Inhibitory effect of mosinone-A on immunohistochemical expression of inflammatory and angiogenic markers in 7, 12-dimethylbenz (a) anthracene induced hamster buccal pouch carcinogenesis

During this process, a disturbance in cell proliferation, dysregulation of cellular differentiation, insufficient apoptosis and genomic instability [1-2] The golden Syrian hamster buccal pouch is an excellent target organ for studying oral carcinogenesis which, under the induction of 7, 12-dimethylbenz [a] anthracene consistently produces squamous cell carcinoma. DMBA, a potent organ and site specific carcinogen is commonly used to induce buccal pouch carcinogenesis in hamsters, Dihydrodiol epoxide, the ultimate carcinogen DMBA, mediate the carcinogenic process by inducing chronic inflammation through the over production of reactive oxygen species (ROS) [3-4]. [...]the mechanism by which Mosinone-A exerts its cytotoxic effect on oral cancer cells are not well understood. [...]we undertook this study to investigate the apoptotic and angiogenic associated proteins during the DMBA induced hamster buccal pouch carcinogenesis. In the current study, we have examined the molecular evidence to prove chemopreventive efficacy of the Mosinone-A in DMBA induced buccal pouch carcinogenesis A number of chemotherapeutic drugs are resistant to cancer treatment, passibly