In multicellular organisms, cell proliferation and death must be regulated
to maintain tissue homeostasis, Many observations suggest that this regulat
ion may be achieved, in part, by coupling the process of cell cycle progres
sion and programmed cell death by using and controlling a shared set of fac
tors. An argument in favor of a link between the cell cycle and apoptosis a
rises from the accumulated evidence that manipulation of the cell cycle may
either prevent or induce an apoptotic response. This linkage has been reco
gnized for tumor suppressor genes such as p53 and RS,the dominant oncogene,
c-Myc, and several cyclin-dependent kinases (Cdks) and their regulators. T
hese proteins that function in proliferative pathways may also act to sensi
tize cells to apoptosis. Indeed, unregulated cell proliferation can result
in pathologic conditions including neoplasias if it is not countered by the
appropriate cell death. Translating the knowledge gained by studying the c
onnection between cell death and cell proliferation may aid in identifying
novel therapies to circumvent disease progression or improve clinical outco
me.