The MYC proto-oncogene has long been implicated in the control of norm
al cell growth and its deregulation is associated with the development
of neoplasia. The MYC protein has a well-established role as a compon
ent of signal-transduction pathways promoting both proliferation and a
poptosis. Because signalling pathways that drive cell death and cell p
roliferation are so tightly coupled, a synergy between genetic lesions
leading to suppression of cell death and those promoting cell prolife
ration is observed during carcinogenesis. We discuss such synergy with
respect to the cooperating oncogenes MYC, RAS and BCL2.