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Molecular cytogenetic analysis of human spermatocytic seminomas
Author(s) -
Verdorfer Irmgard,
Rogatsch Hermann,
Tzankov Alexandar,
Steiner Hannes,
Mikuz Gregor
Publication year - 2004
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1634
Subject(s) - comparative genomic hybridization , fluorescence in situ hybridization , chromosome , fish <actinopterygii> , chromosome 17 (human) , biology , karyotype , pathology , cytogenetics , population , cancer research , microbiology and biotechnology , medicine , genetics , gene , environmental health , fishery
We performed comparative genomic hybridization (CGH) on 8 formalin‐fixed, paraffin wax‐embedded primary spermatocytic seminomas (SS) from 7 patients, one of whom developed metastatic disease. In general, this tumour type is not associated with development of metastases. Since there are only few reported cases of metastatic SS in the literature, this study is the first report of chromosomal constitution in a patient with metastatic disease. Chromosomal imbalances were observed in all 8 tumours analysed by CGH. Frequent copy number alterations were enh(9), dim(16 or 16p), enh(20) and enh(X), each in 6 samples, followed by dim(7) in 4, and enh(1), enh(18) and dim(15), each in 3 samples. In addition to the CGH analysis, interphase fluorescence in situ hybridisation (I‐FISH) was applied to evaluate the CGH results and to define the size of the aberrant cell population. Interphase cytogenetics showed gain of material on chromosomes 9 and X in all tumours analysed. Overall, the I‐FISH results were in agreement with the CGH data. In conclusion, gain of chromosome 9 seems to be restricted to SS and point to an important role for this aberration in the development of this tumour type. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.