Comparative genomic hybridization of microdissected samples from different stages in the development of a seminoma and a non-seminoma

Molecular characterization of hiwi, a human member of the piwi gene family whose overexpression is correlated to seminomas

“…Because of these data, hiwi might be an interesting candidate gene to explain the genetic linkage between the development of TGCTs and the telomeric end of chromosome 12. Moreover, this could explain the ®nding of gain of this chromosomal region in some TGCTs (Looijenga et al, 1999a(Looijenga et al, , 2000Rosenberg et al, 1999;and Lothe, personal communication). Increased hiwi dose might elevate the number or the mitotic activity of spermatogenic stem cells, just like when piwi is overexpressed (Cox et al, 2000).…”

“…The ®rst type of tumors are the seminomas and nonseminomas of adolescents and adults, also known as TGCTs, while the second type are the spermatocytic seminomas of the elderly (reviewed in Looijenga et al, 1999a;Looijenga and Oosterhuis, 1999b). Although these tumors have separate pathogenesis, as demonstrated by their clinical behavior (reviewed in Bosl and Motzer, 1997;Burke and Mosto®, 1993) and chromosomal constitution Looijenga et al, 2000;Rosenberg et al, 1998Rosenberg et al, , 1999van Echten et al, 1995), they all originate from the germ cell lineage. The TGCTs originate from an embryonic germ cell, most likely the malignant counterpart of a primordial germ cell, known as carcinoma in situ (CIS; Jorgensen et al, 1995;Moller, 1989;Skakkebaek, 1972).…”

Overrepresentation of the short arm of chromosome 12 is related to invasive growth of human testicular seminomas and nonseminomas

“…Eight to 25 ng of DNA from each micro-dissected sample and from a normal male were ampli®ed by DOP ± PCR as described before and used for CGH (Telenius et al, 1992;Looijenga et al, 2000).…”

Origin of pluripotent germ cell tumours: The role of microenvironment during embryonic development

“…A recurrent gain of 12p material was demonstrated in the vast majority of overt TGCTs, together with chromosomal aberrations established as typical for TGCTs (Atkin & Baker 1982;Summersgill et al, 2001; and reviewed in Page 7 of 22 A c c e p t e d M a n u s c r i p t 7 von Eyben, 2004). Fascinatingly, the extra 12p material was also observed in several cases of CIS adjacent to overt tumours but was absent in CIS cells with no evidence of invasive growth (Looijenga et al, 2000;Ottesen et al, 2003;Ottesen et al, 2004a;Ottesen et al, 2004b;Skotheim et al, 2006). Whereas gains of 17q were only detected in a few CIS cases (Ottesen et al, 2003;Ottesen et al, 2004b), a recurrent gain of 17q has been associated with non-seminomas in particular, perhaps illustrating the high proliferation potential of this more aggressive tumour (Kraggerud et al, 2002;Skotheim et al, 2002).…”