The myc family of nuclear proto-oncogenes.

Abstract

Several members of the myc family of proto-oncogenes have been described, and some (c-, N-, and L-myc) have been characterized in considerable detail. They are united by a common gene structure and nucleotide homologies that were used to identify some of them initially. Their protein products also have scattered regions of amino acid identity or homology. Although the cellular activities of the various proteins are unknown, some members may play a role in regulating cell growth and differentiation. They share the ability to cooperate with an activated ras gene and cotransform embryonic rodent cells. In naturally occurring tumors, the members of the myc family of oncogenes appear to be activated by genetic changes (proviral insertion, chromosomal translocation, and gene amplification) that augment or otherwise disrupt normally regulated expression. The members of this family of genes differ markedly in their tissue specificity and developmental regulation of expression. This may account in part for the frequent appearance of activated c-myc genes in a wide variety of neoplasms and the limited appearance of activated N- and L-myc genes in tumors of embryonic or neural origin. The c-myc gene may be activated in tumors by a variety of mechanisms, whereas N- and L-myc appear to be activated only by gene amplification. Regulation of expression of the different myc genes also appears to occur by different mechanisms. Finally, the products of the different genes differ in may regions of the protein, and this divergence probably reflects their specific and individual functions.