Additional copies of a 25 Mb chromosomal region originating from 17q23.1-17qter are present in 90% of high-grade neuroblastomas

Meddeb, Mounira; Danglot, Gisèle; Chudoba, Iise; Venuat, A.M.; Bénard, Jean; Avet-Loiseau, Hervé; Vasseur, Béatrice; Paslier, Denis Le; Terrier‐Lacombe, Marie‐José; Hartmann, Olivier; Bernheim, Alain

doi:10.1002/(sici)1098-2264(199611)17:3<156::aid-gcc3>3.0.co;2-3

Cited by 94 publications

(47 citation statements)

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“…neuroblastoma. Recently, it has been shown that gains of 17qter material were present in about 90% of high-grade neuroblastomas (Meddeb et al, 1996). Because neuroblastomas and medulloblastomas are both neuroectodermal tumours, a common tumorigenic event may be proposed, even if no candidate gene has so far been found.…”

Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Avet-Loiseau¹,

et al. 1999

Br J Cancer

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Summary A series of 23 children with primitive neuroectodermal tumours (PNET) were analysed with comparative genomic hybridization (CGH). Multiple chromosomal imbalances have been detected in 20 patients. The most frequently involved chromosome was chromosome 17, with a gain of 17q (11 cases) and loss of 17p (eight cases). Further recurrent copy number changes were detected. Extra copies of chromosome 7 were present in nine patients and gains of 1q were detected in six patients. A moderate genomic amplification was detected in one patient, involving two sites on 3p and the whole 12p. Losses were more frequent, and especially involved the chromosomes 11 (nine cases), 10q (eight cases), 8 (six cases), X (six patients) and 3 (five cases), and part of chromosome 9 (five cases). These recurrent chromosomal changes may highlight locations of novel genes with an important role in the development and/or progression of PNET.

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Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Avet-Loiseau¹,

et al. 1999

Br J Cancer

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“…These findings are supported by earlier studies Plantaz et al, 1997). The association between 1p deletion and 17q gain is not surprising since physical connection between these chromosomes has been seen in the form of unbalanced translocations der(1)t(1p;17q) (Caron et al, 1994;Van Roy et al, 1994;Meddeb et al, 1996;. These translocations result in loss of 1p and gain of 17q, and are thought to occur in the S/G2 phase of the cell cycle (Caron et al, 1994).…”

Section: mentioning

confidence: 99%

“…More recently, comparative genomic hybridization (CGH) studies have shown that extra chromosome 17q material occurs in approximately 70-80% of primary tumours, either as gain of the whole chromosome 17 or the q arm alone (Plantaz et al, 1997;Lastowska et al, 1998;Vandsompele et al, 1998). Using FISH studies Meddeb et al (1996) and Lastowska     et al (1997) showed that 17q can translocate on to a number of chromosome regions other than 1p, and that such rearrangements also results in gain of 17q material. Meddeb et al (1996) reported that among translocations only 17% were (1;17) translocations, whereas the remainder involved various other chromosomes: chromosome 4, 5, 6, 9, 11, 12, 14, 17 and 19.…”

mentioning

confidence: 99%

“…Using FISH studies Meddeb et al (1996) and Lastowska     et al (1997) showed that 17q can translocate on to a number of chromosome regions other than 1p, and that such rearrangements also results in gain of 17q material. Meddeb et al (1996) reported that among translocations only 17% were (1;17) translocations, whereas the remainder involved various other chromosomes: chromosome 4, 5, 6, 9, 11, 12, 14, 17 and 19. Moreover, both groups found that 17q gain also showed correlation to poor prognosis.…”

mentioning

confidence: 99%

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Gain of chromosome arm 17q is associated with unfavourable prognosis in neuroblastoma, but does not involve mutations in the somatostatin receptor 2 (SSTR2) gene at 17q24

