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1                                              RCC cells supported EC survival in coculture assays and
2                                              RCC induced paracrine extracellular signal-regulated kin
3                                              RCC-induced EC survival was sensitive to sunitinib in ha
4 ring of the antiangiogenic response of 786-0 RCC xenografts to sunitinib, which revealed that pretrea
5 5), papillary (n = 5), and medullary (n = 2) RCC and unclassified RCC (uRCC, n = 23).
6 (12 melanoma studies, 5 NSCLC studies, and 3 RCC studies) (a total of 4496 unique patients) were incl
7 (P = 0.022) and TNM stage (P = 0.022) in 304 RCC and 35 normal renal tissues using tissue microarray.
8                                   Of the 306 RCC patients, low MPV levels were detected in 61 (19.9%)
9                     Sixty-three cysts and 49 RCCs underwent unenhanced computed tomography (CT).
10 .5 +/- 0.3; attenuation: cyst 51.9 +/- 21.5, RCC: 34.8 +/- 10.0).
11                        Our study included 53 RCC patients (19 with bone metastases, 25 with visceral
12 n those of RCCs (SI ratio: cyst 2.4 +/- 0.8, RCC 1.5 +/- 0.3; attenuation: cyst 51.9 +/- 21.5, RCC: 3
13          In this paper, we aimed to report a RCC case with metastasis to parotid and submandibular gl
14 ry effect than VHL wild-type Caki-2 and ACHN RCC cell lines.
15 he viability of a renal cell adenocarcinoma (RCC) cell line, 786-O.
16 eview developments in management of advanced RCC from a radiologist's perspective to highlight our cl
17 istration approval for treatment of advanced RCC in a little over a decade.
18 xture analysis in the management of advanced RCC will also be discussed.
19 tatic surveillance and follow-up of advanced RCC.
20 as revolutionized the management of advanced RCC; 10 novel molecular targeted agents and immune check
21 34 patients with previously treated advanced RCC, enrolled between 2008 and 2012, received intravenou
22 n overall survival in patients with advanced RCC.
23 entral in the care of patients with advanced RCC.
24 AR-mediated HIF-2alpha/C-MYC signals against RCC progression.
25 omotes growth and angiogenesis in vivo in an RCC xenograft tumor.
26 ve case-control study, patients with AML and RCC were identified from the pathology database: there w
27 al kidney, primary and metastatic ccRCC, and RCC subtypes.
28 se relationship between SLFN5 expression and RCC aggressiveness raises the possibility of developing
29  the absence or presence of a renal mass and RCC were verified by abdominal CT and by postnephrectomy
30 -related pneumonitis was higher in NSCLC and RCC and during combination therapy.
31 g enzyme E2 were higher in ccRCC tissues and RCC cancer cells than in normal.
32 ession was down-regulated in Wilms tumor and RCC.
33 ing TRAIL, in multiresistant cancers such as RCC.
34 rtant to recognize the key interplay between RCC, RCC therapy, and CKD.
35 , which was followed by a renal cell cancer (RCC) dose-expansion cohort.
36  and tumor suppressors in renal cell cancer (RCC).
37 LCC) compared with right-sided colon cancer (RCC).
38 LCC) compared with right-sided colon cancer (RCC).
39                        Renal cell carcinoma (RCC) - also known as hypernephroma or grawitz tumor - ac
40                        Renal cell carcinoma (RCC) accounts for several percent of all adult malignant
41 on of surveillance for renal cell carcinoma (RCC) after radical or partial nephrectomy remains unknow
42  have a 7-fold risk of renal cell carcinoma (RCC) and 3-fold risk of urothelial carcinoma (UC) compar
43 hly expressed in human renal cell carcinoma (RCC) biopsies and observed abnormal levels of CCR4 ligan
44 l 786-O, RCC4 and A498 Renal Cell Carcinoma (RCC) cell lines expressing high levels of Hypoxia Induci
45 ies and SETD2 isogenic renal cell carcinoma (RCC) cell lines using chromatin immunoprecipitation coup
46 ty and invasiveness of renal cell carcinoma (RCC) cells.
47  past decade, advanced renal cell carcinoma (RCC) has been at the forefront of oncologic innovation.
