ライフサイエンスコーパス: kidney cancer

1 ind of EpCAM negative cancer cell line (293T kidney cancer).

2 hose with a history of malignancy (excluding kidney cancer).

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

4 ostate cancer, hematologic malignancies, and kidney cancer.

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

6 prognostic associations, including RUNX1 in kidney cancer.

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

8 Wilms tumour is the most common childhood kidney cancer.

9 testing for detection of inherited forms of kidney cancer.

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

11 enal fibrosis, renovascular hypertension and kidney cancer.

12 Wilms tumour is a childhood kidney cancer.

13 benefit to patients diagnosed with advanced kidney cancer.

14 rmamentarium in the fight against metastatic kidney cancer.

15 rectomy is associated with increased risk of kidney cancer.

16 ell carcinoma (RCC), the most common form of kidney cancer.

17 tegies directed against these rarer forms of kidney cancer.

18 our(2,3), the most common type of paediatric kidney cancer.

19 gene for the hereditary type of chromophobe kidney cancer.

20 n sporadic and hereditary forms of papillary kidney cancer.

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

22 VHL is the gene for clear cell kidney cancer.

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

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

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

26 ential therapeutic agents for BHD-associated kidney cancer.

27 uterine leiomyomas and an aggressive form of kidney cancer.

28 rgeted therapy in the management of advanced kidney cancer.

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

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

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

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

33 to a worse survival outcome in patients with kidney cancer.

34 tastases, especially those with melanoma and kidney cancer.

35 s well as various sporadic cancers including kidney cancer.

36 for multiple myeloma to 4.91 (4.27-5.65) for kidney cancer.

37 way in lung cancer, and purine metabolism in kidney cancer.

38 ported in the literature to be implicated in kidney cancer.

39 ted Akt activation and survival signaling in kidney cancer.

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

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

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

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 with oral, rectal, liver, skin, breast, and kidney cancers.

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

48 opment and progression of human prostate and kidney cancers.

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

50 come for individuals with either prostate or kidney cancers.

51 ver biliary, melanoma, sarcoma, stomach, and kidney cancers.

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

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

54 yeloma (30.5), testicular cancer (17.0), and kidney cancer (12.5); for transplant recipients, SMRs we

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

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

57 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,

58 .0001) and a greater than 2-fold increase of kidney cancer (4/45 vs 6/155; P = .004) over individuals

59 209314 due to uterine cancer; 421628 due to kidney cancer; 487518 due to liver cancer; 13927 due to

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

61 ere highest for non-Hodgkin lymphoma (10.7), kidney cancer (7.8), and melanoma (5.8).

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

63 the new features with case studies for human kidney cancer, a biomarker study on Parkinson's disease

64 In kidney cancer, a spectrum of histological subtypes exist

65 In 2017, kidney cancer accounted for 393.0 thousand (95% UI: 371.

66 here are no recent articles on the burden of kidney cancer across the world.

67 that of its target genes, which may enhance kidney cancer aggressiveness.

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

69 h HIF target gene expression is amplified in kidney cancer and a new mechanism by which PRDM16 exerts

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

71 l carcinoma (RCC) is the most common type of kidney cancer and comprises several subtypes with unique

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

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

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

75 unexplored oncogenic role for RUNX genes in kidney cancer and indicate that targeting the effects of

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

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

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

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

80 e inter-country differences in the burden of kidney cancer and it is generally higher in countries wi

81 y needed to reduce the risk of recurrence of kidney cancer and of dying of metastatic disease.

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

83 er a tumor suppressive mechanism of PBRM1 in kidney cancer and provide a mechanistic insight into the

84 t, currently in clinical trials for advanced kidney cancer and recurrent glioblastoma, in reducing th

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

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

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

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

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

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

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

92 promising approaches to adjuvant therapy in kidney cancer, and a number of trials are now underway.

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

94 l carcinoma (ccRCC), the most common form of kidney cancer, and causes the accumulation of hypoxia-in

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

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

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

98 Patients with melanoma, kidney cancer, and on long-term anticoagulation had a hi

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

100 Approximately 70% of cases of kidney cancer are localized or locally advanced at diagn

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

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

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

104 This pathway-dependent targeting of kidney cancer arises from the fact that the secretion pa

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

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

107 or multiple myeloma to 6.23% (5.32-7.14) for kidney cancer at age 25-29 years, and ranged from 0.37%

108 erine corpus cancer to 2.95% (2.74-3.16) for kidney cancer at age 45-49 years.

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

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

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

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

113 sure were positively associated with risk of kidney cancer but not with other cancers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 onsible for downregulating FBP1 in liver and kidney cancer cells.

