Abstract
We and others have speculated that elevated expression of c-myc plays an important role in the establishment of the transformed follicle, a preneoplastic lesion essential for the development of the ALV-induced bursal-dependent lymphoma (Baba and Humphries 1985, Clurman and Hayward 1989, Neiman et al 1985). The discovery of base substitutions and missense mutations in some tumor c- myc alleles raises the possibility that qualitative as well as quantitative alterations within the chicken c-myc proto-oncogene may play a role in the genesis and/or progression of bursal lymphomas (Westaway et al 1984). In order to assess the contribution that deregulated expression of an unaltered c-myc allele makes during ALV lymphomagenesis (Hayward et al 1981) , we have constructed a recombinant avian retrovirus, SNVc-myc, that encodes the second and third exons of normal chicken c-myc and expresses only the smaller of the two c-myc proto-oncogene products, pp62c-myc and pp59c-myc (Hann et al 1988). Ultimately, this virus will enable the effects of specific mutations within the context of wild-type pp59c-myc to be assessed.
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Humphries, E.H., Filardo, E.J. (1990). The Transforming Activity of PP59C-MYCis Weaker Than That of v-myc . In: Potter, M., Melchers, F. (eds) Mechanisms in B-Cell Neoplasia 1990. Current Topics in Microbiology and Immunology, vol 166. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75889-8_32
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DOI: https://doi.org/10.1007/978-3-642-75889-8_32
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