This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Corvi, R. Articles by Schwab, M. Search for Related Content PubMed PubMed Citation Articles by Corvi, R. Articles by Schwab, M.

Duplication of N-MYC at Its Resident Site 2p24 May Be a Mechanism of Activation Alternative to Amplification in Human Neuroblastoma Cells¹

Division of Cytogenetics-0130, Deutsches Krebsforschungszentrum, German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany

Amplification of the human N-MYC proto-oncogene is frequently seen either in extrachromosomal double minutes or in homogeneously staining regions of aggressively growing neuroblastomas. N-MYC maps to chromosome 2 band p23–24, but homogeneously staining regions have never been observed at this band, suggesting transposition of N-MYC during amplification. Previous studies had suggested that in cells with amplified N-MYC the chromosomes 2 appear to be unaltered and to carry one apparently normal copy of N-MYC each. In contrast, the contribution of N-MYC to tumors which lack amplification has been unclear. We here show, by fluorescence in situ hybridization, that N-MYC is occasionally duplicated at its resident site in neuroblastoma cell lines previously thought to have a single copy gene. Additionally, we detected duplication in a neuroblastoma cell line carrying amplification. Our results raise the possibility that duplication may, in some neuroblastomas, either be a prelude to amplification or an alternative pathway by which N-MYC becomes activated.

¹ This work was supported by grants from the Deutsche Forschungsgemeinschaft, Dr. Mildred Scheel Stiftung, Heidelberg-Mannheim Comprehensive Cancer Center, and the Israel-Deutsches Krebsforschungszentrum Cooperation Program and is integrated into the frame of the European Communities Concerted Action "Molecular Cytogenetics of Solid Tumors" (BMHI-CT92-0156).

² To whom requests for reprints should be addressed.

Received 6/ 5/95. Accepted 6/23/95.

This article has been cited by other articles:

				D. Williamson, Y.-J. Lu, T. Gordon, R. Sciot, A. Kelsey, C. Fisher, C. Poremba, J. Anderson, K. Pritchard-Jones, and J. Shipley Relationship Between MYCN Copy Number and Expression in Rhabdomyosarcomas and Correlation With Adverse Prognosis in the Alveolar Subtype J. Clin. Oncol., February 1, 2005; 23(4): 880 - 888. [Abstract] [Full Text] [PDF]

				B. Poppe, J. Vandesompele, C. Schoch, C. Lindvall, K. Mrozek, C. D. Bloomfield, H. B. Beverloo, L. Michaux, N. Dastugue, C. Herens, et al. Expression analyses identify MLL as a prominent target of 11q23 amplification and support an etiologic role for MLL gain of function in myeloid malignancies Blood, January 1, 2004; 103(1): 229 - 235. [Abstract] [Full Text] [PDF]

				N Bown Neuroblastoma tumour genetics: clinical and biological aspects J. Clin. Pathol., December 1, 2001; 54(12): 897 - 910. [Abstract] [Full Text] [PDF]