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Hum Pathol ; 44(7): 1412-20, 2013 Jul.
Article in English | MEDLINE | ID: mdl-23434146

ABSTRACT

We present a cohort of 8 renal carcinomas that displayed a variable (5%-95% extent) light microscopic appearance of renal angiomyoadenomatous tumor/clear cell papillary renal cell carcinoma (RAT/CCPRCC) without fulfilling the criteria for these tumors. All but 1 case predominantly (75%-95% extent) showed histopathologic features of conventional clear cell renal cell carcinoma. In 5 of 7 cases with mostly conventional clear renal cell carcinoma (CRCC) morphology, a diagnosis of CRCC was supported by the molecular genetic findings (presence of von Hippel-Lindau tumor suppressor [VHL] mutation and/or VHL promoter methylation and/or loss of heterozygosity [LOH] for 3p). Of the other 2 cases with predominantly characteristic CRCC morphology, 1 tumor did not reveal any VHL mutation, VHL promoter methylation, or LOH for 3p, and both chromosomes 7 and 17 were disomic, whereas the other tumor displayed polysomy for chromosomes 7 and 17 and no VHL mutation, VHL promoter methylation, or LOH for 3p. One tumor was composed primarily (95%) of distinctly RAT/CCPRCC-like morphology, and this tumor harbored a VHL mutation and displayed polysomy for chromosomes 7 and 17. Of the 5 cases with both histomorphologic features and molecular genetic findings of CRCC, we detected significant immunoreactivity for α-methylacyl-CoA racemase in 2 cases and strong diffuse immunopositivity for cytokeratin 7 in 3 cases. Despite the combination of positivity for α-methylacyl-CoA racemase and cytokeratin 7 in 2 cases, there was nothing to suggest of the possibility of a conventional papillary renal cell carcinoma with a predominance of clear cells.


Subject(s)
Adenoma/diagnosis , Angiomyoma/diagnosis , Carcinoma, Papillary/diagnosis , Carcinoma, Renal Cell/diagnosis , Kidney Neoplasms/diagnosis , Adult , Aged , Chromosome Aberrations , Chromosomes, Human, Pair 17 , Chromosomes, Human, Pair 7 , Diagnosis, Differential , Female , Humans , Keratin-7/metabolism , Loss of Heterozygosity , Male , Middle Aged , Mutation , Neoplasms, Multiple Primary/diagnosis , Racemases and Epimerases/metabolism , Von Hippel-Lindau Tumor Suppressor Protein/genetics , von Hippel-Lindau Disease
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