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1 carcinoma histotypes (serous, endometrioid, clear cell).
2 Rlog2 = 1.40 (1.03-1.91)], but not serous or clear cell.
3 d, most notably, two distinct populations of clear cells.
4 microglia respond, microglia are the debris-clearing cell.
6 1.17)], endometrioid [1.20 (1.10-1.32)], and clear cell [1.37 (1.18-1.58)], but not mucinous [0.99 (0
8 stoma) and 68 malignant masses (including 41 clear cell, 20 papillary, and seven chromophobe renal ce
10 Next, syntaxin 6 expression was evaluated in clear cell (786-O and Caki-1) and papillary (Caki-2 and
12 ncanonical signaling by IL6 in human ovarian clear cell adenocarcinoma cell lines and identifies comb
18 ring by risk factors separated endometrioid, clear cell, and low-grade serous carcinomas from high-gr
19 is-related tumors that include endometrioid, clear cell, and seromucinous carcinomas; ii) low-grade s
20 helial cell types including principal cells, clear cells, and basal cells, along with associated supp
21 Further, we found no mutations typical of clear cell carcinoma (Arid1a, Pik3ca), low-grade serous
22 ack of current treatment options for ovarian clear cell carcinoma (CCC) and the cancer is often resis
23 The Cancer Genome Atlas (TCGA) Kidney Renal Clear Cell Carcinoma (KIRC) dataset (n=114, 906 600 SNPs
24 t invasive carcinoma (BRCA) and kidney renal clear cell carcinoma (KIRC) from The Cancer Genome Atlas
25 sing five genomics datasets for Kidney Renal Clear Cell Carcinoma (KIRC) from The Cancer Genome Atlas
30 r serous (OR = 1.43; 95% CI = 0.82-2.49) and clear cell carcinoma (OR = 2.05; 95% CI = 0.36-11.57; P
31 t associations found were between height and clear cell carcinoma (OR per SD increase: 1.36, 95% CI 1
32 sis, together with RNAseq profiling in renal clear cell carcinoma cases (n=392), to compare immune ge
33 Immune gene expression analysis in the renal clear cell carcinoma cohort showed that the presence of
37 l populations from a patient-derived ovarian clear cell carcinoma model which forms malignant ascites
40 carcinoma (ccRCC, also known as kidney renal clear cell carcinoma), papillary (pRCC, also known as ki
48 s and is mutated in more than 50% of ovarian clear cell carcinomas (OCCC), a disease that currently h
49 related with low RARbeta expression in renal clear cell carcinomas and bladder urothelial carcinomas,
50 cy also occurs in poor prognosis endometrial clear cell carcinomas and has some association with endo
51 histotypes (low grade serous, mucinous, and clear cell carcinomas), the inability to directly examin
52 ly, ARID1A is mutated in over 50% of ovarian clear cell carcinomas, which currently have no effective
57 erogeneous uptake patterns are observed with clear cell-cell variations in tumor xenograft tissues, n
58 ed or metastatic renal cell carcinoma with a clear-cell component were recruited from 175 hospitals a
59 ically confirmed renal cell carcinoma with a clear-cell component were recruited from 175 hospitals a
60 three ccRCC epigenetic clusters, including a clear cell CpG island methylator phenotype (C-CIMP) subg
61 Microglia are the principal phagocytes that clear cell debris in the central nervous system (CNS).
64 ion, but the mechanism for this is still not clear; cells grown in 3D have opportunities to develop i
65 nt-naive, advanced renal cell carcinoma with clear cell histology were enrolled in 129 sites (hospita
66 nd Obstetrics [FIGO] stage I-IIa, grade 3 or clear cell histology) or more advanced disease (FIGO sta
67 58 years, 71% of patients were men, 84% had clear cell histology, 53% were at intermediate risk of r
68 rent or metastatic renal cell carcinoma with clear cell histology, a Karnofsky Performance Status of
69 sease; or stage I-III disease with serous or clear cell histology; were aged 18 years and older; and
71 atients initiated treatment, of whom 96% had clear-cell histology, 51% were treatment naive, and 67%
72 h common genomic alterations associated with clear-cell histology, we found that Hippo was one of the
76 ified through The Cancer Genome Atlas (TCGA) clear cell kidney (KIRC) dataset (419 white and 19 Afric
77 high incidence of mTOR mutations observed in clear cell kidney cancer, where VHL loss and HIF activat
79 tain histotypes of ovarian cancer, including clear cell, low-grade serous and endometrioid carcinomas
80 and Methods Eligible patients had untreated clear cell mRCC and Eastern Cooperative Oncology Group p
81 s and Methods Patients with treatment-naive, clear cell mRCC were treated with four cycles of sunitin
83 tiated May 31, 2011, including patients with clear-cell mRCC previously treated with antiangiogenic t
85 ession in transgenic mice, resulted in renal clear cells, multi-layered basement membranes, severe cy
86 ific diagnostic and screening biomarkers for clear cell or papillary RCC and in the differential diag
87 noninvasive biomarkers to diagnose malignant clear cell or papillary renal cell carcinoma (RCC) in a
88 ntrolled trial, patients with a component of clear cell or sarcomatoid histology and who were previou
89 (FIGO; 1988) stage IC-IIA high-grade serous, clear cell, or any poorly differentiated or grade 3 hist
90 onfirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence inte
92 e III/IV high-grade serous, endometrioid, or clear cell ovarian cancer in clinical complete response
94 findings reveal a differential dependency of clear cell ovarian cancers on EGLN1, thus identifying EG
99 glycogen accumulation, and acquisition of a clear cell phenotype in Vhl-deficient renal epithelial c
101 that glycogen accumulation associated with a clear-cell phenotype in hypoxic cancer cells lacking HIF
105 er genes, including VHL, a common initiating clear cell RCC (ccRCC) genetic lesion, and PBRM1 and BAP
107 reclinical models derived from patients with clear cell RCC (ccRCC) who exhibited primary resistance
108 (FSTL1) was significantly down-regulated in clear cell RCC (ccRCC), in particular metastatic ccRCC.
