Furthermore, functional studies have revealed a role for the stress-inducible splice forms of MDM2 in cancer, underscoring the importance of this splicing event and the necessity to gain an understanding of the mechanisms involved in the damage-responsive splicing of MDM2. Using a novel damage-inducible in vitro splicing system we have previously shown that intron 11 of MDM2 contains conserved positive elements that are primarily needed for the efficient full-length splicing of MDM2 (37,38). This evidence concerns the gene MDM2 and cancer.