Members of the myc family of nuclear protooncogenes play roles in cell prol
iferation, differentiation, and apoptosis, Moreover, inappropriate expressi
on of c-myc genes contributes to the development of many types of cancers,
including B cell lymphomas in humans. Although Myc proteins have been shown
to function as transcription factors, their immediate effects on the cell
have not been well defined. Here we have utilized a murine model of lymphom
agenesis (E mu-myc mice) to show that constitutive expression of a c-myc tr
ansgene under control of the Ig heavy-chain enhancer (E mu) results in an i
ncrease in cell size of normal pretransformed B lymphocytes at all stages o
f B cell development. Furthermore, we show that c-Myc-induced growth occurs
independently of cell cycle phase and correlates with an increase in prote
in synthesis. These results suggest that Myc may normally function by coord
inating expression of growth-related genes in response to mitogenic signals
. Deregulated c-myc expression may predispose to cancer by enhancing cell g
rowth to levels required for unrestrained cell division.