Cell Transformation by Andrew Sivak, Alice S. Tu (auth.), J. Celis, A. Graessmann

By Andrew Sivak, Alice S. Tu (auth.), J. Celis, A. Graessmann (eds.)

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Neoplastic Development, Vol. I & II", Academic Press, New York. M. (1982). Cellular transforming genes, Science, 218, 80l. H. (1983). , Nature, 304, 219. -H. & WESTERMARK, B. (1984). Growth factors: Mechanism of action and relation to oncogenes, Cell, lL, 9. F. E. (1984). A relationship between the yeast cell cycle genes CDC4 and CDC36 and the ets sequence of oncogenic virus E26, Nature, 309, 556. S. (1970). Rous sarcoma virus: A function required for the maintenance of the transformed state, Nature, 221 , 1021.

The fact that proto-one genes share common domains with viral genes remains a persuasive argument that proto-one genes may, under certain conditions, be changed into cancer genes. The evidence that most normal proto-one genes are expressed in normal celle suggests that cell-specific domains of proto-one genes may suppress poten- PROTO-one GENES AND CANCER GENES 47 tial oncogenic function. Thus, mutation or removal of suppressors could activate a proto-one gene, as has been predicted for Burkitt's lymphoma.

6 kb), termed mya is deri ved from the protomya gene (22). The gene is defined by a 110,000 dalton 6gag-mya protein, termed pllO (21,24). The proto-mya gene of the chicken has at least 3 exons. The boundaries of the first exon are as yet undefined (25-27). The mya region of MC29 derives four codons possibly from the 3 1 end of the first exon and includes the second and third proto-mya exons (Fig. 1). Three other avian carcinoma viruses MH2, OKlO and CMII also have ona genes with mya sequences (24).

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