Molecular genetic alterations in renal cell carcinomas with tubulocystic pattern: tubulocystic renal cell carcinoma, tubulocystic renal cell carcinoma with heterogenous component and familial leiomyomatosis-associated renal cell carcinoma. Clinicopathologic and molecular genetic analysis of 15 cases

Monika Ulamec, Faruk Skenderi, Ming Zhou, Božo Krušlin, Petr Martínek, Petr Grossmann, Kvetoslava Peckova, Isabel Alvarado-Cabrero, Kristyna Kalusova, Bohuslava Kokoskova, Pavla Rotterova, Milan Hora, Ondrej Daum, Magdalena Dubova, Kevin Bauleth, David Slouka, Maris Sperga, Whitney Davidson, Boris Rychly, Delia Perez MontielMichal Michal, Ondrej Hes (Corresponding Author)

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

The characteristic morphologic spectrum of tubulocystic renal cell carcinoma (TC-RCC) may include areas resembling papillary RCC (PRCC). Our study includes 15 RCCs with tubulocystic pattern: 6 TC-RCCs, 1 RCC-high grade with tubulocystic architecture, 5 TC-RCCs with foci of PRCC, 2 with high-grade RCC (HGRCC) not otherwise specified, and 1 with a clear cell papillary RCC/renal angiomyoadenomatous tumor-like component. We analyzed aberrations of chromosomes 7, 17, and Y; mutations of VHL and FH genes; and loss of heterozygosity at chromosome 3p. Genetic analysis was performed separately in areas of classic TC-RCC and in those with other histologic patterns. The TC-RCC component demonstrated disomy of chromosome 7 in 9/15 cases, polysomy of chromosome 17 in 7/15 cases, and loss of Y in 1 case. In the PRCC component, 2/3 analyzable cases showed disomy of chromosome 7 and polysomy of chromosome 17 with normal Y. One case with focal HGRCC exhibited only disomy 7, whereas the case with clear cell papillary RCC/renal angiomyoadenomatous tumor-like pattern showed polysomies of 7 and 17, mutation of VHL, and loss of heterozygosity 3p. FH gene mutation was identified in a single case with an aggressive clinical course and predominant TC-RCC pattern. The following conclusions were drawn: (1) TC-RCC demonstrates variable status of chromosomes 7, 17, and Y even in cases with typical/uniform morphology. (2) The biological nature of PRCC/HGRCC-like areas within TC-RCC remains unclear. Our data suggest that heterogenous TC-RCCs may be associated with an adverse clinical outcome. (3) Hereditary leiomyomatosis-associated RCC can be morphologically indistinguishable from "high-grade" TC-RCC; therefore, in TC-RCC with high-grade features FH gene status should be tested.

Original languageEnglish
Pages (from-to)521-530
Number of pages10
JournalApplied Immunohistochemistry and Molecular Morphology
Volume24
Issue number7
DOIs
Publication statusPublished - 2016

Keywords*

  • chromosomal aberration
  • hereditary leiomyomatosis-associated renal cell carcinoma
  • kidney
  • papillary renal cell carcinoma
  • tubulocystic renal cell carcinoma

Field of Science*

  • 3.1 Basic medicine

Publication Type*

  • 1.1. Scientific article indexed in Web of Science and/or Scopus database

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