109 e major RCC histological subtypes, including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromop
110 erations found in human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes.
112 ected cohort of patients with non-metastatic clear cell RCC (the MSK peritumoral adipose tissue cohor
117 CC cases (the largest cohort to date) and 74 clear cell RCC cases (ccRCC, the most common RCC subtype
118 nt survival advantage in obese patients with clear cell RCC compared with patients at a normal weight
120 sion parameters useful in differentiation of clear cell RCC from chromophobe and papillary RCCs.
121 values of ER and WR used for differentiating clear cell RCC from other subtypes of RCC were 142 and 3
124 ogic fidelity, these models of papillary and clear cell RCC should be significant contributions to th
125 tients with advanced (ie, stages III and IV) clear cell RCC treated by nephrectomy; after exclusion o
128 population was 33% and 50% in patients with clear cell RCC with sarcomatoid differentiation and 26%
129 d-lower pole of the left kidney diagnosed as clear cell RCC with vascular invasion, liver, lung and b
130 , KDM5C, and BAP1 were absent in multicystic clear cell RCC, mutations of VHL (P = .016) and PBRM1 (P
134 tients with digital CT images and metastatic clear-cell RCC treated with sunitinib were included (n =
136 nts with high-risk (pT3, pT4, node-positive) clear cell renal cancer (ccRCC) in the ASSURE trial (adj
137 ognised as necessary for the pathogenesis of clear cell renal cancer (ccRCC); however, the molecular
138 etermine the phenotypes of isogenic pairs of clear cell renal cancer cells (ccRCC), with or without V
139 reviously untreated patients with metastatic clear cell renal cancer recruited between June 2008 and
144 rt a case of a 56-year-old male patient with clear cell renal carcinoma confirmed on a histopathologi
149 tandard of care for patients with metastatic clear cell renal cell carcinoma (ccRCC) after failure of
150 properties in mouse models of CAIX-positive clear cell renal cell carcinoma (ccRCC) and colorectal c
151 immune checkpoint blockade (ICB) therapy in clear cell renal cell carcinoma (ccRCC) and other solid
152 f flux balance analysis in two cancer types, clear cell renal cell carcinoma (ccRCC) and prostate ade
153 tin 3 (TRPM3) channel promotes the growth of clear cell renal cell carcinoma (ccRCC) and stimulates M
155 e transcriptomic and epigenomic profiling of clear cell renal cell carcinoma (ccRCC) by The Cancer Ge
156 scular area mask (VAM) in H&E micrographs of clear cell renal cell carcinoma (ccRCC) cases from The C
158 The presence of sarcomatoid features in clear cell renal cell carcinoma (ccRCC) confers a poor p
162 ysregulation of chromatin-modifying genes in clear cell renal cell carcinoma (ccRCC) has been uncover
164 netics of Von Hippel-Lindau (VHL)-associated clear cell renal cell carcinoma (ccRCC) has the potentia
168 nd a T cell infiltration score and find that clear cell renal cell carcinoma (ccRCC) is among the hig
178 in-depth immune profiling of samples from 73 clear cell renal cell carcinoma (ccRCC) patients and fiv
179 iptional profiling of a cohort of 50 primary clear cell renal cell carcinoma (ccRCC) samples from The
180 1) was revealed to be downregulated in human clear cell renal cell carcinoma (ccRCC) samples, which w
181 Recent studies have demonstrated that in clear cell renal cell carcinoma (ccRCC) several chromati
184 oit novel compounds with high selectivity to clear cell renal cell carcinoma (ccRCC) with common muta
185 genesis is an important prognostic factor of clear cell renal cell carcinoma (ccRCC), as well as a fa
187 e has transformed the management of advanced clear cell renal cell carcinoma (ccRCC), but the drivers
190 1alpha has been termed a tumor-suppressor in clear cell renal cell carcinoma (ccRCC), primarily based
193 or gene is the signature initiating event in clear cell renal cell carcinoma (ccRCC), the most common
194 ted as an early event in almost all cases of clear cell renal cell carcinoma (ccRCC), the most freque
195 he deregulated functional modules that drive clear cell renal cell carcinoma (ccRCC), we performed co
196 tumor suppressor and is highly expressed in clear cell renal cell carcinoma (ccRCC), where SLC2A3 ex
209 rimethyltransferase, have been identified in clear cell renal cell carcinoma (ccRCC); however it is u
210 C is frequently inactivated in patients with clear cell renal cell carcinoma (ccRCC); however, it is
211 ancer subtypes from The Cancer Genome Atlas: clear cell renal cell carcinoma (ccRCC, also known as ki
212 gle-agent targeted therapies in advanced non-clear cell renal cell carcinoma (ncRCC) compared with cl
213 ociated with an increased risk of developing clear cell renal cell carcinoma (RCC) but, paradoxically
214 l renal cell carcinoma (ncRCC) compared with clear cell renal cell carcinoma (RCC) supports the study
215 s in chromosome 8q24.1 (encompassing MYC) in clear cell renal cell carcinoma and chromosome 11q13.3 (
216 se as defined by RECIST 1.1 in patients with clear cell renal cell carcinoma and how the progression
219 Molecular characterization of the genome of clear cell renal cell carcinoma enabled identification o
220 els of primary and metastatic pVHL-defective clear cell renal cell carcinoma in an on-target fashion.
