Abstract
It is generally believed that, whatever the cause, tumorigenesis usually involves specific genetic alterations in an individual cell which then proliferates to form the tumour mass. Since such alterations may be multiple, and each one as inconspicuous as substituting a single nucleotide base within a genome composed of over 109 base pairs, the task of detecting, let alone circumventing, these events at the molecular level is a daunting one. Considerable research efforts have therefore focused not on the cancer cell itself, but on particular viruses which have been shown to induce these genetic alterations in cells and to cause tumours in animals. Such infectious agents offer two obvious opportunities to the cancer researcher. The first is that if viral infections do indeed cause or predispose individuals to the risk of cancer, then prophylactic measures might prevent these effects. The second is that animal-virus model systems provide considerable scope for experimental manipulation. Most of the viruses discussed in this chapter have genomes about a millionfold less complex than those of the cells they infect. Not only are they simpler to analyse, but the ease with which purified virus particles can be isolated often facilitates the preparation of specific nucleic acid and immunological reagents.
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Wyke, J. & Weiss, R. (eds) (1984) Viruses in human and animal cancers: the current position. Cancer Surveys, 3, No. 1, Oxford University Press, Oxford
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© 1985 Peter B. Farmer and John M. Walker
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Peters, G. (1985). Viruses and Cancer. In: Farmer, P.B., Walker, J.M. (eds) The Molecular Basis of Cancer. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7313-1_4
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DOI: https://doi.org/10.1007/978-1-4684-7313-1_4
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