2003
DOI: 10.1038/sj.onc.1207011
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Abstract: All invasive testicular germ cell tumors of adolescents and adults (TGCTs), that is, seminomas and nonseminomas, show gain of 12p sequences, mostly as isochromosomes. Although several candidate genes have been suggested, the relevant gene(s) have not been identified yet. About 10% of testicular seminomas, however, show a more restricted amplification of the 12p11.2-p12.1 region, in which the various amplicons show an apparent overlap, allowing for the shortest region of amplification overlap approach, aiming a… Show more

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Cited by 71 publications
(68 citation statements)
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“…It is generally assumed that the amplification of tumor genes at this region triggers malignant transformation at the transition from TIN to invasive malignant germ cell tumors. 8,9,31 Since in our patient the amplicon is located at the identical chromosomal region as in testicular germ cell tumors, this observation provides additional evidence in favor of a common pathogenesis of testicular and CNS-GCTs.…”
Section: Restricted Amplification Of 12p12supporting
confidence: 65%
See 1 more Smart Citation
“…It is generally assumed that the amplification of tumor genes at this region triggers malignant transformation at the transition from TIN to invasive malignant germ cell tumors. 8,9,31 Since in our patient the amplicon is located at the identical chromosomal region as in testicular germ cell tumors, this observation provides additional evidence in favor of a common pathogenesis of testicular and CNS-GCTs.…”
Section: Restricted Amplification Of 12p12supporting
confidence: 65%
“…7 In the remaining tumors, gain of chromosomal material of 12p is related to either marker chromosomes or homogeneously staining regions that contain chromosomal material derived from chromosomal band 12p11.2-12.1. 8,9 Additional chromosomal imbalances have also been reported in testicular germ cell tumors. However, these are less frequent and less consistent as compared to gain of 12p.…”
mentioning
confidence: 97%
“…NS, which have a median age at diagnosis of 25, exhibit various stages of differentiation with cells from embryonic, extra-embryonic and somatic tissue types (Mostofi, 1973). Material from the short arm of chromosome 12 is invariably gained in these tumours and in roughly 10% of cases a smaller region of gain at 12p11.2 -p12.1 has been defined (Rodriguez et al, 2003;Zafarana et al, 2003).…”
mentioning
confidence: 99%
“…In addition to 12p, other chromosomal regions have also been identified that are frequently altered in GCTs (von Eyben, 2004), including gains on regions of 2p, 4q, 6p, 7, 8, 17q, 19p, and 21, and losses on chromosomes 4, 10q, 12q, 11, 13, and 18, (Korn et al, 1996;Murty et al, 1999;Kraggerud et al, 2002;Draper et al, 2004;von Eyben, 2004). Sem and NSGCTs have also demonstrated differential copy number gain/loss patterns, with gains of 15q and 22q and high-level amplifications of 12p associated with Sem (Kraggerud et al, 2002;Zafarana et al, 2003) and gains of proximal 17q and losses of 10q associated with NSGCTs .…”
Section: Introductionmentioning
confidence: 99%
“…The vast majority of GCTs manifest this gain as an isochromosome of 12p, while a small proportion show tandem duplication of material from 12p (Atkin and Baker, 1982;Bosl et al, 1989;Murty and Chaganti, 1998). Additionally, a number of tumors show subregional, high-level amplification of 12p (Bourdon et al, 2002;Looijenga and Oosterhuis, 2002;Zafarana et al, 2003). Extensive studies of 12p have identified a number of candidate target genes, including CCND2 and a cluster of stem cell genes at 12p13.31 (Houldsworth et al, 1997;Clark et al, 2004;Korkola et al, 2006).…”
Section: Introductionmentioning
confidence: 99%