ライフサイエンスコーパス: clear cell RCC

1 racteristics across phases, particularly for clear cell RCC.

2 e and the 200 mg dose for previously treated clear cell RCC.

3 h first-line TT for patients with metastatic clear cell RCC.

4 of these novel manifestations of paediatric clear cell RCC.

5 gnificantly from the genotype of multicystic clear cell RCC.

6 ) were significantly more common among solid clear cell RCC.

7 diameter and enhancement parameters of each clear cell RCC.

8 ess can also be valid therapeutic targets in clear cell RCC.

9 tumors (15 of 18) derived from patients with clear cell RCC.

10 use of Nox4 as a target in the treatment of clear cell RCC.

11 and in 13 individuals with familial non-VHL clear cell RCC.

12 ferential diagnostic biomarker of metastatic clear cell RCC.

13 tivity to ferroptotic inducers compared with clear-cell RCC.

14 the clinical management of RCC, particularly clear-cell RCC.

15 The most common subtype (~70% of cases) is clear-cell RCC.

16 candidate biomarker and tumor suppressor in clear-cell RCC.

17 patients with cytokine-refractory metastatic clear-cell RCC.

18 s were significantly higher in patients with clear cell RCC (0.39 +/- 0.08 ng/mg U(Cr); n = 21), comp

19 dexes of 0.64 (95% CI, 0.59 to 0.69) for non-clear-cell RCC, 0.63 (95% CI, 0.56 to 0.69) for papillar

20 mmonly identified single histologic type was clear cell RCC (13/36; 36.1%).

21 L/min/100 g +/- 15.1) was lower than that of clear cell RCC (171.6 mL/min/100 g +/- 61.2, P = .001),

22 nce status 2 or higher (29 of 319 [9%]), non-clear-cell RCC (48 of 437 [11%]) and age 65 years or mor

23 ndependent clinical cohorts of patients with clear cell RCC aged 18 years and older.

24 S-transferase alpha was highly expressed in clear cell RCC, alpha methylacyl racemase in papillary R

25 oter region methylation in 30% (19 of 64) of clear cell RCC and 40% (15 of 38) of papillary RCC, wher

26 expression of MAPK kinase (MKK) and MAPK in clear cell RCC and confirmed the overexpression of MKK1

27 e different from those occurring in sporadic clear cell RCC and do not characteristically involve the

28 1994, 306 patients underwent nephrectomy for clear cell RCC and had paraffin tissue available for rev

29 nce in ER (P=0.001) and WR (P=0.001) between clear cell RCC and other subtypes of RCC.

30 s and has markably lower glucose uptake than clear cell RCC and papillary RCC.

31 thesis-generating study of 233 patients with clear cell RCC and waived the informed consent requireme

32 Two patients had non-clear cell RCC and were excluded from the efficacy analy

33 Analyses by the two major histologic types (clear-cell RCC and papillary RCC) revealed subtype-speci

34 ormance status of 2 or higher, 588 (13%) non-clear-cell RCC, and 1418 (32%) aged 65 years or more.

35 pes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesio

36 egions of 3p associated with LOH in sporadic clear cell RCC as well as homozygous deletion in lung ca

37 Tumor-only screening of clear cell RCC associated with cutaneous (n = 53) and uv

38 reatment of patients with localized resected clear cell RCC based on the results of the KEYNOTE-564 t

39 help explain the pathologic cooperativity in clear-cell RCC between PTEN inactivation and pVHL loss,

40 ns formation were pointed out as a potential clear cell RCC biomarkers.

41 CC cases (the largest cohort to date) and 74 clear cell RCC cases (ccRCC, the most common RCC subtype

42 2 trial, included 162 patients found to have clear cell RCC (cases) and 162 patients with benign rena

43 tion of the VHL gene occurs in most sporadic clear cell RCC (CC-RCC).

44 r suppressor that is lost in the majority of clear cell RCC (ccRCC) cases.

