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1 xtrarenal or BM-derived cells from intrinsic renal cells.
2 se-induced or Wnt3a-induced Wnt signaling in renal cells.
3 nt role in Ca(2+) signaling in renal and non-renal cells.
4 ing previous published evidences obtained in renal cells.
5 iting AMP-activated protein kinase (AMPK) in renal cells.
7 used murine in vitro model for the study of renal cell adenocarcinoma, aldosterone increased RENCA c
8 exhibit enhanced intracellular retention in renal cells, an observation that probably explains the H
9 ntial regulation of Cyp27b1 in renal and non-renal cells and has implications for vitamin D biology i
10 nflammasome and IL-1alpha/beta regulation in renal cells and in experimental kidney disease models.
11 ustained low-level Chi3l1 mRNA expression by renal cells and promoted macrophage persistence and seve
12 d with altered epithelialization/polarity in renal cells and with pronephric cysts and microphthalmia
13 renal hepcidin, both in vivo and in cultured renal cells, and reduced phosphorylation of SMAD kinase
14 ial cell AGEs and RAGE levels, pulmonary and renal cell apoptosis, and the progression of chronic ren
18 itors (SMIs) are commonly used in metastatic renal cell cancer (mRCC) patients; patients often develo
21 isk of upper urinary tract cancer, including renal cell cancer and cancers of the renal pelvis or ure
23 nce for aldosterone serving a causal role in renal cell cancer regulation via its GPER receptor; thus
24 ccumulation in hereditary leiomyomatosis and renal cell cancer tumors is thought to result from fumar
25 PET/CT imaging of 10 subjects with stage IV renal cell cancer was performed after intravenous admini
32 mutation in von Hippel-Lindau (VHL) develop renal cell cancers and hypervascular tumors of the brain
36 nce analysis in two cancer types, clear cell renal cell carcinoma (ccRCC) and prostate adenocarcinoma
37 3) channel promotes the growth of clear cell renal cell carcinoma (ccRCC) and stimulates MAP1LC3A (LC
38 mask (VAM) in H&E micrographs of clear cell renal cell carcinoma (ccRCC) cases from The Cancer Genom
39 esence of sarcomatoid features in clear cell renal cell carcinoma (ccRCC) confers a poor prognosis an
41 n of chromatin-modifying genes in clear cell renal cell carcinoma (ccRCC) has been uncovered through
43 ecent genomic studies of sporadic clear cell renal cell carcinoma (ccRCC) have uncovered novel driver
46 infiltration score and find that clear cell renal cell carcinoma (ccRCC) is among the highest for bo
56 mune profiling of samples from 73 clear cell renal cell carcinoma (ccRCC) patients and five healthy c
57 ofiling of a cohort of 50 primary clear cell renal cell carcinoma (ccRCC) samples from The Cancer Gen
58 aled to be downregulated in human clear cell renal cell carcinoma (ccRCC) samples, which was also ver
59 studies have demonstrated that in clear cell renal cell carcinoma (ccRCC) several chromatin remodelin
60 -Lindau (VHL) are major causes of clear-cell renal cell carcinoma (ccRCC) that may originate from chr
62 an important prognostic factor of clear cell renal cell carcinoma (ccRCC), as well as a factor in gui
63 In the most common form of RCC, clear cell renal cell carcinoma (ccRCC), inactivation of the von Hi
65 arly event in almost all cases of clear cell renal cell carcinoma (ccRCC), the most frequent form of
76 nsferase, have been identified in clear cell renal cell carcinoma (ccRCC); however it is unclear if l
77 ntly inactivated in patients with clear cell renal cell carcinoma (ccRCC); however, it is largely unk
78 pes from The Cancer Genome Atlas: clear cell renal cell carcinoma (ccRCC, also known as kidney renal
80 cytoreductive nephrectomy (CN) in metastatic renal cell carcinoma (mRCC) has become unclear since the
83 is a standard initial therapy in metastatic renal cell carcinoma (mRCC), but chronic dosing requires
89 6.57; P < .001) in patients with melanoma or renal cell carcinoma (N = 60) than lung cancer (N = 153)
90 argeted therapies in advanced non-clear cell renal cell carcinoma (ncRCC) compared with clear cell re
91 Purpose Patients with advanced papillary renal cell carcinoma (PRCC) have limited therapeutic opt
95 The appropriate duration of surveillance for renal cell carcinoma (RCC) after radical or partial neph
96 cipients, for example, have a 7-fold risk of renal cell carcinoma (RCC) and 3-fold risk of urothelial
97 writing (EW) intervention for patients with renal cell carcinoma (RCC) and identified a potential un
99 ined that CCR4 was highly expressed in human renal cell carcinoma (RCC) biopsies and observed abnorma
100 r syndrome associated with susceptibility to renal cell carcinoma (RCC) caused by inactivating mutati
101 ippel-Lindau (VHL)-null 786-O, RCC4 and A498 Renal Cell Carcinoma (RCC) cell lines expressing high le
102 toreductive nephrectomies and SETD2 isogenic renal cell carcinoma (RCC) cell lines using chromatin im
105 morphisms (SNPs) associated with the risk of renal cell carcinoma (RCC) have been identified, yet gen
106 o diagnose malignant clear cell or papillary renal cell carcinoma (RCC) in a screening paradigm.
