate functional variant discovery via decreas

3 ring of the antiangiogenic response of 786-0 RCC xenografts to sunitinib, which revealed that pretrea

4 Using RNA expression profiles from 1,009 RCC samples, we constructed a condition-annotated gene c

5 Of the 306 RCC patients, low MPV levels were detected in 61 (19.9%)

6 nome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-samp

7 n 6 expression was higher in Caki-1 and ACHN RCC cells.

8 and Caki-1) and papillary (Caki-2 and ACHN) RCC cells.

9 ontrol of our current international adjuvant RCC trial, RAMPART.

10 strategy for checkpoint blockade in advanced RCC.

11 eview developments in management of advanced RCC from a radiologist's perspective to highlight our cl

12 xture analysis in the management of advanced RCC will also be discussed.

13 tatic surveillance and follow-up of advanced RCC.

14 ence to safely manage patients with advanced RCC during this pandemic.

15 w standard of care in patients with advanced RCC.

16 tors hold promise as a novel therapy against RCC.

17 age AXL (0.010 mm; 95% CI: 0.003, 0.017) and RCC (0.005 mm; 95% CI: 0.003, 0.007), increased maternal

18 BMI, demonstrate an association with AXL and RCC measured at age 15 years.

19 containing these variants in endothelial and RCC cell lines, and VEGFA rs58159269 increased endotheli

20 factor for inducing antiangiogenic genes and RCC are highly vascularized, which suggests that p53 is

21 ession was down-regulated in Wilms tumor and RCC.

22 tion and migration of RCC cells in vitro and RCC tumor growth in vivo Based on these findings, we pro

23 The condition annotated RCC GCN described herein is a novel data mining resource

24 arcinoma (RCC) with variant histology or any RCC histology with >= 20% sarcomatoid differentiation.

25 ethylation around the TSS was absent in both RCC cell lines and NKE cells.

26 dividuals are asymptomatic at diagnosis, but RCC has a high mortality rate.

27 the language of Region Connection Calculus (RCC-5) to produce consistent alignments of node concepts

28 LCC) compared with right-sided colon cancer (RCC).

29 igher incidence of right-sided colon cancer (RCC).

30 have a 7-fold risk of renal cell carcinoma (RCC) and 3-fold risk of urothelial carcinoma (UC) compar

31 ion and progression in renal cell carcinoma (RCC) and three oncometabolites - fumarate, succinate and

32 hly expressed in human renal cell carcinoma (RCC) biopsies and observed abnormal levels of CCR4 ligan

33 developing clear cell renal cell carcinoma (RCC) but, paradoxically, obesity is also associated with

34 lates proliferation of renal cell carcinoma (RCC) cell lines in vitro.

35 candidate oncogene in Renal Cell Carcinoma (RCC) cells.

36 Renal cell carcinoma (RCC) comprises a diverse group of malignancies arising f

37 genomic alterations in renal cell carcinoma (RCC) encompassing the major RCC histological subtypes, i

38 al excision of primary renal cell carcinoma (RCC) found to be at intermediate or high risk of recurre

39 past decade, advanced renal cell carcinoma (RCC) has been at the forefront of oncologic innovation.

40 andscape of metastatic renal cell carcinoma (RCC) has been revolutionized over the past two decades,

41 tients with metastatic renal cell carcinoma (RCC) has evolved dramatically.

42 t pathways of advanced renal cell carcinoma (RCC) have considerably evolved in the past 5 years, pres

43 s across all stages of renal cell carcinoma (RCC) in plasma (area under the receiver operating charac

44 Renal cell carcinoma (RCC) incidence is increasing worldwide.

45 Renal cell carcinoma (RCC) is a cancer with poor prognosis, and the 5-year sur

46 Cystic renal cell carcinoma (RCC) is almost certainly overdiagnosed and overtreated.

47 Renal cell carcinoma (RCC) is one of the most aggressive urologic cancers, how

48 Renal cell carcinoma (RCC) is one of the most lethal urological tumors.

49 Renal cell carcinoma (RCC) is polyresistant to chemo- and radiotherapy and bio

50 thase de-repression in renal cell carcinoma (RCC) is poorly understood.

