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Detection of chromosomal DNA gains and losses in testicular germ cell tumors by comparative genomic hybridization
Author(s) -
Korn W. Michael,
Weghuis Daniel E. M. Olde,
Suijkerbuijk Ron F.,
Schmidt Ulrich,
Otto Thomas,
du Manoir Stanislas,
van Kessel Ad Geurts,
Harstrick Andreas,
Seeber Siegfried,
Becher Reinhard
Publication year - 1996
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199610)17:2<78::aid-gcc2>3.0.co;2-y
Subject(s) - comparative genomic hybridization , biology , germ cell , germ cell tumors , dna , in situ hybridization , genomic dna , cancer research , genetics , microbiology and biotechnology , genome , gene , gene expression , chemotherapy
To extend the results of conventional cytogenetic analysis of testicular germ cell tumors (TGCTs), we applied the new molecular cytogenetic method of comparative genomic hybridization (CGH), which enables the detection of chromosomal imbalances without the need for dividing cells. DNA from II TGCTs was studied by CGH. In all tumors examined, gain of 12p, mostly of the whole p arm, could be demonstrated. However, in three tumors, an amplification of 12p material restricted to the chromosomal bands 12p11.2‐p12.1 was found. Further fluorescence in situ hybridization (FISH) analysis using a yeast artificial chromosome (YAC) that was previously mapped to that region revealed multiple copies of that chromosomal segment in interphase nuclei of these tumors. This finding is an important clue to the localization of candidate protooncogenes at 12p involved in TGCTs. Gains of small chromosomal regions at 2p, 4q, 6p, and 19p were also detected recurrently. Furthermore, gains of chromosomes 8, 14, 21, and X as well as loss of chromosome 13 were frequent findings. In conclusion, CGH provides new insights into genetic alterations of TGCTs. By using CGH, chromosomal subregions could be identified that may harbor genes involved in the pathogenesis of this malignancy. Genes Chromosom Cancer 17:78–87 (1996). © 1996 Wiley‐Liss, Inc.