𝔖 Bobbio Scriptorium
✦   LIBER   ✦

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

✍ Scribed by Jannie van Echten; J. Wolter Oosterhuis; Leendert H. J. Looijenga; Mirjam van de Pol; Janneke Wiersema; Gerard J. Te Meerman; Heimen Schraffordt Koops; Dirk Th. Sleijfer; Bauke De Jong


Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
922 KB
Volume
14
Category
Article
ISSN
1045-2257

No coin nor oath required. For personal study only.

✦ Synopsis


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 I02 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 I2p. i( I 2p), 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( I2p) are higher in NS than in SE. This may suggest that i( I2p) is involved in tumor progression. Besides i( I2p), several clonal structural chromosomal abnormalities were found, but none appeared t o be specific. SE and NS had chromosome numbers in the triploid range, with significantly higher numbers in SE than in NS (average modal chromosome number of 73.4 in SE and 65.0 in NS). Both in SE and NS, some chromosomes were significantly underrepresented (e.g., I I, 13, 18, and Y) and others overrepresented (e.g., 7, 8, 12, 2 I, 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. Genes Chromosom Cancer /4:/33-/44 (1995). 0 1995 Wiley-Liss, Inc.