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.