Epithelial ovarian Wortmannin cancer continues to be the leading cause of death among gynecological malignancies. The lack of effective methods for prevention, early detection and treatment recurrent ovarian tumors creates a pressing need to understand its pathogenesis and identify molecular targets for therapy. Cancer is a disease involving multistep dynamic changes in the genome. However, the oncogenic events and their cooperation that promote malignant transformation in ovarian carcinoma remain largely unknown. Phosphatidylinositol-39 kinase is an intracellular signal transducer with lipid substrate specificity implicated in a wide range of cancer-associated signaling pathways including tumor cell metabolism, survival and proliferation. It is recruited and activated by multiple receptor tyrosine kinases and generates second messengers via phosphorylation of membrane inositol lipids at the D3 position. PI-3 kinase was first recognized as a putative oncogene because of its ability to bindpolyoma middle T antigen. This expedient approach means that many genes encoding proteins with uncharacterized functions may be disregarded as potential therapeutic or diseasepreventive targets. These assumptions have several consequences. Mitochondrial functional measures in the soleus muscle were not affected by either MPred or FR treatment but the plantaris muscle did show limited changes. FR resulted in a decrease in COX activity in the plantaris muscle but this difference appears to have had minimal impact on ATP generating capacity with either of the substrate combinations used. This suggests that there was either ample reserve capacity of the COX enzyme or other compensatory regulation occurred. In comparison, a reduction in ATP production rate with pyruvate + malate in plantaris muscle was the only mitochondrial function change resulting from MPred treatment. Since ATP production rate with the fatty acid substrate palmitoyl-carnitine was maintained in the MPred plantaris it is likely that an early step specific to pyruvate metabolism, such as transport into the mitochondria, was affected by MPred treatment and responsible for the differential results. This interpretation would also suggest that most of the remaining common pathways leading to ATP synthesis remain unchanged during MPred treatment. It is presently unclear why pyruvate metabolism would be selectively affected by glucocorticoid action in the mixed oxidative-glycolytic plantaris but not in soleus., which has higher oxidative capacity. This finding is, however, consistent with the pattern of muscle-specific effects of glucocorticoid action, which has been shown, for example to induce greater atrophy in white/glycolytic muscles compared to the predominantly oxidative soleus. First, the diversity in many chemical libraries is not utilized. Second, focusing on the pathogen enzymes most likely to be essential to all life increases the likelihood that a compound will also have activity against the host.