48 iated with the risk of renal cell carcinoma (RCC) have been identified, yet genetic predisposition co
49 lear cell or papillary renal cell carcinoma (RCC) in a screening paradigm.
50                        Renal cell carcinoma (RCC) is a cancer with poor prognosis, and the 5-year sur
51                        Renal cell carcinoma (RCC) is a heterogeneous disease made up of a number of d
52             Paediatric renal cell carcinoma (RCC) is a rare neoplasm which differs significantly in i
53                        Renal cell carcinoma (RCC) is one of the most aggressive urologic cancers, how
54                        Renal cell carcinoma (RCC) is polyresistant to chemo- and radiotherapy and bio
55                        Renal cell carcinoma (RCC) occurs in approximately 3% of TSC patients, and typ
56                        Renal cell carcinoma (RCC) of clear-cell type (ccRCC), the most common type, b
57                     As renal cell carcinoma (RCC) patients often present with osteolytic metastases,
58 mpared with clear cell renal cell carcinoma (RCC) supports the study of combination regimens.
59 ve identified multiple renal cell carcinoma (RCC) susceptibility loci.
60 patients with advanced renal cell carcinoma (RCC) treated with nivolumab in a phase I study with expa
61 b, have revolutionized renal cell carcinoma (RCC) treatment.
62 ung cancer (NSCLC), or renal cell carcinoma (RCC) were eligible for a meta-analysis.
63 s and 50 patients with renal cell carcinoma (RCC) were evaluated.
64                     In renal cell carcinoma (RCC), cells deficient in the von Hippel-Lindau (VHL) tum
65 ted from patients with renal cell carcinoma (RCC), colorectal carcinoma, or colorectal liver metastas
66      Kidney cancer, or renal cell carcinoma (RCC), is a disease of increasing incidence that is commo
67 stance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the develop
68 a)-dependent manner in renal cell carcinoma (RCC), yet the role of long noncoding RNAs (LncRNAs) invo
69 tients with metastatic renal cell carcinoma (RCC).
70 tiation of subtypes of renal cell carcinoma (RCC).
71 tients with metastatic renal cell carcinoma (RCC).
72 1 (PD-L1) antibody, in renal cell carcinoma (RCC).
73 n important pathway in renal cell carcinoma (RCC).
74 of targeted therapy in renal cell carcinoma (RCC).
75 overexpressed in human renal cell carcinoma (RCC).
76  malignant glioma, and renal cell carcinoma (RCC).
77 gnostic evaluations of renal cell carcinoma (RCC).
78 fied six risk loci for renal cell carcinoma (RCC).
79 ole remains unclear in renal cell carcinoma (RCC).
80 rst-line treatment for renal cell carcinoma (RCC).
81 d by dose expansion in renal cell carcinoma (RCC).
82 wth and progression of renal cell carcinoma (RCC).
83 m-3 from patients with renal cell carcinoma (RCC).
84      Kidney cancer [or renal cell carcinoma (RCC)] is known as "the internist's tumor" because it has
85  melanoma (n = 16) and renal cell carcinoma (RCC; n = 15).
86 n resected unfavorable renal cell carcinoma [RCC]), the largest adjuvant trial published to date.
87 inst kidney cancer (or renal cell carcinoma, RCC); however, drug resistance frequently occurs via sub
88            Clear cell renal cell carcinomas (RCC) frequently display inactivation of von Hippel-Linda
89 to the development of renal cell carcinomas (RCC).
90 opsy-proved stage T1a renal cell carcinomas (RCCs) treated with percutaneous microwave ablation.
91 and seven chromophobe renal cell carcinomas [RCCs[) that were 1.1-4.0 cm in diameter (mean, 2.7 cm +/
92 s demonstrate that MYC overexpression causes RCC and points to the inhibition of glutamine metabolism
93                                           CC-RCC treatment with ROCK inhibitors is cytotoxic and cyto
94          Clear cell renal cell carcinoma (CC-RCC) is the most lethal of all genitourinary cancers.
95 le factor (HIF) beta in the VHL-deficient CC-RCC had a protective effect against Y-27632 treatment, m
96  for selective targeting of VHL-deficient CC-RCC in multiple genetic backgrounds by clonogenic assays
97 e colony-forming ability of VHL-deficient CC-RCC, thus mimicking the effect of Y-27632 treatment, whe
98  potential therapeutics for VHL-deficient CC-RCC.
