It is conceivable that agonists that goal more than a simple PPAR may be suitable for treating or preventing cancer. Bezafibrate is a pot PPAR agonist but some of its effects are mediated by PPAR 7. A number of studies claim that bezafibrate could prevent colon tumorigenesis in both rat 199 201 and human cancer models 202. Service for the idea that this really is mediated by PPAR originates from data showing that a specific PPAR agonist, methylclofenopate, also inhibits intestinal conjugating enzyme tumorigenesis 203. The molecular mechanisms underlying the effects of bezafibrate and methylclofenopate on colon tumorigenesis remain elusive. Bezafibrate can induce terminal differentiation, also trigger expansion arrest and apoptosis in Burkitts lymphoma cells and these effects are enhanced by co treatment with medroxyprogesterone acetate 204. These changes are mediated simply by a rise in the creation of 15 deoxy 12,14 prostaglandin J2, an all natural ligand of PPAR 204. More over, bezafibrate causes similar changes in growth, differentiation and apoptosis Lymph node in B cell chronic lymphocytic leukemia cells, and co treatment with MPA increases these effects via a similar system mediated by increased production of 15 dPGJ2 and apparent activation of PPAR 205. These observations suggest that the pan PPAR agonist bezafibrate might target myeloid cancers by way of a mechanism that increases PPAR exercise. As bezafibrate initiates PPAR, it remains a chance that PPAR is required for these effects but it’s not been established up to now. The new clinical trial demonstrating that bezafibrate is chemopreventive for colon cancer in humans 202, supports the hypothesis that development of pan PPAR agonists with relatively lower affinity for the PPARs could be appropriate for future chemopreventive ways. Indeed, reports suggest that high affinity combined PPAR agonists may cause cancers, including bladder cancer, liposarcomas and hemangiosarcomas, in long-term bioassays 206, indicating that topical Hedgehog inhibitor the usage of low affinity agents might be a more appropriate approach. Recognition of new double or pan PPAR agonists could possibly be possible since PPAR ligands can cause unique alterations in gene expression located in part on differential employment of co activators 191. This might result in characterization of substances that not show negative side effects related to PPAR ligands including professional carcinogenic effects in pre-clinical models 206, 207. In fact, pan and double PPAR agonists may also help offset unwanted effects observed with increased selective PPAR agonists. For example, weight gain or bone fractures observed in a reaction to administration of PPAR agonists 187 190, 206 might be offset by agonist activity for PPAR or PPARB/, which could increase lipid catabolism and stimulate osteoblast activity in bone 208.