Apoptosis or programmed cell death, is a mechanism of cellular demise which is believed to play a role in many physiological processes, and which when defective, can contribute to the pathogenesis of cancer. Apoptosis is stimulated in cells by the p53 tumor suppresser, Bax and El A proteins and inhibited by overexpression of Bcl-2 and adenovirus E1B 19 kDa oncoproteins. A role for altered apoptosis in cancer comes from recent reports which have documented that inactivation of p53 (which promotes apoptosis) and/or overexpression of bcl-2 (which inhibits apoptosis) occurs in numerous cancers. Recent work from our laboratory has shown that inactivation of p53 (either by physical complex formation between p53 and Human Papillomavirus (HPV) type 16- or 18- E6 protein or by mutation of p53), is associated with increased expression of bcl-2 in cervical carcinoma cells. The combination of inactive p53 and increased expression of bcl-2 may lead to inhibition of apoptosis and thereby contribute to the development or progression of cervical cancer.