99 29286, selectively targeted VHL-deficient CC-RCC.
100 nthetically lethal with VHL deficiency in CC-RCC.
101 Hippel-Lindau (VHL) gene occurs in 90% of CC-RCC, driving cancer progression.
102  inhibited growth of subcutaneous 786-OT1 CC-RCC tumors in mice.
103 r that is lost in the majority of clear cell RCC (ccRCC) cases.
104                                   Clear cell RCC (ccRCC) showed more intense contrast enhancement tha
105 s significantly down-regulated in clear cell RCC (ccRCC), in particular metastatic ccRCC.
106 und in human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes.
107 P=0.001) and WR (P=0.001) between clear cell RCC and other subtypes of RCC.
108 n were pointed out as a potential clear cell RCC biomarkers.
109             The genotype of solid clear cell RCC differed significantly from the genotype of multicys
110 ters useful in differentiation of clear cell RCC from chromophobe and papillary RCCs.
111 R and WR used for differentiating clear cell RCC from other subtypes of RCC were 142 and 38 with area
112 thological result was reported as clear cell RCC metastasis.
113 ty, these models of papillary and clear cell RCC should be significant contributions to the field of
114 e of the left kidney diagnosed as clear cell RCC with vascular invasion, liver, lung and brain metast
115 ovel manifestations of paediatric clear cell RCC.
116  from the genotype of multicystic clear cell RCC.
117  digital CT images and metastatic clear-cell RCC treated with sunitinib were included (n = 275).
118  ER of clear cell, papillary and chromophobe RCC were 188+/-49.7, 35+/-8.9, and 120+/-41.6 respective
119  WR of clear cell, papillary and chromophobe RCCs were 28.6+/-6.8, 47.6+/-5.7 and 42.7+/-10, respecti
120 n (GCC), Regional Certification Commissions (RCCs), and National Certification Committees (NCCs) prov
121  and clear cell RCC (ccRCC), the most common RCC subtypes.
122 luding 47 moderately and five highly complex RCCs.
123 of the patients had pathologically confirmed RCC in further evaluation.
124 nd 19 patients with pathologically confirmed RCC.
125 etrospective study recruited 306 consecutive RCC patients between January 2009 and December 2009.
126 luated based on the residual carbon content (RCC).
127 ]FDA, with overall radiochemical conversion (RCC) more than 3-fold higher than wild-type FlA1.
128 human endogenous retrovirus HERV-E (named CT-RCC HERV-E).
129  peptides predicted to be products of the CT-RCC HERV-E envelope transcript-stimulated CD8(+) T cells
130 eutic strategies for targeting VHL-deficient RCC.
131 al that cystine deprivation in VHL-deficient RCCs presents an attractive therapeutic opportunity that
132 sitivity of urine AQP1 and PLIN2 to diagnose RCC.
133                               To distinguish RCC subtypes based on contrast enhancement features of C
134 e nearly two times more likely to experience RCC-specific death (95% CI, 1.5 to 2.6; P < .001); EZH2
135 ate 2 (FRS2) phosphorylation in fibroblasts, RCC broadly induced low-level fibroblast growth factor r
136 light MCAM and LAMA4 as prime candidates for RCC prognosis and therapeutic targeting.
137 nd independent negative prognostic value for RCC.
138 used to accurately differentiate fp-AML from RCC on unenhanced CT images.
139 nign hemorrhagic or proteinaceous cysts from RCC, although prospective assessment will be needed to c
140 ight on the mechanisms underlying TFE-fusion RCCs and suggest a possible therapeutic strategy based o
141 TFE-fusion renal cell carcinomas (TFE-fusion RCCs) are caused by chromosomal translocations that lead
142 acologic suppression of MARCKS in high-grade RCC cell lines in vitro led to a decrease in cell prolif
143 the anti-apoptotic factor BIRC7 in MiTF-high RCC tumors, suggesting a potential therapeutic role for
144                                     However, RCC is under-recognized by the nephrology community, suc
145 evealed that the mouse tumors mimicked human RCC.
146  we undertook an extensive analysis of human RCC tissue employing combined grade-dependent proteomics
147 ation through stabilization of HIF-1alpha in RCC.
148  that enables TRAIL to activate caspase-8 in RCC.
