Amplified DNA with limited homology to myc cellular oncogene is shared by human neuroblastoma cell lines and a neuroblastoma tumour

Manfred Schwab, Kari Alitalo, Karl Heinz Klempnauer, Harold E. Varmus, J. Michael Bishop, Fred Gilbert, Garrett Brodeur, Milton Goldstein, Jeffrey Trent

Research output: Contribution to journalArticlepeer-review

Abstract

Amplified cellular genes in mammalian cells frequently manifest themselves as double minute chromosomes (DMs) and homogeneously staining regions of chromosomes (HSRs)1,2. With few exceptions both karyotypic abnormalities appear to be confined to tumour cells3,4. All vertebrates possess a set of cellular genes homologous to the transforming genes of RNA tumour viruses, and there is circumstantial evidence that these cellular oncogenes are involved in tumorigenesis5. We have recently shown that DMs and HSRs in cells of the mouse adrenocortical tumour Yl6 and an HSR in the human colon carcinoma COLO3207 contain amplified copies of the cellular oncogenes c-Ki-ras and c-myc, respectively. Both DMs and HSRs are found with remarkable frequency in cells of human neuroblastomas 4,8-15. We show here that a DNA domain detectable by partial homology to the myc oncogene is amplified up to 140-fold in cell lines derived from different human neuroblastomas and in a neuroblastoma tumour, but not in other tumour cells showing cytological evidence for gene amplification. By in situ hybridization we found that HSRs are the chromosomal sites of the amplified DNA. The frequency with which this amplification appears in cells from neuroblastomas and its apparent specificity raise the possibility that one or more of the genes contained within the amplified domain contribute to tumorigenesis.

Original languageEnglish (US)
Pages (from-to)245-248
Number of pages4
JournalNature
Volume305
Issue number5931
DOIs
StatePublished - Dec 1 1983

ASJC Scopus subject areas

  • General

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