We made use of HDONAs to identify 'early' target genes downstream of COX-2. Earlier studies in other cell systems have demonstrated the ability of COX-2 to regulate gene expression, such as the expression of MDR1 (Patel et al, 2002) . Specific studies of differential gene expression in colon cancer cells (using suppressive subtractive hybridisation and differential screening) have previously demonstrated altered expression of genes involved in cell proliferation and viability (Zhang and DuBois, 2001) , however high NSAID doses and long time points make a direct comparison with our expression studies difficult. We chose to look at early time points following treatment with the highly selective COX-2 inhibitor SC236 to identify crucial early responses. COX-2 independent effects of SC236 have been described (He et al, 2006) . However, we chose to use SC236 at a dose which was associated with only modest changes in rates of apoptosis but where we observed rescue by co-incubation with PGE 2 , in the belief that study of a more subtle but specific phenotypic change would yield more significant findings.