149 R, 2.85; 95% CI, 1.60-5.08; P < .001) and in RCC for all-grade pneumonitis (OR, 1.59; 95% CI, 1.32-1.
150 tudies and combinations with atezolizumab in RCC.
151 Hippel-Lindau (VHL)-dependent manner both in RCC cell culture and clinical specimens.
152                            Loss of DAB2IP in RCC cells enhances their sensitivities to growth factor
153              After validation experiments in RCC cell lines that were wild-type or mutant for the Von
154 cal analysis of MCAM and LAMA4 expression in RCC and colorectal carcinoma blood vessels.
155                             The incidence in RCC was higher than in melanoma for all-grade pneumoniti
156  the first time that CHIP may be involved in RCC angiogenesis through regulating VEGF secretion and e
157            In this study, C1QBP knockdown in RCC cell influenced expression of multiple genes associa
158 tration rate) and serum sclerostin levels in RCC patients (r = 0.05; p = 0.74) and controls (r = 0.06
159 ed to investigate serum sclerostin levels in RCC patients.
160  observed abnormal levels of CCR4 ligands in RCC patient plasma.
161             Following knockdown of MARCKS in RCC cells, the IC50 of the multikinase inhibitor regoraf
162  assess the occurrence of bone metastases in RCC patients.
163 ent predictor of adverse clinical outcome in RCC.
164 dence of antitumor activity, particularly in RCC.
165 and VEGF-VEGFR2 (VEGF receptor 2) pathway in RCC.
166 ical mediators of an aggressive phenotype in RCC.
167        To identify the function of PIK3R1 in RCC, we examined its expression in normal kidney, pRCC a
168 ased cellular migration and proliferation in RCC cell lines.
169           Overall, PIK3R1 down-regulation in RCC promotes propagation, migration, EMT and stem-like p
170 suppression, which was highly represented in RCC compared with other metabolic pathways.
171 that sorafenib overcomes TRAIL resistance in RCC by a mechanism that does not rely on Mcl-1 down-regu
172 n, was frequently epigenetically silenced in RCC, and DAB2IP loss was correlated with the overall sur
173 revealed vascular MCAM as highly specific in RCC, where it was induced strongly by VEGF, which is hig
174 isease settings as therapeutic strategies in RCC.
175 n was also shown to predict poor survival in RCC, but not in colorectal carcinoma.
176 constitute a potential therapeutic target in RCC.
177 ion homogeneity and higher lesion entropy in RCCs (P </= .01).
178 ntially expressed in many cancers, including RCC, and is down-regulated in metastatic versus primary
179          The data suggested that MYC-induced RCC up-regulated the glutaminolytic pathway instead of t
180 (all P < .001) in the 19 patients with known RCC (AQP1 median [95% CI], 225.0 [121.0-450.0] ng/mg uri
181 ot the RAS oncogene, initiates and maintains RCC.
182                            The low malignant RCC cell line 786-O was chronically treated with sunitin
183 uation was also performed to the renal mass (RCC) of the patient.
184  RNAs (LncRNAs) involved in hypoxia-mediated RCC progression remains unclear.
185 azol-2-yl)ethyl sulfide impeded MYC-mediated RCC tumor progression.
186  regulatory subunit of PI3K, in a metastatic RCC (mRCC), while the mutation was absent in the corresp
187 by prolonged sunitinib therapy in metastatic RCC.
188        Consequently, treatment of metastatic RCC represents an unmet clinical need.
189 l-product-inspired drugs to treat metastatic RCC.
190                    A patient with metastatic RCC experienced a partial response (78% shrinkage, progr
191 ar survival rate of patients with metastatic RCC is 5-10%.
192 server agreement in patients with metastatic RCC treated with sunitinib.
193  months, including a patient with metastatic RCC with progression-free survival of > 3.9 years.
194 titumor activity in patients with metastatic RCC.
195 ng may then lead to differentially modulated RCC progression in a VHL-dependent manner.
196  maps of metabolites and lipids in the mouse RCC samples.
197 with aberrant RNA splicing in a SETD2 mutant RCC and SETD2 knockout cell line.
198 xic cell cycle progression in the VHL-mutant RCC cells while derepress it in the VHL-restored RCC cel
199          Risks of disease recurrence and non-RCC death were estimated by using parametric models for
200 competing risk factors of recurrence and non-RCC death.