51 w that angiogenesis in renal cell carcinoma (RCC) is regulated through AXL/S100A10 signaling and supp

52 Renal cell carcinoma (RCC) is the most common type of kidney cancer and compri

53 3 tumors from advanced renal cell carcinoma (RCC) patients identifies molecular subsets associated wi

54 and response to ICB in renal cell carcinoma (RCC) remains to be resolved.

55 neous ablation for cT1 renal cell carcinoma (RCC) remains underused, partially because of heterogeneo

56 Renal cell carcinoma (RCC) subtypes are characterized by distinct molecular pr

57 biopsy, with triage of renal cell carcinoma (RCC) to PN or ablation depending on risk factors for wor

58 sistance in metastatic renal cell carcinoma (RCC) treated with antiangiogenic therapy.

59 Human renal cell carcinoma (RCC) tumors were stained for the NK cell receptors CD56,

60 to the progression of renal cell carcinoma (RCC) via a novel epitranscriptomic mechanism that involv

61 wave ablation (MWA) of renal cell carcinoma (RCC) with and without pyeloperfusion.

62 patients with advanced renal cell carcinoma (RCC) with variant histology or any RCC histology with >=

63 treatment for stage I renal cell carcinoma (RCC), albeit without supportive level I evidence.

64 tromal tumors (GISTs), renal cell carcinoma (RCC), and pancreatic cancer, has been reported to inhibi

65 e been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directl

66 In renal cell carcinoma (RCC), cells deficient in the von Hippel-Lindau (VHL) tum

67 atients had metastatic renal cell carcinoma (RCC), endometrial cancer, squamous cell carcinoma of the

68 with increased risk of renal cell carcinoma (RCC), the most common form of kidney cancer.

69 om three patients with renal cell carcinoma (RCC), were imaged.

70 therapy in metastatic renal cell carcinoma (RCC).

71 the cells of origin of renal cell carcinoma (RCC).

72 role of syntaxin 6 in renal cell carcinoma (RCC).

73 e yet to be studied in renal cell carcinoma (RCC).

74 fied six risk loci for renal cell carcinoma (RCC).

75 malignant glioma, and renal cell carcinoma (RCC).

76 gnostic evaluations of renal cell carcinoma (RCC).

77 nly poorly analyzed in renal cell carcinoma (RCC).

78 bination in metastatic renal cell carcinoma (RCC).

79 RC) is the most common renal cell carcinoma (RCC).

80 melanoma (n = 16) and renal cell carcinoma (RCC; n = 15).

81 n resected unfavorable renal cell carcinoma [RCC]), the largest adjuvant trial published to date.

82 renal oncocytoma, and renal cell carcinomas (RCC).

83 tological subtypes of renal cell carcinomas (RCCs) and carries a decidedly poor prognosis.

84 opsy-proved stage T1a renal cell carcinomas (RCCs) treated with percutaneous microwave ablation.

85 Categorizing RCC samples as CREB1 negative or positive, respectively,

86 CC-RCC treatment with ROCK inhibitors is cytotoxic and cyto

87 Clear cell renal cell carcinoma (CC-RCC) is the most lethal of all genitourinary cancers.

88 for selective targeting of VHL-deficient CC-RCC in multiple genetic backgrounds by clonogenic assays

89 e colony-forming ability of VHL-deficient CC-RCC, thus mimicking the effect of Y-27632 treatment, whe

90 potential therapeutics for VHL-deficient CC-RCC.

91 29286, selectively targeted VHL-deficient CC-RCC.

92 inhibited growth of subcutaneous 786-OT1 CC-RCC tumors in mice.

93 ncluding VHL, a common initiating clear cell RCC (ccRCC) genetic lesion, and PBRM1 and BAP1 which are

94 Clear cell RCC (ccRCC) showed more intense contrast enhancement tha

95 models derived from patients with clear cell RCC (ccRCC) who exhibited primary resistance to VEGFRi a

96 histological subtypes, including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromophobe RCC (c

97 ed V2R expression and activity in clear cell RCC (ccRCC).

98 t of patients with non-metastatic clear cell RCC (the MSK peritumoral adipose tissue cohort).

99 clinical cohorts of patients with clear cell RCC aged 18 years and older.

100 arkably lower glucose uptake than clear cell RCC and papillary RCC.

