Abstract
Background: Gastric cancer (GC) remains the third leading cause of cancer–related death worldwide. While inflammation is a well–established driver of gastric tumorigenesis, only a small subset of GC patients responds to immunotherapy. The understanding of the tumour microenvironment, which suppresses anti–tumour immune responses, is a field of great interest. One proposed mechanism of immune escape is silencing tumour–antigen expression by DNA methylation, and thereby avoiding immune recognition. DNA methyltransferases (DNMTs) are the enzymes responsible for DNA methylation and hence, for the epigenetic silencing of gene expression of tumour–antigens and other immune–related molecules. DNMTs are often overexpressed in solid tumours. Epigenetic drugs inhibiting these DNMTs have shown anti–tumour effects in combination with immune checkpoint inhibitors by re-activating the expression of tumour antigens, amongst others. Here we are studying the role of DNMTs in GC mouse models and the possibility of combining DNMT inhibitors with immunotherapy for the treatment of GC.
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