45 er genes, including VHL, a common initiating clear cell RCC (ccRCC) genetic lesion, and PBRM1 and BAP

46 ChRCC is distinct from clear cell RCC (ccRCC) in terms of genetics, genomics, m

47 the most common form of kidney cancer, with clear cell RCC (ccRCC) representing about 85% of all RCC

48 Tumorgrafts from VHL-mutant clear cell RCC (ccRCC) retained metabolic features of hu

49 Clear cell RCC (ccRCC) showed more intense contrast enha

50 reclinical models derived from patients with clear cell RCC (ccRCC) who exhibited primary resistance

51 (FSTL1) was significantly down-regulated in clear cell RCC (ccRCC), in particular metastatic ccRCC.

52 e major RCC histological subtypes, including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromop

53 whole-genome and transcriptome sequencing of clear cell RCC (ccRCC), the most common form of the dise

54 erations found in human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes.

55 alyses of human sRCC tumors compared against clear cell RCC (ccRCC), with validation spatially and in

56 in the most common subtype of kidney cancer, clear cell RCC (ccRCC).

57 demonstrated V2R expression and activity in clear cell RCC (ccRCC).

58 s: Nine studies comprising 152 patients (133 clear cell RCC [ccRCC], 19 other RCC subtypes) were incl

59 In the clear cell RCC clustering, two subgroups emerged that co

60 nt survival advantage in obese patients with clear cell RCC compared with patients at a normal weight

61 The genotype of solid clear cell RCC differed significantly from the genotype

62 SCR1-TFE3 driven by Pax8-Cre (a credentialed clear cell RCC driver) disrupted nephrogenesis and glome

63 eam signaling pathways are also modulated by clear cell RCC-dysregulated miRs.

64 prognostic significance in 41 nonmetastatic clear cell RCC extending beyond the renal capsule.

65 velopment, causing neonatal death, while the clear cell RCC failed driver, Sglt2-Cre, induced aggress

66 Eligible patients had metastatic clear-cell RCC following progression on 1 to 2 prior lin

67 sion parameters useful in differentiation of clear cell RCC from chromophobe and papillary RCCs.

68 lidated, may assist in the discrimination of clear cell RCC from oncocytoma, papillary RCC, and chrom

69 olding of enhancement helped to discriminate clear cell RCC from oncocytoma, papillary RCC, and chrom

70 values of ER and WR used for differentiating clear cell RCC from other subtypes of RCC were 142 and 3

71 as present in 32 tissue sections (91%) of 35 clear cell RCC (group 1).

72 ediate-risk and high-risk clear-cell and non-clear-cell RCC groups in contemporary data, supporting i

73 Two patients with clear cell RCC had germline BAP1 alterations in the sett

74 histopathologically confirmed malignancies, clear-cell RCC had the lowest uptake (SUV(max) 3.4), and

75 Sixty-four patients with metastatic non-clear-cell RCC histology were the subjects of this retro

76 is an important factor in the development of clear cell RCC, however: loss of VHL can result in tumor

77 udy identified 5872 patients with metastatic clear cell RCC in the National Cancer Database from Janu

78 e von Hippel-Lindau protein as the basis for clear cell RCC, in addition to the well designed clinica

79 In clear cell RCC, increased emphasis is being placed on ta

80 interesting new approach in the treatment of clear cell RCC is antibody-mediated therapy with the chi

81 r the differentiation of minimal fat AML and clear cell RCC is poor.

82 Clear cell RCC is the most common histologic subtype (75

83 Metastatic non-clear-cell RCC is characterized by a resistance to syste

84 h first-line TT for patients with metastatic clear cell RCC (IT group: hazard ratio [HR], 0.60 [95% C

85 ly decreased uptake of (111)In-girentumab in clear cell RCC lesions.

