ArticleNucleic acids research1994
Megabase-scale analysis of the origin of N-myc amplicons in human neuroblastomas.
Article in Nucleic acids research, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Selective targeting of genome amplifications and repeat elements by CRISPR-Cas9 nickases to promote cancer cell death.Nature communications · 2025Article
- Glioblastoma proto-oncogene SEC61gamma is required for tumor cell survival and response to endoplasmic reticulum stress.Cancer research · 2009Article
- Clinical implications of a slight increase in the gene dosage of MYCN in neuroblastoma determined using quantitative PCR.Pediatric surgery international · 2008Article
- Genes proximal and distal to MYCN are highly expressed in human neuroblastoma as visualized by comparative expressed sequence hybridization.The American journal of pathology · 2008Article
- Activation of anaplastic lymphoma kinase is responsible for hyperphosphorylation of ShcC in neuroblastoma cell lines.Oncogene · 2002Article
- Gene amplification in PNETs/medulloblastomas: mapping of a novel amplified gene within the MYCN amplicon.Journal of medical genetics · 2000Article
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Authors and funding
6 authors.
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Abstract
In order to elucidate the initiation of the N-myc gene amplification, we have analyzed the original structures of the N-myc amplicons among 38 human neuroblastomas. Nineteen DNAs isolated from the N-myc amplicons recognized a continuous stretch totally encompassing a 5.5 megabase region spanning the normal N-myc gene. The co-amplification profiles with these DNAs showed that two of them, which mapped into a 300 kb region flanking the N-myc gene, were commonly amplified in most specimens, while others were differentially amplified among various subsets. These profiles enabled us to divide the N-myc amplicons into several groups and outline their original domains as a continuous stretches, pointing to the existence of 'consensus sites' for the ends of the initial domains in the original region. In one cell line, the domain was found to be several times larger than that of the derivative amplicon; and the rearranged sites identified within the amplicons, which showed no site specificity, were consistent with those deduced from the domain structure. These results lead to a model in which N-myc gene amplification is initiated at some consensus sites by a preferential mechanism and followed by a random loss of the domain structures during subsequent stages.
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