101 he largest cohort to date) and 74 clear cell RCC cases (ccRCC, the most common RCC subtype) with matc

102 advantage in obese patients with clear cell RCC compared with patients at a normal weight.

103 k of recurrence, or patients with clear cell RCC only.

104 ty, these models of papillary and clear cell RCC should be significant contributions to the field of

105 advanced (ie, stages III and IV) clear cell RCC treated by nephrectomy; after exclusion of 59 (39%)

106 The complex interplay between the clear cell RCC tumour and peritumoral adipose tissue microenvironme

107 Patients with metastatic clear cell RCC who experienced progression after at least one syste

108 was 33% and 50% in patients with clear cell RCC with sarcomatoid differentiation and 26% in patients

109 common subtype (~70% of cases) is clear-cell RCC.

110 ccRCC), papillary RCC (pRCC) and chromophobe RCC (chRCC).

111 particular, renal oncocytoma and chromophobe RCC, which present the most significant morphologic over

112 helper cell signature, was increased in CIMP RCC.

113 sland methylator phenotype-associated (CIMP) RCCs and metabolically divergent chRCCs, and new biomark

114 clear cell RCC cases (ccRCC, the most common RCC subtype) with matched gender and tumor grade.

115 The river continuum concept (RCC) has been historically used as a model to predict th

116 s four regulator of chromosome condensation (RCC) repeats, homologous to those found in the eukaryoti

117 etrospective study recruited 306 consecutive RCC patients between January 2009 and December 2009.

118 Analyzing 453 consecutive RCC tumors by immunohistochemistry, weakly negative, but

119 nfidence interval (CI)] only red cell count (RCC) (p = 0.004), red cell distribution width (RDW) (p <

120 s (BP), respiratory-cardiovascular coupling (RCC), central chemoreflex function, cardiac autonomic co

121 tion, we explore reduced complexity crosses (RCCs) between phenotypically divergent, yet genetically

122 mage-guided percutaneous cryoablation of cT1 RCC and to compare outcomes for CT versus MRI guidance.

123 yoablation for solitary pathology-proven cT1 RCC between August 2000 and July 2017.

124 ficant capture of renal cell carcinoma CTCs (RCC-CTCs) remains elusive due to their heterogenous surf

125 (AXL; mm), and radius of corneal curvature (RCC; mm).

126 aft models, Tolvaptan and OPC31260 decreased RCC tumor growth by reducing cell proliferation and angi

127 ovel capture platform is developed to detect RCC-CTCs through integration of dendrimer-mediated multi

128 ineered capture platform effectively detects RCC-CTCs for their potential use as tumor biomarkers.

129 application of this resource, we discovered RCC GCN edges and modules that were associated with gene

130 nd tumour metabolism, as well as within each RCC subtype, of which some correlated with differences i

131 ls; developing non-invasive methods of early RCC detection; establishing the feasibility, public acce

132 Eight RCC recurrence models (University of California at Los A

133 dge, the first prospective study to evaluate RCC risk in relation to various pesticides.

134 ted adjuvant trial data to validate existing RCC prediction models and demonstrate a sharp decrease i

135 (0.021 mm; 95% CI: 0.015, 0.028) and flatter RCC (0.008 mm; 95% CI: 0.006, 0.010).

136 (0.067 mm; 95% CI: 0.032, 0.10) and flatter RCC (0.023 mm; 95% CI: 0.013, 0.034) and increasing birt

137 ing birth weight was associated with flatter RCC (0.005 mm; 95% CI: 0.0003, 0.009).

138 ORR(week24) was as follows: RCC, 63% (19/30; 95% CI, 43.9% to 80.1%); endometrial ca

139 98, 95% CI 0.84-1.14), increase the risk for RCC.

140 and a new analysis shows that screening for RCC could potentially be cost-effective.

141 b should not be used as adjuvant therapy for RCC.

142 he expansion of immunotherapies approved for RCCs has generated a search for biomarkers that might be

143 Lastly, an antibody cocktail targeting four RCC-CTC surface receptors, which included epithelial cel

144 acologic suppression of MARCKS in high-grade RCC cell lines in vitro led to a decrease in cell prolif

145 responses in patients with variant histology RCC or RCC with >= 20% sarcomatoid differentiation.

146 n and 26% in patients with variant histology RCC.