86 Pathological result was reported as clear cell RCC metastasis.

87 Clear cell RCC most commonly manifested with a mixed enh

88 , KDM5C, and BAP1 were absent in multicystic clear cell RCC, mutations of VHL (P = .016) and PBRM1 (P

89 This pattern was highly predictive of clear cell RCC (odds ratio of 22 and 54 for readers 1 an

90 th high risk of recurrence, or patients with clear cell RCC only.

91 fusion of oncocytoma was higher than that of clear cell RCC (P < .001).

92 necrosis and larger size were predictive of clear cell RCC (P<.001) for all lesions, whereas low SI

93 These subtypes include clear cell RCC, papillary RCC and chromophobe RCC.

94 and biopsy slides into five related classes: clear cell RCC, papillary RCC, chromophobe RCC, renal on

95 ing the elucidation of the von Hippel-Lindau/clear cell RCC pathway.

96 2)-kinase (JNK), is selectively activated in clear cell RCC patient specimens.

97 (111)In-girentuximab uptake in the tumor in clear cell RCC patients, especially in the group treated

98 protein profilin1 (Pfn1) is overexpressed in clear cell RCC predominantly in tumor-associated vascula

99 This preliminary radiogenomics analysis of clear cell RCC revealed associations between CT features

100 untranslated region of VHL, nearly tripling clear cell RCC risk (odds ratio 2.72, 95% confidence int

101 reening and direct sequencing in 35 sporadic clear cell RCC samples without VHL gene inactivation and

102 ogic fidelity, these models of papillary and clear cell RCC should be significant contributions to th

103 -1 expression is a poor prognostic factor in clear-cell RCC that is associated with activation of an

104 ected cohort of patients with non-metastatic clear cell RCC (the MSK peritumoral adipose tissue cohor

105 tients with advanced (ie, stages III and IV) clear cell RCC treated by nephrectomy; after exclusion o

106 tients with digital CT images and metastatic clear-cell RCC treated with sunitinib were included (n =

107 Tissues from 248 consecutive clear cell RCC tumors obtained from 2000 to 2003 were st

108 The majority of sporadic clear-cell RCC tumors are characterized by VHL tumor sup

109 The complex interplay between the clear cell RCC tumour and peritumoral adipose tissue mic

110 nty-four patients with histologically proven clear-cell RCC undergoing surgical evaluation for possib

111 ts with multiple GU malignancies, especially clear cell RCC, urothelial carcinoma, and rare GU tumors

112 ome were assessed in data from patients with clear-cell RCC, using Cox proportional hazards regressio

113 olumab showed promising efficacy in most non-clear-cell RCC variants tested in this trial, particular

114 Genomic findings in non-clear-cell RCC variants warrant further study as predict

115 In clear cell RCC, VHL loss generates pseudohypoxia that ex

116 tients with previously untreated, metastatic clear cell RCC were randomly assigned to receive either

117 fty treatment-naive patients with metastatic clear cell RCC were randomly assigned to sunitinib 50 mg

118 ochemistry; while patients with melanoma and clear cell RCC were screened for MITF p.E318K alteration

119 tients with previously untreated, metastatic clear-cell RCC were randomly assigned to receive either

120 majority of work in kidney cancer deals with clear cell RCC, which is the most common variant of this

121 Patients (N = 106) had metastatic clear-cell RCC, which had progressed despite previous cy

122 cur in a large majority of sporadic cases of clear-cell RCC, which have high intrinsic resistance to

123 Patients with metastatic clear cell RCC who experienced progression after at leas

124 7x (sB7x) and investigated 101 patients with clear cell RCC who underwent nephrectomy between 2003 an

125 prospective trials with these agents in non-clear cell RCC will further clarify their use in the fut

126 In contrast to the general population, clear cell RCC with 3p abnormalities represent only a sm

127 enotype-phenotype correlations were seen for clear cell RCC with pathogenic BAP1/ MITF alterations an

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 lated in the majority of a series of primary clear cell RCC with VHL inactivation.