Molecular biology and genetic of human neuroblastoma

Washington University School of Medicine, St. Louis, MO 63110.
Cancer Genetics and Cytogenetics (Impact Factor: 1.93). 10/1989; 41(2):153-74. DOI: 10.1016/0165-4608(89)90243-4
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Available from: Garrett M Brodeur,
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    • "The power of FISH was best illustrated by the finding of whole chromosome 17 and partial 17q gain as the most frequent recurrent chromosomal change in NB (Savelyeva et al., 1994; Van Roy et al., 1994; Vandesompele et al., 1998, 2001; Speleman and Bown, 2000). Only one cytogenetic study referred to chromosome 17 involvement in NB, all other previously conducted cytogenetic analysis overlooked the non-random involvement of chromosome 17 in NB (Gilbert et al., 1984; Brodeur and Fong, 1989). FISH studies including 24-colour M-FISH (Speicher et al., 1996) revealed gain of 17q in the majority of cell lines and high-stage tumors , most often as the result of unbalanced translocations (Van Roy et al., 2001; Schleiermacher et al., 2003). "
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    ABSTRACT: In the past few years high throughput methods for assessment of DNA copy number alterations have witnessed rapid progress. Both 'in house' developed BAC, cDNA, oligonucleotide and commercial arrays are now available and widely applied in the study of the human genome, particularly in the context of disease. Cancer cells are known to exhibit DNA losses, gains and amplifications affecting tumor suppressor genes and proto-oncogenes. Moreover, these patterns of genomic imbalances may be associated with particular tumor types or subtypes and may have prognostic value. Here we summarize recent array CGH findings in neuroblastoma, a pediatric tumor of the sympathetic nervous system. A total of 176 primary tumors and 53 cell lines have been analyzed on different platforms. Through these studies the genomic content and boundaries of deletions, gains and amplifications were characterized with unprecedented accuracy. Furthermore, in conjunction with cytogenetic findings, array CGH allows the mapping of breakpoints of unbalanced translocations at a very high resolution.
    Cytogenetic and Genome Research 02/2006; 115(3-4):273-82. DOI:10.1159/000095924 · 1.56 Impact Factor
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    • "Deletion of chromosome 1p is an independent indicator of poor prognosis (Christiansen and Lampert, 1988; Hayashi et al, 1989) and may be the most discriminant prognostic factor (Caron et al, 1996; Rubie et al, 1997). Early studies showing deletion in 70% of samples concentrated on advanced tumours and cell lines (Brodeur and Fong, 1989; Weith et al, 1989), which were likely to be a nonrepresentative group of aggressive, progressive tumours. Del(1p) is less often found in stage 1 and 2 tumours (Hayashi et al, 1989; Ambros et al, 1995). "
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    ABSTRACT: Neuroblastoma is the commonest extracranial solid tumour in children. There are a number of molecular genetic features known which are of prognostic importance and which are used to direct therapy. Identification and targeting of high-risk individuals with intensive therapeutic regimens may allow an improvement in survival rates. The most powerful biological parameters associated with prognosis in this malignancy are chromosomal changes, especially MYCN amplification, deletion of chromosome 1p and aneuploidy. Rapid characterization of these aberrations at the time of diagnosis is paramount if stratification according to risk group is to be achieved. This paper describes the rapid detection of del(1p), MYCN amplification and trisomy using interphase fluorescence in situ hybridization on imprints from fresh tumour biopsies. The results are related to those obtained by standard molecular methods and karyotyping.
    British Journal of Cancer 08/2000; 83(1):40-9. DOI:10.1054/bjoc.2000.1280 · 4.84 Impact Factor
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    • "We have sought evidence for amplification or overexpression of a number of other oncogenes in a panel of neuroblastoma cell lines and primary tumors, but none was found (Brodeur and Fong, 1989). Although N-ras was first identified as the transforming gene of a human neuroblastoma cell line, subsequent studies of primary neuroblastomas by ourselves and others (Ballas et al., 1988; Ireland, 1989; Moley et al., 1991) indicate that ras activation by mutation of codons 12, 13, 59, or 61 is rare. "
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    ABSTRACT: Tumors of the peripheral nervous system include neuroblastomas, pheochromocytomas, and neuroepitheliomas. Neuroblastomas and pheochromocytomas are adrenergic in origin and share certain genetic features, whereas neuroepitheliomas are thought to be cholinergic and are characterized by distinct genetic features. Neuroblastomas are characterized by deletion of the short arm of chromosome 1 (1p), amplification of the MYCN proto-oncogene, and hyperdiploidy in subsets of tumors. All three of these genetic features have prognostic value in subsets of patients. Allelic loss of 14q also occurs with increased frequency, but the prognostic importance of this abnormality is not known yet. Pheochromocytomas have not been studied as extensively, but allelic loss for 1p appears to be a frequent change, and no clear examples of oncogene activation have been identified to date. Neuroepitheliomas are characterized by translocation between chromosomes 11 and 22. Although they have a characteristic pattern of proto-oncogene expression, it is not clear that any of these oncogenes are activated specifically, and no sites of allelic loss have been identified to date. Thus, cytogenetic and molecular analysis of neuroblastomas, pheochromocytomas, and neuroepitheliomas are useful in distinguishing them from each other and from other tumors in selected cases. Furthermore, certain genetic markers are useful in predicting clinical behavior, especially for neuroblastoma.
    Cancer and metastasis reviews 01/1992; 10(4):321-33. DOI:10.1007/BF00554794 · 7.23 Impact Factor
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