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1 gnificantly from the genotype of multicystic clear cell RCC.
2 ) were significantly more common among solid clear cell RCC.
3  diameter and enhancement parameters of each clear cell RCC.
4 ess can also be valid therapeutic targets in clear cell RCC.
5 tumors (15 of 18) derived from patients with clear cell RCC.
6  use of Nox4 as a target in the treatment of clear cell RCC.
7  of these novel manifestations of paediatric clear cell RCC.
8  and in 13 individuals with familial non-VHL clear cell RCC.
9 ferential diagnostic biomarker of metastatic clear cell RCC.
10  candidate biomarker and tumor suppressor in clear-cell RCC.
11 patients with cytokine-refractory metastatic clear-cell RCC.
12 s were significantly higher in patients with clear cell RCC (0.39 +/- 0.08 ng/mg U(Cr); n = 21), comp
13 L/min/100 g +/- 15.1) was lower than that of clear cell RCC (171.6 mL/min/100 g +/- 61.2, P = .001),
14 nce status 2 or higher (29 of 319 [9%]), non-clear-cell RCC (48 of 437 [11%]) and age 65 years or mor
15  S-transferase alpha was highly expressed in clear cell RCC, alpha methylacyl racemase in papillary R
16 oter region methylation in 30% (19 of 64) of clear cell RCC and 40% (15 of 38) of papillary RCC, wher
17  expression of MAPK kinase (MKK) and MAPK in clear cell RCC and confirmed the overexpression of MKK1
18 e different from those occurring in sporadic clear cell RCC and do not characteristically involve the
19 1994, 306 patients underwent nephrectomy for clear cell RCC and had paraffin tissue available for rev
20 nce in ER (P=0.001) and WR (P=0.001) between clear cell RCC and other subtypes of RCC.
21 thesis-generating study of 233 patients with clear cell RCC and waived the informed consent requireme
22 ormance status of 2 or higher, 588 (13%) non-clear-cell RCC, and 1418 (32%) aged 65 years or more.
23 pes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesio
24 egions of 3p associated with LOH in sporadic clear cell RCC as well as homozygous deletion in lung ca
25 help explain the pathologic cooperativity in clear-cell RCC between PTEN inactivation and pVHL loss,
26 ns formation were pointed out as a potential clear cell RCC biomarkers.
27 tion of the VHL gene occurs in most sporadic clear cell RCC (CC-RCC).
28 r suppressor that is lost in the majority of clear cell RCC (ccRCC) cases.
29                                              Clear cell RCC (ccRCC) showed more intense contrast enha
30  (FSTL1) was significantly down-regulated in clear cell RCC (ccRCC), in particular metastatic ccRCC.
31 whole-genome and transcriptome sequencing of clear cell RCC (ccRCC), the most common form of the dise
32 erations found in human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes.
33                                       In the clear cell RCC clustering, two subgroups emerged that co
34                        The genotype of solid clear cell RCC differed significantly from the genotype
35 eam signaling pathways are also modulated by clear cell RCC-dysregulated miRs.
36  prognostic significance in 41 nonmetastatic clear cell RCC extending beyond the renal capsule.
37 sion parameters useful in differentiation of clear cell RCC from chromophobe and papillary RCCs.
38 lidated, may assist in the discrimination of clear cell RCC from oncocytoma, papillary RCC, and chrom
39 olding of enhancement helped to discriminate clear cell RCC from oncocytoma, papillary RCC, and chrom
40 values of ER and WR used for differentiating clear cell RCC from other subtypes of RCC were 142 and 3
41 as present in 32 tissue sections (91%) of 35 clear cell RCC (group 1).
42      Sixty-four patients with metastatic non-clear-cell RCC histology were the subjects of this retro
43 is an important factor in the development of clear cell RCC, however: loss of VHL can result in tumor
44 e von Hippel-Lindau protein as the basis for clear cell RCC, in addition to the well designed clinica
45                                           In clear cell RCC, increased emphasis is being placed on ta
46 interesting new approach in the treatment of clear cell RCC is antibody-mediated therapy with the chi
47 r the differentiation of minimal fat AML and clear cell RCC is poor.
48                               Metastatic non-clear-cell RCC is characterized by a resistance to syste
49 ly decreased uptake of (111)In-girentumab in clear cell RCC lesions.
50          Pathological result was reported as clear cell RCC metastasis.
51                                              Clear cell RCC most commonly manifested with a mixed enh
52 , KDM5C, and BAP1 were absent in multicystic clear cell RCC, mutations of VHL (P = .016) and PBRM1 (P
53        This pattern was highly predictive of clear cell RCC (odds ratio of 22 and 54 for readers 1 an
54 fusion of oncocytoma was higher than that of clear cell RCC (P < .001).
55  necrosis and larger size were predictive of clear cell RCC (P<.001) for all lesions, whereas low SI
56 ing the elucidation of the von Hippel-Lindau/clear cell RCC pathway.
57 2)-kinase (JNK), is selectively activated in clear cell RCC patient specimens.
58  (111)In-girentuximab uptake in the tumor in clear cell RCC patients, especially in the group treated
59   This preliminary radiogenomics analysis of clear cell RCC revealed associations between CT features
60 reening and direct sequencing in 35 sporadic clear cell RCC samples without VHL gene inactivation and
61 ogic fidelity, these models of papillary and clear cell RCC should be significant contributions to th
62 -1 expression is a poor prognostic factor in clear-cell RCC that is associated with activation of an
63 tients with digital CT images and metastatic clear-cell RCC treated with sunitinib were included (n =
64                 Tissues from 248 consecutive clear cell RCC tumors obtained from 2000 to 2003 were st
65                     The majority of sporadic clear-cell RCC tumors are characterized by VHL tumor sup
66 nty-four patients with histologically proven clear-cell RCC undergoing surgical evaluation for possib
67                                           In clear cell RCC, VHL loss generates pseudohypoxia that ex
68 tients with previously untreated, metastatic clear cell RCC were randomly assigned to receive either
69 tients with previously untreated, metastatic clear-cell RCC were randomly assigned to receive either
70 majority of work in kidney cancer deals with clear cell RCC, which is the most common variant of this
71            Patients (N = 106) had metastatic clear-cell RCC, which had progressed despite previous cy
72 cur in a large majority of sporadic cases of clear-cell RCC, which have high intrinsic resistance to
73 7x (sB7x) and investigated 101 patients with clear cell RCC who underwent nephrectomy between 2003 an
74  prospective trials with these agents in non-clear cell RCC will further clarify their use in the fut
75       In contrast to the general population, clear cell RCC with 3p abnormalities represent only a sm
76 d-lower pole of the left kidney diagnosed as clear cell RCC with vascular invasion, liver, lung and b
77 lated in the majority of a series of primary clear cell RCC with VHL inactivation.

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