147 f MTHFD2 was significantly elevated in human RCC tissues, and MTHFD2 knockdown strongly reduced xenog

148 levels in various cancer cells and in human RCC tumors correlate with higher histone acetylation lev

149 tigated V2R expression and activity in human RCC tumors, and its role in RCC tumor growth.

150 atlas (TCGA) database, and analysis of human RCC tumor tissue microarrays, cDNA arrays and tumor biop

151 Immunofluorescence staining on human RCC samples demonstrated the advantages of NKp30 targeti

152 0-year oncologic outcomes of PCA for stage I RCC in a prospective manner.

153 a retrospective analysis of the IMmotion150 RCC study also suggests that PBRM1 mutation reduces bene

154 In RCC, as in many other solid malignancies, clinicians rel

155 tus to the metabolic state of tumor cells in RCC.

156 NKp30 and NKp46 costained in RCC samples, demonstrating the expression of these recep

157 A5B is a HIF target gene highly expressed in RCC that promotes in vivo tumor growth.

158 tment response or prognostication feature in RCC, emerging research suggests that the identification

159 he de-repression of the GM2-synthase gene in RCC.

160 idence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and D

161 In this study, C1QBP knockdown in RCC cell influenced expression of multiple genes associa

162 observed abnormal levels of CCR4 ligands in RCC patient plasma.

163 F-2alpha form a positive feedforward loop in RCC, promoting metabolic reprograming and tumor growth.

164 Following knockdown of MARCKS in RCC cells, the IC50 of the multikinase inhibitor regoraf

165 a identifies PAX8 as a candidate oncogene in RCC and provides a potential biomarker to monitor its ac

166 ical mediators of an aggressive phenotype in RCC.

167 We show that restoration of PRDM16 in RCC cells suppresses in vivo tumor growth.

168 ts function as a marker of poor prognosis in RCC patients.

169 pocyte differentiation, is down-regulated in RCC and shows a differential expression pattern for two

170 that sorafenib overcomes TRAIL resistance in RCC by a mechanism that does not rely on Mcl-1 down-regu

171 mRNA to increase the sunitinib resistance in RCC.

172 ctivity in human RCC tumors, and its role in RCC tumor growth.

173 ditional preclinical and clinical studies in RCC.

174 alone, and develop personalized therapies in RCC and other indications.

175 me days (IWDs) of 38 pesticides and incident RCC in the Agricultural Health Study, a prospective coho

176 ips (edges) specific to conditions including RCC subtype and tumor stage.

177 Indirect RCC-5 modeling of intensional (property-based) node conc

178 tory evidence that obesity and DBP influence RCC risk.

179 s into specific chemicals that may influence RCC risk among pesticide applicators.

180 ere associated with genetic lesions in known RCC driver genes, including VHL, a common initiating cle

181 f patients who had nephrectomy for localised RCC at MSK.

182 edictive and prognostic models for localized RCC showed a substantial decrease in each of the predict

183 cell carcinoma (RCC) encompassing the major RCC histological subtypes, including clear cell RCC (ccR

184 Whole-genome sequences of substrains make RCCs possible by supporting the development of array- an

185 Risk of metachronous RCC was 6%.

186 become the first-line therapy for metastatic RCC patients.

187 sponse and disease progression in metastatic RCC treated with vascular endothelial growth factor rece

188 ery 3 weeks is safe and active in metastatic RCC.

189 fter adjustment for International Metastatic RCC Database (IMDC) risk score (0.68, 0.48-0.96).

190 als.gov identifier: NCT00749320), metastatic RCC perfusion was measured with ASL MRI before and durin

191 Consequently, treatment of metastatic RCC represents an unmet clinical need.

192 pects of the molecular biology of metastatic RCC, with an emphasis on predictive and prognostic bioma

193 ab and nivolumab in patients with metastatic RCC after prior treatment with anti-PD-1 pathway-targete

194 ar survival rate of patients with metastatic RCC is 5-10%.

195 Forty-five patients with metastatic RCC were included.

196 eptable toxicity in patients with metastatic RCC who had prior treatment with checkpoint inhibition.

197 Patients with metastatic RCC who received prior anti-PD-1 pathway-targeted therap

198 We enrolled patients with metastatic RCC with no prior checkpoint inhibitor exposure.

199 months, including a patient with metastatic RCC with progression-free survival of > 3.9 years.

