Chromosomes 1 and 12 abnormalities in pediatric germ cell tumors by interphase fluorescence in situ hybridization

Bussey, Kimberly J.; Lawce, Helen J.; Himoe, Eleanor; Shu, Xiao Ou; Suijkerbuijk, Ron F.; Olson, Susan B.; Magenis, R. Ellen

doi:10.1016/s0165-4608(00)00380-0

Cited by 25 publications

(24 citation statements)

References 23 publications

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“…In contrast, Perlman et al detected loss at 1p in five of seven cases analyzed with conventional cytogenetic techniques, indicating significant observer-dependent differences in the assessment of 1p alterations (Perlman et al, 1994). Complementary FISH analyses using a 1p36 cosmid probe coupled with a centromeric or 1q probe reported a relative reduction in the number of 1p36 signals compared to the centromeric or 1q signals in up to 80% of childhood YSTs (Jenderny et al, 1996;Perlman et al, 1996;Stock et al, 1996;Bussey et al, 2001). However, since conventional chromosomal CGH revealed infrequent loss at distal 1p but frequent gain of 1q, including the centromeric region, there has been some debate whether the results of the FISH studies were related to gain of 1q rather than loss of 1p Schneider et al, 2001Schneider et al, (a), 2002.…”

Section: Discussionmentioning

confidence: 87%

“…Chromosomal loss at 1p has also been noted in several cases of adolescent testicular and ovarian GCTs and in pediatric GCTs (Perlman et al, 1994;Bussey et al, 1999;Perlman et al, 2000;Mostert et al, 2000;Schneider et al, 2001(a); Bussey et al, 2001;Schneider et al, 2002;van Echten et al, 2002). Of note, these studies were based on FISH, CGH, or cytogenetic analyses, which detect chromosomal copy number loss but do not determine true allelic loss.…”

Section: Discussionmentioning

confidence: 99%

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Imbalances of chromosome arm 1p in pediatric and adult germ cell tumors are caused by true allelic loss: A combined comparative genomic hybridization and microsatellite analysis

Zahn

Sievers

Alemazkour

et al. 2006

Genes Chromosomes & Cancer

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Previous studies on childhood germ cell tumors (GCTs) report highly variable frequencies of losses at chromosome arm 1p. Since deletions at 1p portend a poor prognosis in other embryonal tumors, this study aims to clarify the question of the frequency of true allelic loss at 1p and whether it constitutes a prognostic parameter. We analyzed 13 GCTs from different gonadal and extragonadal sites of children (4 teratomas, 9 malignant GCTs) and 18 GCTs of adolescents and adults (3 teratomas; 15 malignant GCTs) using automated microsatellite analysis with 23 polymorphic markers and chromosomal "high resolution" comparative genomic hybridization (HR-CGH). With this combined approach, we detected loss of heterozygosity (LOH) at 1p in 8/9 childhood malignant GCTs with concordant data from HR-CGH and microsatellite analyses. In contrast, LOH at 1p was not detected in childhood teratomas (0/4) and constituted a rare event in GCTs of adolescence and adulthood (3/18). The commonly deleted region was located at distal 1p36-pter, with a proximal boundary between the markers D1S450 and D1S2870. These data unequivocally demonstrate that deletion at 1p is common in childhood GCTs and results in allelic loss. This observation argues for the presence of a classical tumor suppressor at distal 1p. Considering the high frequency of LOH at 1p and the overall favorable prognosis of childhood GCTs, a prognostic impact of LOH at 1p in childhood GCTs appears unlikely. However, since two postpubertal tumors with LOH at 1p progressed, a prognostic relevance in this age group seems possible, warranting a prospective evaluation.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Imbalances of chromosome arm 1p in pediatric and adult germ cell tumors are caused by true allelic loss: A combined comparative genomic hybridization and microsatellite analysis

Zahn

Sievers

Alemazkour

et al. 2006

Genes Chromosomes & Cancer

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“…1,2,[75][76][77][78][79][80] While virtually all adult cases are aneuploid, pediatric cases are mostly diploid, particularly teratomas, although yolk sac tumors may be nondiploid. Imprinting studies suggest that both arise from primordial germ cells but at a different stage of germ cell development.…”

Section: Molecular Biology Of Germ Cell Tumorsmentioning

confidence: 99%

“…i(12p) and 12p amplification are rare events in pediatric tumors. Bussey et al 77 found that 12p amplification in childhood GCT was age dependent and only seen in patients above the age of 9 years. On the other hand, pediatric tumors are characterized by deletions of 1p, particularly region p36, loss of 6q, and structural abnormalities of chromosome 2 and 3p.…”

Section: Molecular Biology Of Germ Cell Tumorsmentioning

confidence: 99%

Origins and molecular biology of testicular germ cell tumors

2005

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“…By contrast, the pattern of genomic gains and losses between the histological subtypes was broadly similar, except for gains of chromosome 15 in seminomas compared to nonseminomas (Looijenga, 2001). In the paediatric population, DNA ploidy was found to be variable (diploid, triploid and tetraploid) (Looijenga and Oosterhuis, 1999;Bussey et al, 2001;Schneider et al, 2001) while ovarian GCTs are mostly diploid, independent of age (Surti et al, 1990).…”

Section: Chromosomal Aberrationsmentioning

confidence: 99%

Age‐related biological features of germ cell tumors

Collinson

Murray

Orsi

et al. 2013

Genes Chromosomes & Cancer

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Germ cell tumours (GCTs) are rare but clinically and pathologically diverse tumours that occur in an extensive range of age groups, from children to older adults and which include both seminomatous and nonseminomatous tumours. Current clinical management for both male and female teenagers and young adults (TYAs) with GCTs remains inconsistent, alternating between paediatric and adult multidisciplinary oncology teams, based on locally defined age cut-offs. We therefore reviewed available literature to determine the biological similarities and differences between GCTs in young children [0-12 years (y)], TYAs (13-24y), and older adults (>24y). GCTs arising in paediatric and adult populations in general showed marked molecular biological differences within identical histological subtypes, whereas there was a distinct paucity of available data for GCTs in the TYA population. These findings highlight that clinical management based simply on chronological age may be inappropriate for TYA and suggests that the optimal future management of GCTs should consider specific molecular biological factors in addition to clinical parameters in the context of patient specific age group specialty. 3 AimsThe aim of this review was to analyse molecular biological studies of germ cell tumours (GCTs) arising in the paediatric (≤12y) and older adult (>24y) age groups for key similarities and differences in an attempt to identify where the biology of GCTs from teenagers and young adult (TYA) patients lies within this framework. The review discusses current knowledge in this area and also highlights gaps that still need to be addressed. In the UK, the TYA age group includes male and females aged 13-24y; accordingly we have used this definition for the purposes of this review).The aims were achieved through a synthesis and analysis of available biological data for GCTs in children, TYAs and older adults. We anticipated that the goal would be to use a combination of both clinical and biological risk factors to improve clinical management decisions for TYA patients with GCTs (Murray et al., 2009).

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Chromosomes 1 and 12 abnormalities in pediatric germ cell tumors by interphase fluorescence in situ hybridization

Cited by 25 publications

References 23 publications

Imbalances of chromosome arm 1p in pediatric and adult germ cell tumors are caused by true allelic loss: A combined comparative genomic hybridization and microsatellite analysis

Imbalances of chromosome arm 1p in pediatric and adult germ cell tumors are caused by true allelic loss: A combined comparative genomic hybridization and microsatellite analysis

Origins and molecular biology of testicular germ cell tumors

Age‐related biological features of germ cell tumors

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