“…Growth arrest in wild-type P53 is dependent on transcriptional activation of P21, which ultimately inhibits cyclin complexes and arrests cells in the G1 to S phase transition (Clarke et al, 1993;Chang et al, 1997;Bouvard et al, 2000). Through the activation of BAX, a proapoptotic gene, and downregulation of BCL-2, an anti-apoptotic gene, P53 plays an essential role in apoptosis (Lane, 1992;Clarke et al, 1993;elDeiry et al, 1994;Silvestrini et al, 1994;Gallo et al, 1999;Sionov and Haupt, 1999;Dijkema et al, 2000;Jackel et al, 2000). It follows that cellular response to radiation may be dependent on a normally functioning P53 gene.…”