200 the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identi

201 Two new RCC subtypes were defined by distinct epigenetic and met

202 2alpha expression, and PHD3 knockdown in non-RCC cells resulted in the expected increase in HIF-2alph

203 e 3 Trial to Study Efficacy in Nonmetastatic RCC) was a randomized, double-blind, placebo-controlled

204 re (Continuous Linear Enhanced Assessment of RCC, or CLEAR score).

205 or receptor (c-Met), improves the capture of RCC cells by up to 80%.

206 tumor samples of two independent cohorts of RCC patients (N = 265 and N = 345); we used immunohistoc

207 erview of genomic evidence in the context of RCC and its potential predictive and prognostic value.

208 prevalence of RCC and stage distribution of RCC detected by screening; and evaluating the potential

209 f individual pesticides and the incidence of RCC.

210 ty of MPV value as a prognostic indicator of RCC.

211 its downstream pathways are the mainstay of RCC development and progression.

212 e how the underlying molecular mechanisms of RCC provide specific targets for novel anticancer agents

213 ce of Pfn1 in proliferation and migration of RCC cells and in soluble Pfn1's involvement in vascular

214 erein reduces proliferation and migration of RCC cells in vitro and RCC tumor growth in vivo Based on

215 titumor activity in the RENCA mouse model of RCC.

216 of screening; establishing the prevalence of RCC and stage distribution of RCC detected by screening;

217 ilencing leads to decreased proliferation of RCC cell lines.

218 Finally, we show that reconstitution of RCC cells with a PRDM16 mutant unable to bind CtBPs null

219 higher body mass index increases the risk of RCC (ORSD: 1.56, 95% confidence interval [CI] 1.44-1.70)

220 statistically significant increased risk of RCC among the highest users of 2,4,5-T compared with nev

221 EZH2 expression accurately predicts risk of RCC death beyond existing clinicopathologic models, part

222 aft rejection, can also increase the risk of RCC in transplant patients.

223 l and synthetic compounds for sensitizers of RCC cells to TRAIL-mediated apoptosis led to identificat

224 to PAX8 silencing and identifies a subset of RCC cases with poor survival.

225 Discrimination of three subtypes of RCC was also achieved on the basis of DESI-MS imaging da

226 oding RNA FILNC1, which inhibits survival of RCC by downregulating c-Myc and c-Myc-dependent metaboli

227 h antiangiogenic agents for the treatment of RCC.

228 n of CREB1 protein in the clear cell type of RCC (ccRCC) and analysis of in-house ccRCC cell lines su

229 carcinoma (PRCC) is the most common type of RCC in end-stage kidney disease (ESKD).

230 on to improving our current understanding of RCC, TCGA RCC studies are an invaluable resource that pr

231 The simplified genetic architecture of RCCs often permit immediate identification of causal var

232 In this study MWAs of RCCs were successfully performed using pyeloperfusion as

233 The effect on RCC risk was estimated by calculating odds ratios (ORSD)

234 in human tumors, whereas tumor cells in one RCC sample expressed the peripheral NK marker CD56.

235 es in patients with variant histology RCC or RCC with >= 20% sarcomatoid differentiation.

236 ameters for differentiating ccRCC from other RCC subtypes are aorta-based corrected AV and aorta-base

237 more intense contrast enhancement than other RCC subtypes.

238 resses more aggressively compared with other RCC subtypes, but it is challenging to diagnose TFE3-RCC

239 ed relatively consistent compared with other RCCs, but further investigation of the tumour-immune cel

240 ose uptake than clear cell RCC and papillary RCC.

241 including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromophobe RCC (chRCC).

242 hen MRI findings are indicative of papillary RCC.

243 naged by using MRI to help predict papillary RCC for surveillance.

244 based on histological subtype, the papillary RCC subtype exhibited a significant correlation between

245 nostic biomarker for patients with papillary RCC and syntaxin 6 inhibitors hold promise as a novel th

246 Pathological RCC was observed in HF rats (peak coherence >0.5 between

247 by patient-derived renal cell carcinomas (PD-RCC), and selective inactivation of PI3Kbeta reduced PD-

248 elective inactivation of PI3Kbeta reduced PD-RCC-stimulated EC spheroid sprouting.

