The three most common genetic abnormalities occurring in malignant lym
phomas involve alterations resulting in the deregulated expression of
the c-myc and bcl-2 oncogenes and the inactivation of the p53 tumor su
ppressor gene. Relevant strains of genetically engineered mice, includ
ing bcl-2-Ig and E mu-myc transgenic mice and p53 knockout mice, have
been used to prospectively examine the regulation of apoptotic cell de
ath by these genes, individually and in combination, and their contrib
ution to in vivo lymphomagenesis. The potential importance of the ther
apeutic induction of apoptosis is discussed.