Chromosomal analysis of neuroblastoma

Hafez, Michael J.; el-Meadday, M; Sheir, Mahmoud; Al-Tonbarry, Y; Nada, Nadia; I, el-Desoky

doi:10.1038/bjc.1985.34

Cited by 13 publications

(4 citation statements)

References 15 publications

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“…This chromosomal region has been implicated in the development of neuroblastoma. Tumor cells derived from 70 % of patients with neuroblastoma exhibit a deletion of part of the short arm of chromosome 1 [39]. Molecular analysis of a number of neuroblastoma cell lines indicates that the deletions cluster at position 1p32 [40].…”

Section: Discussionmentioning

confidence: 99%

Human and mouse homologs of the Saccharomyces cerevisiaeRAD54 DNA repair gene: evidence for functional conservation

et al. 1996

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The tissue-specific expression of mHR54 is consistent with a role for the gene in recombination. The complementation experiments show that the DNA repair function of Rad54 is conserved from yeast to humans. Our findings underscore the fundamental importance of DNA repair pathways: even though they are complex and involve multiple proteins, they seem to be functionally conserved throughout the eukaryotic kingdom.

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Section: Discussionmentioning

confidence: 99%

Human and mouse homologs of the Saccharomyces cerevisiaeRAD54 DNA repair gene: evidence for functional conservation

et al. 1996

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“…The short-arm deletions usually involved the part distal to 1p32, although reports about the affected region on 1p were not always consistent. Most of the early studies showed long terminal deletions (Brodeur et al, 1981;Gilbert et al, 1982;Hafez et al, 1985), whereas recent investigations could restrict the region of interest to 1p36 (Fong et al, 1989;Weith et al 1989;Cheng et al, 1995;White et al, 1995;Bauer et al, 2001;Maris et al, 2001). Some authors have proposed two different loci on 1p containing at least two tumor-suppressor genes (Schleiermacher et al, 1994;Takeda et al, 1994;Mora et al, 2000), with the second more proximal one showing less prognostic relevance compared to the distal 1p36 (Mora et al, 2000).…”

Section: Introductionmentioning

confidence: 93%

Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations

Spitz

Hero

Westermann

et al. 2002

Genes Chromosomes & Cancer

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Chromosomal alterations in 1p36 were investigated in 196 neuroblastoma tumors using fluorescence in situ hybridization. Additionally, by using the same technique, it was determined whether MYCN was amplified in 149 of these. The most frequent finding was a deletion in 1p36, leading to monosomy of this region (29 cases, 15%). Furthermore, we found tumors with at least two intact copies of chromosome 1 and additional 1p36-deleted copies. Altogether, 21 tumors (11%) displayed this imbalance of 1p36. Similar to the cases with deletion, imbalances were predominantly found in stage 4 tumors (81%), and they were significantly associated with an increased patient age (P = 0.01). Nearly all 1p-deleted tumors showed amplification of MYCN (24/27 analyzed samples, 89%), whereas only 8 of 21 (38%) with imbalance did. Eight cases with imbalance were investigated for loss of heterozygosity (LOH) using microsatellite markers in 1p35-36. Only 4 displayed 1p36 LOH, whereas the remaining 4 were heterozygous. Both patients with deletion of 1p and with imbalance had a poor outcome [3-year rate of event-free-survival (EFS): 33 +/- 15% and 41 +/- 15%], which was significantly worse compared to the outcome of patients without 1p alterations (3-year EFS: 70 +/- 5%; P = 0.01 and P = 0.0059). We conclude that besides monosomic short arm deletions, imbalance of 1p36 is a strong marker of a poor prognosis in neuroblastoma and not necessarily associated with MYCN amplification and LOH.

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“…1970). Cells from at least 70% of these tumors exhibit a loss of the distal portion of the short arm of chromosome 1 (Brodcur et al" 1981: Haag ct al" 1981Gilbert et al" 1982;Hafez, et al" 1985). Other chromosomal abnormalities associated with this tumor include double minute chromosomes (DMs) and homoge neously staining regions (HSRs) that are believed to represent the amplification of M YCN and its surrounding genes (Montgomery etal.. 1983: Kohletal.. 1984Hafez etal.. 1985: Shiloh et al.…”

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confidence: 99%

Molecular analysis of chromosome 1 abnormalities in neuroblastoma

Ritke¹,

Shah²,

Valentine

et al. 1989

Cytogenet Genome Res

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Tumor cells from 70% of neuroblastoma patients contain a deletion of part of the short arm of chromosome 1, indicating that this chromosomal region includes a gene involved in tumor formation. To more precisely evaluate the boundaries and mechanisms involved in generating these deletions, we have examined four neuroblastoma cell lines using a combination of somatic cell hybridization, isozyme analysis, and nucleic acid hybridization employing both standard and restriction fragment length polymorphic probes. The data suggest that the truncation of chromosome 1 in these neuroblastomas was most likely due to a complex translocation and deletion mechanism rather than a simple unbalanced translocation or terminal or interstitial deletion. This conclusion is supported by the frequent removal of MYCL from the altered chromosome 1 to another chromosome. Furthermore, the data suggest that the frequency of breakpoints previously assigned by karyotypic analysis to bands other than lp32 in neuroblastomas may be overestimated. Finally, this study identified a breakpoint at 1p32 that was localized between the genes JUN and MYCL for one neuroblastoma thus establishing the order of these genes as centromere, JUN, MYCL, telomere. We conclude that the observed breakpoints within chromosome 1p in human neuroblastoma are not as variable as previously described and suggest the results of this study provide evidence for the involvement of specific DNA sequences within lp32 in the generation of neuroblastoma.

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Chromosomal analysis of neuroblastoma

Cited by 13 publications

References 15 publications

Human and mouse homologs of the Saccharomyces cerevisiaeRAD54 DNA repair gene: evidence for functional conservation

Human and mouse homologs of the Saccharomyces cerevisiaeRAD54 DNA repair gene: evidence for functional conservation

Fluorescence in situ hybridization analyses of chromosome band 1p36 in neuroblastoma detect two classes of alterations

Molecular analysis of chromosome 1 abnormalities in neuroblastoma

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