Cell Hybridisation

  • J. M. Boyle
Part of the Handbook of Experimental Pharmacology book series (HEP, volume 72)

Abstract

It has been suggested that cell fusion could be an early event in the neoplastic process (Miller 1974). In this chapter we examine the evidence for the occurrence of cell fusion in vivo, and explore the possibility that drug resistance can derive from mutations that accumulate in the enlarged gene pool of the hybrid cell. Since there is little direct information concerning the expression of drug resistance in hybrid cells in vivo, we shall discuss the implications for chemotherapy of the lessons learnt from the study of drug resistance in hybrid cells in vitro. The fusion of two cells is but one means of increasing cell ploidy (review, Brodsky and Uryvaeva 1977), so much of this discussion may be applicable to polyploid cells in general. Emphasis is placed on resistance to antitumour agents which exclusively involve nuclear genes. Mutants deficient in mitochondrial protein synthesis and respiratory functions coded by both nuclear and mitochondrial DNA are providing interesting insights into nuclear/cytoplasmic relationships, but to date none of these have involved antitumour drug resistance and will not be discussed. The interested reader can find information on this topic reviewed by Wright et al. (1980) and background reading on somatic-cell genetics in Harris (1970), Ephrussi (1972), Davidson and De La Cruz (1974), Ringertz and Savage (1976) and Shows and Sakaguchi (1980).

Keywords

Sarcoma Dexamethasone Cytosine Colchicine Corticosterone 

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© Springer-Verlag Berlin Heidelberg 1984

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  • J. M. Boyle

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