ABSTRACT
I. INTRODUCTION It is now well established that defects in the normal mechanisms that control programmed cell death (PCD) occur commonly in cancers. Cell numbers in the body are governed not only by cell division, which determines the rate of cell production, but also by cell death, which sets the rate of cell loss. In the course of a typical day, an average adult produces, and in parallel eradicates, —50 to 70 billion cells, representing approximately 1 million cells per second. Normally, these two processes of cell division and cell death are tightly coupled so that no net increase in cell numbers occurs or so that such increases represent only temporary responses to environmental stimuli. However, alterations in the expression or function of genes that control PCD can upset this delicate balance, contributing to the expansion of neoplastic cells (reviewed in Ref. 1).
