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Statements

Subject Item
n2:RIV%2F00216208%3A11140%2F14%3A10210868%21RIV15-MSM-11140___
rdf:type
skos:Concept n13:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1016/j.anndiagpath.2013.12.003
dcterms:description
We report 3 cases of primary renal cell tumor simulating atrophic kidney with distinct gross, morphologic, immunohistochemical, and molecular genetic features. The tumors were retrieved out of more than 17 000 renal tumors from the Plzen Tumor Registry. Tissues for light microscopy had been fixed, embedded, and stained with hematoxylin and eosin using routine procedures. The tumors were further analyzed using immunohistochemistry, array comparative genomic hybridization, and human androgen receptor. Analyses of VHL gene and loss of heterozygosity (LOH) 3p were also performed. The patients were 2 women and 1 man, with ages ranging from 29 to 35 years (mean, 31.3 years). Grossly, the neoplasms were encapsulated and round with largest diameter of 3.5 cm (mean, 3.2 cm). Follow-up available for all patients ranged from 2 to 14 years (mean, 8 years). No aggressive behavior was noted. Histologically, akin to atrophic (postpyelonephritic) kidney parenchyma, the tumors were composed of follicles of varying sizes that were filled by eosinophilic secretion. Rare areas contained collapsed follicles. Each follicle was endowed with a small capillary. The stroma was loose, inconspicuous, and focally fibrotic. Two types of calcifications were noted: typical psammoma bodies and amorphous dark-blue stained calcified deposits. Immunohistochemically, tumors were strongly positive for cytokeratins (OSCAR), CD10, and vimentin, with weak immunopositivity for CAM5.2 and AE1-AE3. WT1 and cathepsin K were weakly to moderately focally to diffusely positive. Tumors were negative for cytokeratin 20, carbonic anhydrase IX, parvalbumin, HMB45, TTF1, TFE3, chromogranin A, thyroglobulin, PAX8, and ALK. Only, 1 case was suitable for molecular genetic analyses. No mutations were found in the VHL gene; no methylation of VHL promoter was noted. No numerical aberrations were found by array comparative genomic hybridization analysis. We report 3 cases of primary renal cell tumor simulating atrophic kidney with distinct gross, morphologic, immunohistochemical, and molecular genetic features. The tumors were retrieved out of more than 17 000 renal tumors from the Plzen Tumor Registry. Tissues for light microscopy had been fixed, embedded, and stained with hematoxylin and eosin using routine procedures. The tumors were further analyzed using immunohistochemistry, array comparative genomic hybridization, and human androgen receptor. Analyses of VHL gene and loss of heterozygosity (LOH) 3p were also performed. The patients were 2 women and 1 man, with ages ranging from 29 to 35 years (mean, 31.3 years). Grossly, the neoplasms were encapsulated and round with largest diameter of 3.5 cm (mean, 3.2 cm). Follow-up available for all patients ranged from 2 to 14 years (mean, 8 years). No aggressive behavior was noted. Histologically, akin to atrophic (postpyelonephritic) kidney parenchyma, the tumors were composed of follicles of varying sizes that were filled by eosinophilic secretion. Rare areas contained collapsed follicles. Each follicle was endowed with a small capillary. The stroma was loose, inconspicuous, and focally fibrotic. Two types of calcifications were noted: typical psammoma bodies and amorphous dark-blue stained calcified deposits. Immunohistochemically, tumors were strongly positive for cytokeratins (OSCAR), CD10, and vimentin, with weak immunopositivity for CAM5.2 and AE1-AE3. WT1 and cathepsin K were weakly to moderately focally to diffusely positive. Tumors were negative for cytokeratin 20, carbonic anhydrase IX, parvalbumin, HMB45, TTF1, TFE3, chromogranin A, thyroglobulin, PAX8, and ALK. Only, 1 case was suitable for molecular genetic analyses. No mutations were found in the VHL gene; no methylation of VHL promoter was noted. No numerical aberrations were found by array comparative genomic hybridization analysis.
dcterms:title
Distinctive renal cell tumor simulating atrophic kidney with 2 types of microcalcifications. Report of 3 cases Distinctive renal cell tumor simulating atrophic kidney with 2 types of microcalcifications. Report of 3 cases
skos:prefLabel
Distinctive renal cell tumor simulating atrophic kidney with 2 types of microcalcifications. Report of 3 cases Distinctive renal cell tumor simulating atrophic kidney with 2 types of microcalcifications. Report of 3 cases
skos:notation
RIV/00216208:11140/14:10210868!RIV15-MSM-11140___
n3:aktivita
n5:S n5:P n5:I
n3:aktivity
I, P(ED2.1.00/03.0076), S
n3:cisloPeriodika
2
n3:dodaniDat
n6:2015
n3:domaciTvurceVysledku
n11:6058884 n11:9711783 n11:7629990 n11:9342710 n11:2975491 n11:3182975
n3:druhVysledku
n9:J
n3:duvernostUdaju
n14:S
n3:entitaPredkladatele
n10:predkladatel
n3:idSjednocenehoVysledku
11808
n3:idVysledku
RIV/00216208:11140/14:10210868
n3:jazykVysledku
n20:eng
n3:klicovaSlova
HUMARA; Comparative genomic hybridization; Thyroid-like renal tumor; Atrophic renal parenchyma-like tumor; Kidney
n3:klicoveSlovo
n12:Kidney n12:HUMARA n12:Thyroid-like%20renal%20tumor n12:Comparative%20genomic%20hybridization n12:Atrophic%20renal%20parenchyma-like%20tumor
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[ABC575E2CA86]
n3:nazevZdroje
Annals of Diagnostic Pathology
n3:obor
n18:FP
n3:pocetDomacichTvurcuVysledku
6
n3:pocetTvurcuVysledku
12
n3:projekt
n8:ED2.1.00%2F03.0076
n3:rokUplatneniVysledku
n6:2014
n3:svazekPeriodika
18
n3:tvurceVysledku
Pivovarčíková, Kristýna Grossmann, Petr Hes, Ondřej Hora, Milan Michal, Michal Petersson, Fredrik Kuroda, Naoto Straka, Lubomir Svajdler, Marian de Souza, Tulio Geraldo Kacerovská, Denisa Martínek, Petr
n3:wos
000333440600009
s:issn
1092-9134
s:numberOfPages
7
n15:doi
10.1016/j.anndiagpath.2013.12.003
n16:organizacniJednotka
11140