Novel pharmacologic approach to enhance the epigenetic and immune priming effect of decitabine in patients with advanced non-small cell lung cancer
نویسندگان
چکیده
Background DNA methyl transferase 1 (DNMT-1) is a key epigenetic enzyme in cancer cells which inactivates proliferation terminating genes and downregulates the expression of cancer related proteins and neoantigens by hypermethylation. Prolonged exposure of tumor cells to DAC is required for sufficient demethylation. Clinical use of decitabine to target DNMT-1 is restricted by its short in vivo half-life (about 10 minutes) due to rapid inactivation by the enzyme cytidine deaminase (CDA) present in tissues. Tetrahydrouridne(THU), an oral inhibitor of CDA can overcome the pharmacokinetic (PK) limitation.
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