249 - 9.4) with 100 stage T1a N0M0 biopsy-proved RCCs (median diameter, 2.6 cm +/- 0.8) underwent percuta

250 6% men) with single, sporadic, biopsy-proven RCC (median size +/- standard deviation, 2.8 cm +/- 1.4)

251 cipants with single, sporadic, biopsy-proven RCC were included to calculate the 10-year overall survi

252 Eighteen biopsies of proven RCC were treated with 20 sessions of MWA.

253 additional exploration in patients with rare RCC, particularly those with PD-L1-positive tumors.

254 lly, conventional treatments for sarcomatoid RCCs (sRCCs) have shown little efficacy, and median surv

255 In summary, RCCs enhance discovery-based genetics of complex traits.

256 ancers, however, the mechanism on supporting RCC carcinogenesis is still not clear.

257 o increase sunitinib sensitivity to suppress RCC progression.

258 oving our current understanding of RCC, TCGA RCC studies are an invaluable resource that provides the

259 histopathology whole-slide images of 74 TFE3-RCC cases (the largest cohort to date) and 74 clear cell

260 ubtle morphological differences between TFE3-RCC and ccRCC and contribute to a potential guideline fo

261 es with significant differences between TFE3-RCC and ccRCC.

262 1.2 translocation renal cell carcinoma (TFE3-RCC) generally progresses more aggressively compared wit

263 ypes, but it is challenging to diagnose TFE3-RCC by traditional visual inspection of pathological ima

264 earning models are built to distinguish TFE3-RCC from ccRCC.

265 contribute to a potential guideline for TFE3-RCC diagnosis.

266 These facts suggest that RCC meets some of the criteria for screening, and a new

267 The RCC GCN contains binary gene coexpression relationships

268 f DOM exported from fluvial systems, and the RCC may be significantly limited in predicting DOM quali

269 Because the RCC-5 alignments fundamentally reflect the trained, logi

270 stinguishing features were found between the RCC subtypes, including in chromosomal alterations and t

271 titatively assess the importance of both the RCC and land use as environmental drivers controlling DO

272 aminase inhibition with CB-839 or BPTES, the RCC cell lines SN12PM-6-1 (SN12) and 786-O exhibited dec

273 xpression allowed to further distinguish the RCC patients with high Fuhrman grade, high tumor stage,

274 response rate was 21% overall and 27% in the RCC subset.

275 ating land use among other controls into the RCC to better predict the fate and quality of DOM export

276 rts a predominantly repressive effect on the RCC transcriptome including suppression of the gene enco

277 sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in

278 nt of a novel therapy to better suppress the RCC progression.

279 e expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines r

280 ed variability that can be attributed to the RCC.

281 matin nuclear fraction of cells and uses the RCC-like domain to interact with Ran.

282 enes at these regions that may contribute to RCC susceptibility.

283 risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework.

284 ygenic biomarkers and their relationships to RCC tumors with specific molecular and mutational profil

285 ptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR/AXL signaling.

286 Efforts to diagnose and treat RCC at a curable stage result in many benign neoplasms a

287 Here we have shown that VHL-/- RCC cells rely on RC-derived aspartate to maintain de no

288 Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-effects models.

289 No association with RCC risk was seen for lipids, overall type 2 diabetes, o

290 mental variables, and their association with RCC risk was subsequently evaluated in a genome-wide ass

291 We found evidence of associations with RCC for four herbicides (2,4,5-T, atrazine, cyanazine, a

292 in clinical responses in some patients with RCC and combinatorial approaches involving checkpoint bl

293 This is of concern as patients with RCC have the poorest clinical outcomes among all CRC pat

294 dity of this assay to identify patients with RCC using urine cell-free DNA (cfDNA; AUROC of 0.86).

295 ractory disease, including one patients with RCC with ongoing response > 3.5 years.

296 of nephrectomy samples from 56 patients with RCC, we found that MARCKS expression and its phosphoryla

297 rds was undertaken to identify patients with RCC, who were treated with MWA with and without adjuncti

298 Tumors from women with RCC were nutrient-deplete, showing enhanced energy produ

299 deplete metabolic subphenotype in women with RCC, with implications for tumor progression and outcome

300 resulted in increasing VEGF-A in the VHL-wt RCC cells.