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

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

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

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

135 Kidney cancer confined by the renal capsule can be surgi

136 Network analysis of the kidney cancer data in the TCGA database with ProGAdNet a

137 Analyses of bladder, lung, and kidney cancer data indicate that the tRF-mRNA wiring can

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

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

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

141 nal and reproductive factors could influence kidney cancer development.

142 her Wilms tumor (nephroblastoma; a childhood kidney cancer) develops from a premalignant background,

143 Wilms' tumor (WT), the most common childhood kidney cancer, develops in association with an underlyin

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

145 most highly mutated tumor suppressor gene in kidney cancer, encodes PBRM1.

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

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

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

149 ereas it might function as an oncoprotein in kidney cancer, for example, by targeting phosphatase and

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

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

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

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

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

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

156 Kidney cancer globally accounts for more than 131,000 de

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

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

159 The field of hereditary kidney cancer has begun to mature following the identifi

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

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

162 Kidney cancer has unique features that make this maligna

163 f autophagy in polycystic kidney disease and kidney cancer have also been described.

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

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

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

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

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

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

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

171 , RUNX1 deletion in a genetic mouse model of kidney cancer improved overall survival and reduced tumo

172 -adjusted life years (DALYs) associated with kidney cancer in 195 countries, from 1990 to 2017.

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

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

175 dullary carcinoma (RMC) is a rare and deadly kidney cancer in patients of African descent with sickle

176 population-based cohort of 699 patients with kidney cancer in Queensland, Australia (2012-2013).

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

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

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

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

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

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

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

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

185 over 50 children with different subtypes of kidney cancer, including Wilms tumours, malignant rhabdo

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

187 ically significant CKD following surgery for kidney cancer is associated with increased morbidity and

188 Kidney cancer is associated with renal vein or inferior

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

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

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

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

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

194 ar mechanisms involving SPOP in prostate and kidney cancers is needed to improve our understanding of

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

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

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

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

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

200 1 (WT1) gene in humans can lead to childhood kidney cancer, life-threatening glomerular nephropathy a

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

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

203 ated positively with all-cause, diabetes and kidney cancer mortality, and negatively with external ca

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

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

206 95% Confidence Interval [CI] 3.50-7.61) and kidney cancer (OR 2.50; 95% CI 1.69-3.72).

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

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

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

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

211 component of the management of patients with kidney cancer, particularly those who undergo radical re

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

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

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

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

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

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

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

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

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

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

222 The Trust Family Fund for Kidney Cancer Research.

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

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

225 ly reducing angiogenesis in a mouse model of kidney cancer resistant to PD-1 blockade.

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

227 Kidney cancer risk also was increased in liver recipient

228 or renewed efforts to reduce exposure to the kidney cancer risk factors and to improve the prevention

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

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

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

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

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

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

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

236 In kidney cancer, RP subtypes map to molecular subtypes rel

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

238 1 and p21 correlate with each other in human kidney cancer samples.

239 edback loop that is deregulated in liver and kidney cancer.See related article by Liao et al., p.

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

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

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

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

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

245 r suppressor in prostate cancer; however, in kidney cancer, SPOP largely accumulates in the cytoplasm

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

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

248 illary renal cell carcinoma (pRCC) and rarer kidney cancer subtypes, integrating whole-genome sequenc

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

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

251 (ccRCC), but they are less studied for other kidney cancer subtypes.

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

253 rane receptor CD74) in prostate, bladder and kidney cancers suggest that it is a pro-tumorigenic fact

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

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

256 Hereditary kidney cancer syndromes offer valuable insight into the

257 molecules but has yet to be used to enhance kidney cancer targeting.

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

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

260 and renal cell carcinoma (HLRCC), a type of kidney cancer that harbors fumarate hydratase (FH)-inact

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

262 association between hypertension and risk of kidney cancer, the current meta-analysis suggested that

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

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

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

266 nd will likely continue as central tenets of kidney cancer therapeutics.

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

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

269 d for imaging of target metabolites in human kidney cancer tissue.

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

271 int inhibition is a well-established part of kidney cancer treatment, and rapid advances continue to

272 RI could be further developed to personalize kidney cancer treatment.

273 tumorigenesis have been highly actionable in kidney cancer treatments, and will likely continue as ce

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

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

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

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

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

279 The considerable burden of kidney cancer was attributable to high body mass index (

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

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

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

283 7138 Medicare beneficiaries with early-stage kidney cancer, we identified 1925 patients (27.0%) treat

284 ients' risk of CKD arising after surgery for kidney cancer, we tested models in a population-based co

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

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

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

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

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

290 fluorophore for hyperfluorescence imaging of kidney cancers, which cannot be achieved with hepatobili

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

292 P4 is a potential tumor suppressor for human kidney cancer, whose downregulation is correlated with Y

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

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

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

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

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

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

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

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