115 l carcinoma (ncRCC) compared with clear cell renal cell carcinoma (RCC) supports the study of combina
117 d long-term safety in patients with advanced renal cell carcinoma (RCC) treated with nivolumab in a p
119 lay an essential role in the pathogenesis of renal cell carcinoma (RCC) under normoxic conditions, th
120 noma, non-small cell lung cancer (NSCLC), or renal cell carcinoma (RCC) were eligible for a meta-anal
123 ant endothelium collected from patients with renal cell carcinoma (RCC), colorectal carcinoma, or col
125 ation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rat
126 ctor-2alpha (HIF-2alpha)-dependent manner in renal cell carcinoma (RCC), yet the role of long noncodi
144 sorafenib vs placebo in resected unfavorable renal cell carcinoma [RCC]), the largest adjuvant trial
147 s </= 10% of pheochromocytoma or early-onset renal cell carcinoma and </= 40% of CNS hemangioblastoma
151 second-line targeted therapy for metastatic renal cell carcinoma at 19 centres in Canada, USA, Greec
154 ne treatment in a xenograft model using ACHN renal cell carcinoma cells did not differ from vehicle c
156 ght to validate the International Metastatic Renal Cell Carcinoma Database Consortium (IMDC) model in
158 nfiltrated lymphocytes from 16 patients with renal cell carcinoma demonstrated 56% of a strong tumor-
160 characterization of the genome of clear cell renal cell carcinoma enabled identification of the roles
161 had been functionally disabled in the human renal cell carcinoma environment without unleashing unde
162 ed melanoma, non-small cell lung cancer, and renal cell carcinoma has hastened the need to better cha
164 systemic therapy in patients with metastatic renal cell carcinoma have not been studied in the settin
166 resent the case of endovascular treatment of renal cell carcinoma in patient with solitary kidney.
168 tocrine/paracrine signaling in patients with renal cell carcinoma is associated with poor prognosis o
169 suppress ccRCC progression.The incidence of renal cell carcinoma is higher in males than in females
172 ce after nephrectomy in localised clear cell renal cell carcinoma is well characterised by clinical a
175 ium (IMDC) model in patients with metastatic renal cell carcinoma receiving next-line targeted therap
177 surveillance, periodic self-examination, and renal cell carcinoma surveillance should be encouraged i
178 71.9 years +/- 10.9) with 217 biopsy-proven renal cell carcinoma tumors treated with thermal ablatio
179 ment-naive progressive metastatic clear cell renal cell carcinoma were enrolled between September 201
182 tic or locally advanced (or both) clear-cell renal cell carcinoma were randomly assigned (3:2) to rec
183 l of 361 patients with metastatic clear cell renal cell carcinoma were randomly assigned equally to a
184 ents from France with stage I-III clear cell renal cell carcinoma who had also undergone nephrectomy.
