RET/PTC3 Oncogene's Inflammatory Properties and Hashimoto's Thyroiditis

 RET/PTC3 Oncogene's Inflammatory Properties and Hashimoto's Thyroiditis 


Various components of the ability to fight of infection in a host are collectively termed as immune system. Swelling, redness, pain and heat at the site of infection are hallmark of the active immune system and are defined as inflammation. Generally, more robust the inflammatory reaction is, the better it is for the host to clear the infection. Cancers are different as they are said to be actively causing the development of inflammation. The reason is that increased blood flow to the site of cancer brings more and more nutrients and other mediators which contradictorily help expand the cancer growth. We however believe that to be inaccurate, at best reflecting certain cancers only. We investigate papillary thyroid carcinoma (PTC) which is one of the most prevalent endocrine tumor known, accounting for about 85% of the thyroid malignancies. The incidence of thyroid cancers is on the rise too, in USA and in the world, especially among women. A specific type of PTC caused by a protein termed RP3 is associated with increased inflammation and leads to benign cancers. Not only that, this type of PTC has been found to be associated with Hashimoto’s Thyroiditis (HT), a chronic inflammatory disease condition of thyroid, very prevalent in US population and again 80-90% prevalent in women. We again believe that against the popular assumption, presence of HT as a chronic inflammatory condition enhances the immune response against PTC leading to its regression. We have developed various novel versions of RP3 protein which do and do not cause the development of inflammation. These unique proteins will be put in various cancers and will be tested for tumor growth. Our assumption is that absence of inflammation will lead to bigger and aggressive tumors. Further, in order to understand the relationship of PTC and HT, we are going to develop a mouse model where the RP3 protein will be turned on in thyroid along with induction of HT and the progression of PTC cancer assessed. We think that this will reduce the PTC growth or cause its regression. Our study is therefore a novel way to understand the role of inflammation in cancer development. The study will define the mechanism behind cancer growth or regression and pave way for new therapeutic strategies for treating cancers. 


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