No abstract

These results indicate that biochemical apoptotic processes are initiated concomitant with etoposide-induced cell cycle arrest and are interrupted by Bcl-2 overexpression. However, the aberrant mitotic events induced by etoposide are sufficient to kill these cells even in the absence of apoptosis.

These results indicate that Bcl-2 enhances clonogenic survival of human epithelial tumor cells in an agent-specific fashion, which may be determined by the initial cytotoxic lesion induced by a particular drug.

These results indicate that staurosporine potentiates apoptosis through events which occur downstream of DNA damage, and implicate unscheduled activation of cyclin A-dependent kinase during inhibition of DNA synthesis as a possible cause.