201 x-0 disease but a CCI >/= 2, the risk of non-RCC death exceeded that of abdominal recurrence risk alr
202 pT1Nx-0 disease and a CCI </= 1, risk of non-RCC death exceeded that of abdominal recurrence risk at
203  estimated at the point when the risk of non-RCC death exceeded the risk of recurrence.
204 he risk of recurrence versus the risk of non-RCC death.
205 e 3 Trial to Study Efficacy in Nonmetastatic RCC) was a randomized, double-blind, placebo-controlled
206 as a novel agent for elimination of VHL-null RCC cells via apoptosis is warranted for further investi
207 re (Continuous Linear Enhanced Assessment of RCC, or CLEAR score).
208 -the-art knowledge of the molecular basis of RCC and its treatment and imaging will help ensure that
209 anding of the molecular and genetic basis of RCC has revolutionized the management of advanced RCC; 1
210                              The etiology of RCC is still unknown and metastatic involvement can be s
211                   In the most common form of RCC, clear cell renal cell carcinoma (ccRCC), inactivati
212           In patients with with a history of RCC, both past and present, a thyroid mass, especially c
213 ty of MPV value as a prognostic indicator of RCC.
214          The mean serum sclerostin levels of RCC patients and controls were 45.8 pmol/l and 45.1 pmol
215 e how the underlying molecular mechanisms of RCC provide specific targets for novel anticancer agents
216  contribute to progression and metastasis of RCC.
217 ly localized to vessels in a murine model of RCC, offering an opportunity for endothelial-specific ta
218 titumor activity in the RENCA mouse model of RCC.
219                                In a panel of RCC cell lines, we observed nuclear accumulation of beta
220 e also interrogate the vascular phenotype of RCC xenografts exhibiting acquired resistance to sunitin
221 2 or higher was identified as a predictor of RCC for both readers, with no significant difference in
222 k and unfavorable postoperative prognosis of RCC, possibly by down-regulating FSTL1 expression in ren
223 a role in the development and progression of RCC, we identified the best overall drug combination, be
224  have been associated with increased risk of RCC and can result in HIF pathway activation, chromatin
225  EZH2 expression accurately predicts risk of RCC death beyond existing clinicopathologic models, part
226 aft rejection, can also increase the risk of RCC in transplant patients.
227 icantly associated with an increased risk of RCC, with an odds ratio of 2.004 (95% confidence interna
228 a mechanism that explains the sensitivity of RCC tumor growth to GLS1 inhibitors and supports the dev
229 l and synthetic compounds for sensitizers of RCC cells to TRAIL-mediated apoptosis led to identificat
230 een kidney confinement and distant spread of RCC, because this difference affects diagnostic and ther
231 howed no difference between the subgroups of RCC patients with regard to visceral or bone metastases
232 iating clear cell RCC from other subtypes of RCC were 142 and 38 with areas under the curve of 0.937
233                              The subtypes of RCC were as follows: clear cell carcinomas (n=23), papil
234 between clear cell RCC and other subtypes of RCC.
235 3 had biomarker concentrations suggestive of RCC and were found to have an imaged renal mass by CT.
236 oding RNA FILNC1, which inhibits survival of RCC by downregulating c-Myc and c-Myc-dependent metaboli
237  was correlated with the overall survival of RCC patients.
238               Chronic sunitinib treatment of RCC cell lines activated both AXL and MET, induced EMT-a
239 l class of therapeutics for the treatment of RCC with potent preclincal efficacy as well as improved
240 e therapeutic approaches in the treatment of RCC, by modulating SLFN5 expression.
241 nase inhibitor approved for the treatment of RCC, has been shown to sensitize cancer cells to TRAIL-i
242 , pathology, and approaches for treatment of RCC.
243 eport the first detailed genetic analysis of RCCs in TSC patients.
244  can be modified to enhance sensitization of RCCs to TRAIL-mediated apoptosis, thereby assisting deve
245 ysts were significantly higher than those of RCCs (SI ratio: cyst 2.4 +/- 0.8, RCC 1.5 +/- 0.3; atten
246 ameters for differentiating ccRCC from other RCC subtypes are aorta-based corrected AV and aorta-base
247        When differentiating ccRCC from other RCC subtypes, a cut-off AV of 86-89 HU, aorta-based corr
248 nts with papillary features but not in other RCC variants.
