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Trisomy 7 and 17 mark papillary renal cell tumours irrespectively of variation of the phenotype.
  1. Ildiko Balint
  1. Laboratory of Molecular Oncology, Medical Faculty, University of Heidelberg, Germany
    1. Adrianna Szponar
    1. Laboratory of Molecular Oncology, Medical Faculty, University of Heidelberg, Germany
      1. Anna Jauch
      1. Institute of Human Genetics, Medical Faculty, University of Heidelberg, Germany
        1. Gyula Kovacs (gyula.kovacs{at}urz.uni-heidelberg.de)
        1. Laboratory of Molecular Oncology, Medical Faculty, University of Heidelberg, Germany

          Abstract

          Background: Papillary renal cell tumours (RCT) have been described as a genetic entity. Recently, papillary RCTs are divided into small (type 1) and large (type 2) cell tumours. Subsequent DNA analyses resulted in controversial data regarding putative genetic changes marking type 1 and type 2 tumours.

          Aim: The aim of this study was to improve our original description, that papillary RCT is a genetic entity regardless of the phenotypic variation.

          Methods: We have analysed DNA from 163 papillary RCTs including 82 multiplex tumours from 8 hereditary cases for copy number changes by chromosomal CGH and/or for allelic changes at chromosome 7 and 17 by microsatellites and compared the results of genetic analysis to the cytological characteristics of tumours.

          Results: We have detected alterations of chromosome 7 and 17 at similar frequency in papillary RCTs from small to large cell characteristics, from nuclear grade 1 to 3 and from 3 mm to 16 cm in diameter in size.

          Conclusion: Trisomies of chromosomes 7 and 17 are specific genetic alterations in papillary RCTs irrespectively of their size, grade and cellular differentiation.

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