185 tter than that of sorafenib in patients with renal cell carcinoma who had progressed on previous VEGF
186 in 942 patients with stage I-III clear cell renal cell carcinoma who had undergone a nephrectomy at
187 urvival benefit for patients with metastatic renal cell carcinoma who have progressed after one previ
188 cal need exists for patients with metastatic renal cell carcinoma who have progressed on VEGF-targete
189 hibitor everolimus in patients with advanced renal cell carcinoma who progressed after previous VEGFR
190 y, previously treated patients with advanced renal cell carcinoma who were randomly assigned to nivol
191 chromophobe, or unclassified non-clear cell renal cell carcinoma with no history of previous systemi
192 standard first-line treatment in metastatic renal cell carcinoma with postulated favourable immunomo
193 cRNA-SARCC (Suppressing Androgen Receptor in Renal Cell Carcinoma) is differentially regulated by hyp
195 ys, and tumor evolution and heterogeneity in renal cell carcinoma, as well as the most recent advance
196 the transcription factor HNF4A in clear cell renal cell carcinoma, despite no differential expression
197 cy in other patient tumor samples (including renal cell carcinoma, glioblastoma multiforme, head and
199 older with advanced or metastatic clear-cell renal cell carcinoma, measurable disease, and previous t
200 presence of BAP1-associated cancers such as renal cell carcinoma, mesothelioma and meningioma, but n
201 oma, but not in another approved malignancy, renal cell carcinoma, or when data were pooled across al
203 a phase 2 study in patients with metastatic renal cell carcinoma, overall survival was associated wi
204 d tissues from patients and murine models of renal cell carcinoma, pancreatic ductal adenocarcinoma,
205 come in patients with stage I-III clear cell renal cell carcinoma, providing a more accurate and indi
206 nitially effective against kidney cancer (or renal cell carcinoma, RCC); however, drug resistance fre
208 In patients with metastatic non-clear cell renal cell carcinoma, sunitinib improved progression-fre
228 expressed in kidney, and is downregulated in renal cell carcinoma; also, its low expression correlate
229 nesis has had some success in tumors such as renal cell carcinoma; however, angiogenesis inhibitors h
230 ater with completely resected non-metastatic renal-cell carcinoma and adequate cardiac, renal, and he
232 y of sunitinib in patients with locoregional renal-cell carcinoma at high risk for tumor recurrence a
233 Among patients with locoregional clear-cell renal-cell carcinoma at high risk for tumor recurrence a
235 fically suppressed growth in patient-derived renal-cell carcinoma cells with endogenous PIK3Cbeta(D10
237 th treatment-naive, asymptomatic, metastatic renal-cell carcinoma from five hospitals in the USA, Spa
240 ents with locoregional, high-risk clear-cell renal-cell carcinoma to receive either sunitinib (50 mg
242 bout the genetic basis of sporadic papillary renal-cell carcinoma, and no effective forms of therapy
243 ogenic agents that are effective in advanced renal-cell carcinoma, in patients with resected local di
247 nitiation of systemic therapy for metastatic renal-cell carcinoma; a decision that was made at the di
249 is inactivated in the majority of clear cell renal cell carcinomas (ccRCC), but genetic ablation of V
252 A subset of familial and sporadic clear cell renal cell carcinomas (ccRCCs) is believed to develop fr
253 is inactivated in the majority of clear cell renal cell carcinomas (ccRCCs), leading to inappropriate
254 ncluded renal oncocytomas and non-clear cell renal cell carcinomas (nccRCCs), consisting of papillary
255 he histomorphological subtyping of papillary renal cell carcinomas (pRCCs) has improved the predictio
258 for 100 consecutive biopsy-proved stage T1a renal cell carcinomas (RCCs) treated with percutaneous m
260 ar cell, 20 papillary, and seven chromophobe renal cell carcinomas [RCCs[) that were 1.1-4.0 cm in di
262 infiltrate in human lung adenocarcinomas and renal cell carcinomas can be reliably dissected with mas
264 ificant portion of aggressive non-clear cell renal cell carcinomas that have no standard therapy.
267 ently mutated in a significant percentage of renal cell carcinomas, raising the possibility that the
268 d in a distinct subgroup of type 2 papillary renal-cell carcinomas that was characterized by poor sur
271 l carcinoma, which accounts for 15 to 20% of renal-cell carcinomas, is a heterogeneous disease that c
272 ar characterization of 161 primary papillary renal-cell carcinomas, using whole-exome sequencing, cop
274 DK4/6) pathway is activated in parallel with renal cell-cycle entry but before the development of AKI
277 p27b1 is also expressed at low levels in non-renal cells, in which transcription was modulated exclus
279 In damaged kidneys and cytokine-stimulated renal cells, JQ1 reduced the nuclear levels of RelA NF-k
280 y) and polarized (Madin-Darby canine kidney) renal cell lines and electrophysiology on Xenopus oocyte
282 Intrarenal crystals trigger inflammation and renal cell necroptosis, processes that involve TNF recep
286 Infiltrating leukocytes interacting with renal cells play a critical role during the initiation a
289 kidney-specific control module governed by a renal cell-specific chromatin structure located distal t
292 trol mineral homeostasis and second in extra-renal cells to regulate target genes linked to specific
293 ed activation of the IFN response in primary renal cells, tracheal epithelial cells, and a chicken ce
295 is not clear whether HIF signaling in other renal cell types also contributes to the regulation of E
297 by these peptides, is expressed in different renal cell types, including podocytes, where its functio
298 that this activity is triggered in isogenic renal cells upon their transformation independently of t
299 atrix protein increase by activating AMPK in renal cells, we examined whether H2S inhibits high gluco
300 and PCDH9, and increased ICAM5 in muscle and renal cells, while ICAM5 knockdown reduced HIST1H3E expr
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