v-myc is the viral homolog of c-myc transduced by several acute transformin
g retroviruses, many of which encode this gene as a Gag-Myc fusion protein,
The v-myc oncogene can transform several lineages of mammalian and avian c
ells either alone or in cooperation with other oncogenes, While the Gag por
tion of the Gag-Myc fusion protein and the nuclear localization signal each
appear to be dispensable for transformation, the N- and C-termini of the M
yc sequence have been found to be essential for transformation. All v-myc g
enes contain point mutations which seem to confer a greater potency to v-my
c in the process of transformation, proliferation, and apoptosis, In v-myc-
transformed myelomonocytic cells, secondary events occur, such as the expre
ssion of colony stimulating factor-1 (CSF-1) which play a critical role in
immortalization and subsequent tumor progression, Inhibition of the autocri
ne loop of CSF-I was found to induce apoptosis in the immortalized cells, W
hile overexpression of v-Myc blocks terminal differentiation of hematopoiet
ic cells, this is not sufficient to block the differentiation of certain ne
ural and skeletal muscle cells. Recent developments on the effects of v-myc
on cell growth, transformation, differentiation and apoptosis are discusse
d in this review.