249 the CDC signature is closer to that of other RCC subtypes than to UTUC, which is similar to that of b
250 more intense contrast enhancement than other RCC subtypes.
251     Such a novel manifestation of paediatric RCC has not been described previously in literature.
252 ssive biological behaviour of the paediatric RCC in our case and the consequent atypical imaging find
253 s showed multifocal TSC-associated papillary RCC (PRCC).
254 r detecting malignancy, most often papillary RCC.
255 ening biomarkers for clear cell or papillary RCC and in the differential diagnosis of imaged renal ma
256                     Eighteen of 20 papillary RCCs were hypovascular.
257 he highest miR-126 expression, and papillary RCCs exhibited the lowest expression.
258 lear cell RCC from chromophobe and papillary RCCs.
259 oven case of clear cell variety of pediatric RCC which showed invasion into the pelvicalyceal system
260 here is no consensus for posttransplantation RCC or UC screening as supporting data are limited.
261 tion was absent in the corresponding primary RCC (pRCC).
262        We evaluated the potential of primary RCC cultures (derived from tumors and tumor grafts) to s
263 - 9.4) with 100 stage T1a N0M0 biopsy-proved RCCs (median diameter, 2.6 cm +/- 0.8) underwent percuta
264  to recognize the key interplay between RCC, RCC therapy, and CKD.
265  Patients with advanced treatment-refractory RCC treated with nivolumab demonstrated durable response
266 CC), World Health Organization (WHO) region (RCC), or globally (GCC).
267 study demonstrated that C1QBP could regulate RCC metastasis by regulating the GSK3/beta-Catenin/L1CAM
268                           C1QBP may regulate RCC cell adhesion and invasion through influencing the p
269          In vitro, CHIP negatively regulated RCC cell migration, invasion and angiogenesis.
270 ng cabozantinib in anti-angiogenic resistant RCC.
271 veral from patients with sunitinib-resistant RCC, were established.
272 cells while derepress it in the VHL-restored RCC cells.
273 s suitable for an efficient digestion, since RCC was lower than 18% and the agreement with certified
274 ancers, however, the mechanism on supporting RCC carcinogenesis is still not clear.
275 tive and safe treatment option for stage T1a RCC, regardless of tumor complexity.
276                           Our data show that RCC activates EC through VEGF-dependent and -independent
277 aminase inhibition with CB-839 or BPTES, the RCC cell lines SN12PM-6-1 (SN12) and 786-O exhibited dec
278 response rate was 21% overall and 27% in the RCC subset.
279                         We conclude that the RCC risk allele at 12p12.1 maps to rs7132434, a function
280                                   Therefore, RCC is labeled the internist's tumor.
281     We present an individualized approach to RCC surveillance that bases the duration of follow-up on
282 enes at these regions that may contribute to RCC susceptibility.
283 , and medullary (n = 2) RCC and unclassified RCC (uRCC, n = 23).
284 s containing sunitinib-treated and untreated RCC tissues were stained with MET and AXL antibodies.
285 ckpoint, and suppressed the growth of VHL-/- RCC cells.
286               Here we have shown that VHL-/- RCC cells rely on RC-derived aspartate to maintain de no
287  Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-effects models.
288  Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-effects models.
289 ts for most of the mortality associated with RCC.
290              Results Fifty-one patients with RCC (N = 22) were enrolled, including 30 (59%) with one
291        A total of 8-14% of the patients with RCC has head and neck metastasis.
292 alivary gland mass detected in patients with RCC history.
293 anoma and four of 15 evaluable patients with RCC treated at 20 mug/kg (overall response rate, 27%).
294 ractory disease, including one patients with RCC with ongoing response > 3.5 years.
295 of nephrectomy samples from 56 patients with RCC, we found that MARCKS expression and its phosphoryla
296 e fat at unenhanced CT) and 84 patients with RCC.
297  survival in a large cohort of patients with RCC.
298 SNPs within FSTL1-coding genomic region with RCC risk and postoperative prognosis.
299                       66-year old woman with RCC history was referred to our radiology department for
300  (27 M, 7 F, aged 25-72 ys: mean 45 ys) with RCC.

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