222 ur recurrence after nephrectomy in localised clear cell renal cell carcinoma is well characterised by
224 (Guangzhou, Guangdong, China) with localised clear cell renal cell carcinoma to examine 44 potential
225 with treatment-naive progressive metastatic clear cell renal cell carcinoma were enrolled between Se
226 A total of 361 patients with metastatic clear cell renal cell carcinoma were randomly assigned e
227 of 626 patients from France with stage I-III clear cell renal cell carcinoma who had also undergone n
228 cal outcome in 942 patients with stage I-III clear cell renal cell carcinoma who had undergone a neph
229 papillary, chromophobe, or unclassified non-clear cell renal cell carcinoma with no history of previ
230 ulation by the transcription factor HNF4A in clear cell renal cell carcinoma, despite no differential
231 glioma multiforme, breast, colorectal, skin, clear cell renal cell carcinoma, hepatic and prostate ca
232 linical outcome in patients with stage I-III clear cell renal cell carcinoma, providing a more accura
236 3 and 2014 included patients with metastatic clear cell renal cell carcinoma, with at least one targe
247 essor gene is inactivated in the majority of clear cell renal cell carcinomas (ccRCC), but genetic ab
248 tumor evolution have been well described for clear cell renal cell carcinomas (ccRCC), but they are l
249 he earliest genetic event in the majority of clear cell renal cell carcinomas (ccRCC), leading to acc
254 suppressor is inactivated in the majority of clear cell renal cell carcinomas (ccRCCs), leading to in
256 mors that included renal oncocytomas and non-clear cell renal cell carcinomas (nccRCCs), consisting o
259 tute a significant portion of aggressive non-clear cell renal cell carcinomas that have no standard t
260 usion-weighted MRI may be useful to identify clear cell renal cell carcinomas with higher growth rate
265 von Hippel-Lindau (VHL) are major causes of clear-cell renal cell carcinoma (ccRCC) that may origina
270 thod to previously published datasets of 100 clear-cell renal cell carcinoma and 99 non-small-cell lu
271 ctivity of cabozantinib in patients with non-clear-cell renal cell carcinoma is poorly characterised.
272 nd prospective ongoing studies targeting non-clear-cell renal cell carcinoma subtypes and specific mo
274 cohort study of patients with metastatic non-clear-cell renal cell carcinoma treated with oral caboza
275 med metastatic or locally advanced (or both) clear-cell renal cell carcinoma were randomly assigned (
276 d patients with histologically confirmed non-clear-cell renal cell carcinoma who received cabozantini
277 years and older with advanced or metastatic clear-cell renal cell carcinoma, measurable disease, and
282 sphorylated STAT3 are remarkably elevated in clear-cell renal-cell carcinoma relative to adjacent nor
283 ed 615 patients with locoregional, high-risk clear-cell renal-cell carcinoma to receive either suniti
285 we dissect the molecular mechanisms by which clear cells respond to luminal ATP and adenosine to modu
286 ] per birth, 0.78; 95% CI, 0.74 to 0.83) and clear cell (RR, 0.68; 95% CI, 0.61 to 0.76) carcinomas (
287 5% CI, 1.08 to 1.46) but a decreased risk of clear cell (RR, 0.72; 95% CI, 0.55 to 0.94) tumors (P-he
288 a, salivary-duct cancer, ovarian cancer, and clear-cell sarcoma and among patients with colorectal ca
289 terminus of BCOR in 23 of 27 (85%) pediatric clear cell sarcomas of the kidney (CCSK) from two indepe
293 irmed a deregulation of CREB1 protein in the clear cell type of RCC (ccRCC) and analysis of in-house
299 orts an obesity paradox in patients with the clear cell variant; however, population-based cohort dat
300 very unusual, pathologically proven case of clear cell variety of pediatric RCC which showed invasio