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Use of small molecule activity in upregulation of Class I MHC and change in tumour cytokine profile in metastatic murine epithelial carcinoma. Dada, Sarah


Cancer is a devastating disease that is responsible for the death of a quarter of Canadians. Cancer is the result of cells that gain genetic mutations or epigenetic changes that incur abnormal, uncontrolled proliferation. Oftentimes, such mutations give rise to the metastatic form of cancer, which is capable of moving throughout the body to distant sites. Adaptive immunity, including Cytolytic T cells (CTLs), are intended to kill tumours based on tumour specific antigen presented on Major Histocompatability Complex (MHC) Class I. However, metastatic tumours are capable of escaping such death through the downregulation of Antigen presentation machinery (APM), including MHC Class I. Here, we investigate the role of the small molecule Cannabigerol in upregulating class I MHC and altering cytokine signalling in metastatic tumours, and the consequent CTL tumour killing ex-vivo. Additionally, we determined the impact of Cannabigerol on immune infiltrates and tumour burden in vivo. Small molecules which enhance the efficacy of the CTL killing through upregulation of tumour-antigen bound MHC class I killing would be beneficial for therapeutic use through increased tumour killing, as well as reduced tumour metastasis, and would result in a prolonged host survival.

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