CYP1B1 has been suggested to be exploited for the development of targeted anticancer therapies. Our study indicates that caution should be observed as this therapy may not be applicable universally to all cancers. The fact that CYP1B1 expression is higher in the Ascomycin normal tissues might aid to the development of chemopreventive drugs for oral cancer. In the light of the knowledge that CYP1B1 plays a role in carcinogenesis, drugs that inhibit CYP1B1 might be useful prophylactic agents. During a clinical examination of the oral cavity of a patient, it is often possible to distinguish normal tissue, premalignant lesion and malignant tumor. An Indian survey showed that 80% of the malignancies of the oral cavity arise from premalignant lesions, such as leukoplakia, erythroplakia, and oral submucous fibrosis. The presence of such premalignant lesions would enable prophylactic treatments which otherwise are not possible in most of other cancers. Apart from drugs that inhibit CYP1B1, prodrugs that are activated by CYP1B1 might also be used as prophylactic drugs since they would result in depletion of the cells expressing it, enabling reduction in the risk to develop a malignant lesion. In summary, the CYP1B1 downregulation in oral tumor tissues as compared to their matched normal tissues contradicts many studies which state that CYP1B1 is overexpressed in tumors. This downregulation is consistent over a range of tumor stages and independent of the gender of the patient, site of the lesion and etiology of the carcinogenesis. On the basis of our observations, we suggest that a level of caution should be observed for treatments based on CYP1B1 overexpression in tumors. Lipoprotein-associated phospholipase A2, also known as plasma platelet activating factor acetylhydrolase, is unique among members of the phospholipase A2 superfamily due to its origin, its association with circulating lipoproteins, and its substrate preference for polar phospholipids, including those generated during the oxidation of low-density lipoprotein. Lp-PLA2 is secreted by monocytes, macrophages, T lymphocytes, and mast cells, and catalyzes the hydrolysis of oxidized LDL, which produces the proinflammatory mediators lysophosphatidylcholine and oxidized fatty acid. There has been a growing interest in Lp-PLA2 because of its key role in lipid metabolism and in initiating inflammation. Epidemiological and clinical studies have indicated that Lp-PLA2 is a marker for cardiovascular risk, with higher plasma Lp-PLA2 mass or activity correlating with a higher risk for cardiovascular events independent of systemic inflammation and other conventional risk factors. Many studies found correlations Terbuthylazine between Lp-PLA2 and triglycerides, LDL-cholesterol, high-density lipoprotein cholesterol, body mass index, age, sex, use of postmenopausal hormones, and smoking. Lp-PLA2 has been associated with an increased incidence of ischemic stroke among nonusers of hormone therapy in postmenopausal women independent of traditional cardiovascular risk factors.