et al. 1999

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Deletion of chromosome arm 1p and amplification of the MYCN oncogene are well-recognized genetic alterations in neuroblastoma cells. Recently, another alteration has been reported; gain of the distal part of chromosome arm 17q. In this study 48 neuroblastoma tumours were successfully analysed for 17q status in relation to known genetic alterations. Chromosome 17 status was detected by fluorescence in situ hybridization (FISH). Thirty-one of the 48 neuroblastomas (65%) showed 17q gain, and this was significantly associated with poor prognosis. As previously reported, 17q gain was significantly associated with metastatic stage 4 neuroblastoma and more frequently detected than both deletion of chromosome arm 1p and MYCN amplification in tumours of all stages. 17q gain also showed a strong correlation to survival probability ( P = 0.0009). However, the most significant correlation between 17q gain and survival probability was observed in children with low-stage tumours (stage 1, 2, 3 and 4S), with a survival probability of 100% at 5 years from diagnosis for children with tumours showing no 17q gain compared to 52.5% for those showing 17q gain ( P = 0.0021). This suggests that 17q gain as a prognostic factor plays a more crucial role in low-stage tumours. Expression of the somatostatin receptor 2 (SSTR2), localized in chromosome region 17q24, has in previous studies been shown to be positively related to survival in neuroblastoma. A point mutation in the SSTR2 gene has earlier been reported in a human small-cell lung cancer. In this study, mutation screening of the SSTR2 gene in 43 neuroblastoma tumours was carried out with polymerase chain reaction-based single-stranded conformation polymorphism/heteroduplex (SSCP/HD) and DNA sequencing, and none of the tumours showed any aberrations in the SSTR2 gene. These data suggest that mutations in the SSTR2 gene are uncommon in neuroblastoma tumours and do not correlate with either the 17q gain often seen or the reason some tumours do not express SSTR2 receptors. Overall, this study indicates that gain of chromosome arm 17q is the most frequently occurring genetic alteration, and that it is associated with established prognostic factors. © 1999 Cancer Research Campaign

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“…Several studies performed in neuroblastoma tumors have identified a common amplified region ranging from 17q21.3 to 17qter with a highly variable localization of the breakpoint region [2,22]. Identification of one or more genes located in the long arm of chromosome 17 is of large clinical interest since an effect of their altered expression may be responsible for the altered phenotype [23].…”

Section: Discussionmentioning

confidence: 99%

Influence of 17q gain and promoter polymorphisms on mRNA expression of somatostatin receptor type 2 in neuroblastoma

Simi

Pinzani

Raggi

et al. 2007

Clinica Chimica Acta

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Background: Neuroblastoma, the most frequent solid extracranial tumor in children, is characterized by a wide spectrum of clinical behaviours. We previously reported that high expression of somatostatin receptor type-2 (sst2) mRNA is associated to increased overall and event free survival. Several genetic abnormalities are detected in neuroblastomas, frequently involving balanced and/or unbalanced gain on the long arm on chromosome 17, the same region containing sst2 gene. Methods: In this study we detected balanced and/or unbalanced 17q gain in 50 neuroblastomas. Since two polymorphisms in sst2 promoter (− 57 C N G and − 83 A N G) were previously described as responsible for an in vitro reduction of sst2 mRNA expression, promoter sequencing was also performed in the same samples. The results were compared to sst2 mRNA expression, measured by real-time RT-PCR. Results: The frequency of 17q gain (14/50 neuroblastomas) was significantly associated to sst2 mRNA over-expression (Fischer's exact test: p = 0.0012). The sst2 expression was significant higher both in balance and unbalance 17q amplifications (ANOVA: p = 0.04). Conversely, we found a reduction of sst2 mRNA in neuroblastomas with − 57 C N G promoter polymorphism (ANOVA: p = 0.03). Conclusion: We highlighted that 17q gain and promoter polymorphisms can play a role into the regulation of sst2 expression in neuroblastomas.

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Additional copies of a 25 Mb chromosomal region originating from 17q23.1-17qter are present in 90% of high-grade neuroblastomas

Cited by 94 publications

References 30 publications

Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Gain of chromosome arm 17q is associated with unfavourable prognosis in neuroblastoma, but does not involve mutations in the somatostatin receptor 2 (SSTR2) gene at 17q24

Influence of 17q gain and promoter polymorphisms on mRNA expression of somatostatin receptor type 2 in neuroblastoma

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