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No recurrent structural abnormalities apart from i(12p) in primary germ cell tumors of the adult testis.

Authors
  • van Echten, J
  • Oosterhuis, J W
  • Looijenga, L H
  • van de Pol, M
  • Wiersema, J
  • te Meerman, G J
  • Schaffordt Koops, H
  • Sleijfer, D T
  • de Jong, B
Type
Published Article
Journal
Genes, chromosomes & cancer
Publication Date
Oct 01, 1995
Volume
14
Issue
2
Pages
133–144
Identifiers
PMID: 8527395
Source
Medline
License
Unknown

Abstract

Malignant transformation may be caused by gene deregulation resulting from specific chromosomal rearrangements, by amplification, by mutations in proto-oncogenes, by loss of tumor suppressor genes, or a combination of these. We investigated the role of numerical and structural chromosomal abnormalities in 102 cytogenetically abnormal cases of primary testicular germ cell tumors of adolescents and adults (TGCT) [32 seminomas (SE) and 70 nonseminomatous germ cell tumors (NS)]. We confirmed that an isochromosome for 12p, i(12p), is the only consistent structural chromosomal abnormality in TGCT, present in about 70% of our cases. Both the frequency and the number of copies of i(12p) are higher in NS than in SE. This may suggest that i(12p) is involved in tumor progression. Besides i(12p), several clonal structural chromosomal abnormalities were found, but none appeared to be specific. SE and NS had chromosome numbers in the triploid range, with significantly higher numbers in SE than in NS (average modal chromosome numbers of 73.4 in SE and 65.0 in NS). Both in SE and NS, some chromosomes were significantly underrepresented (e.g., 11, 13, 18, and Y) and others overrepresented (e.g., 7, 8, 12, 21, and X). In SE, a significantly higher copy number of chromosomes 7, 15, 19, and 22 was found and a significantly lower number of chromosome 17, compared with NS. These chromosomes may play an important role in the differentiation of TGCT.

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