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1 is up-regulated in RCC and down-regulated in oncocytoma.
2 pe 2 papillary, chromophobe, TFE3, TFEB, and oncocytoma.
3 ignant renal cell carcinoma (RCC) and benign oncocytoma.
4 y be a molecular basis for the occurrence of oncocytomas.
5 rentiation between clear cell carcinomas and oncocytomas.
6 f 12 (25%) clear cell RCCs, but 0 of 4 renal oncocytomas.
7 in was detected primarily in chromophobe RCC/oncocytomas.
8 mples, including nonpapillary, papillary and oncocytomas.
9 multiple chromosomal arms in CDCs and renal oncocytomas.
10 ing diversion of tumor progression to benign oncocytomas.
11 %) sporadic renal tumors: 2 of 7 (29%) renal oncocytomas, 1 of 9 (11%) chromophobe RCCs, 4 of 11 (36%
12 x10(-3) mm(2)/s; p<0.05 and in patients with oncocytoma - 2.75+/-0.27x10(-3) mm(2)/s vs. 2.11+/-0.25x
16 enal tumors of different cell types: 7 renal oncocytomas, 9 chromophobe renal cell carcinomas (RCCs),
17 of the renal cell carcinoma, 5 patients with oncocytoma and 5 patients with angiomyolipoma (AML).
19 itary kidney cancer syndromes, like familial oncocytoma and the Birt-Hogg-Dube syndrome, have been id
20 can be used to differentiate solid RCCs from oncocytomas and characterize the histologic subtypes of
21 167 primary human tumors that included renal oncocytomas and non-clear cell renal cell carcinomas (nc
23 he five false-positive masses included three oncocytomas and two Bosniak category 3 cystic lesions.
24 in BHD(d/+) mice including oncocytic hybrid, oncocytoma, and clear cell with concomitant loss of hete
25 f 170 clear cell RCCs, 57 papillary RCCs, 49 oncocytomas, and 22 chromophobe RCCs were evaluated for
26 uding pyelonephritis, renal cysts, adenomas, oncocytomas, and normal kidney, did not express the MN/C
28 RCCs were distinguished from chromophobe RCC/oncocytomas based on large-scale gene expression pattern
30 y chromophobe renal cell carcinoma and renal oncocytoma but not by clear cell renal cell carcinoma or
31 e further distinguished from chromophobe RCC/oncocytomas by overexpression of vimentin and class II m
34 ilies (chromophobe: amylases 1A, 1B, and 1C; oncocytoma: general transcription factors 2H2, 2B, 2C, a
35 iomyoma renal cell carcinoma, familial renal oncocytoma, hereditary nonpolyposis colon cancer, and me
37 RCCs including papillary, nonpapillary, and oncocytomas in order to determine whether allelic loss c
38 of clear cell RCCs was greater than that of oncocytomas in the corticomedullary (125 HU vs 106 HU, P
40 even segments), clear cell (three segments), oncocytoma (nine segments), and papillary type 2 (two se
42 ients with RCC but is nearly undetectable in oncocytoma, other tumors, and urinary tract inflammation
43 t helped to discriminate clear cell RCC from oncocytoma, papillary RCC, and chromophobe RCC with accu
45 ma (RCC) specimens (chromophobe, clear cell, oncocytoma, papillary type 1, and papillary type 2) usin
47 d tumor fate from adenomas and carcinomas to oncocytomas-rare, predominantly benign tumors characteri
48 l chromophobe renal cell carcinoma and renal oncocytoma seem to originate from the A-type intercalate
49 e 26 benign small renal masses (including 18 oncocytomas, seven lipid-poor angiomyolipomas, and one h
50 ns; 24 (12%), chromophobe adenomas; 14 (7%), oncocytomas; six (3%), lipid-poor angiomyolipomas; and 1
54 e chromophobe RCC, five sarcomatoid RCC, two oncocytomas, three transitional cell carcinomas (TCC) of
56 family of neoplasms ranging from the benign oncocytoma, to the indolent papillary and chromophobe ca
62 hree families classified with familial renal oncocytoma were identified with BHD mutations, which rep
63 ations, chromophobes, clear-cell tumors, and oncocytomas were composed exclusively of noncoding DNA.
66 llecting duct carcinomas (CDCs) and 13 renal oncocytomas were studied using highly informative micros
68 d to derive a cohort of 298 cases of RCC and oncocytoma with preoperative multiphasic multidetector C
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