Abstract
Gene amplification can be defined as an increase in the copy number of a restricted region of the genome. Originally discovered as a mechanism of drug resistance in cultured cell lines, it also occurs during tumourigenesis, more frequently in solid tumours than in hemopoietic malignancies (for review, Alitalo and Schwab, 1986; Schwab and Amler, 1990). Two types of chromosomal structures, the homogeneously staining regions (hsr) and double minute chromosomes (dmin), are currently regarded as hallmarks of gene amplification, hsr consist of chromosomal regions that fail to exhibit bands. They can vary in size and do not usually reside at the native locus of the amplified gene (Wahl, 1989). dmin are small paired acentric elements that replicate autonomously once per cell cycle and segregate randomly between daughter cells at mitosis (Wahl, 1989). Thus, unequal segregation of these structure provides means to increase the copy number of certain DNA sequences during a single cell cycle. Submicroscopic circular molecules, called episomes, were found in cells with amplified genes and might represent precursors of dmin (Carroll et al., 1988; Van Hoff et al., 1988; Wahl, 1989).
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© 1997 The Organizing Committee of the 12th International Chromosome Conference, Madrid, Spain
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Muleris, M., Almeida, A., Gerbault-Seureau, M., Dutrillaux, A.M., Malfoy, B., Dutrillaux, B. (1997). Characterization of amplified DNA sequences in human cancers. In: Henriques-Gil, N., Parker, J.S., Puertas, M.J. (eds) Chromosomes Today. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-1537-4_9
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DOI: https://doi.org/10.1007/978-94-009-1537-4_9
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