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Glossary A2aR Adenosine A2a receptor ACSS Acetyl-CoA synthetase ACT Adoptive cell transfer ADP Adenosine diphosphate AhR Aryl hydrocarbon receptor AKT Protein kinase B ALDH1A3 Aldehyde dehydrogenase 1 family member A3 ALPK1 ADP-heptose activates alpha kinase 1 AMP Adenosine monophosphate APC Antigen-presenting cell Arg1 Arginase 1 ATB Antibiotic ATP Adenosine triphosphate CA Cholic acid CARs Synthetic receptors CAR-T Chimeric antigen receptor T cell CCL C-C motif chemokine ligand CCR C-C chemokine receptor CD Cluster of differentiation CDCA Chenodeoxycholic acid c-di-AMP Cyclic di-adenosine monophosphate cGAS Cyclic guanosine monophosphate AMP synthase CHIP Hsc70-interacting protein CHPS Capsular heteropolysaccharide COX-2 Cyclooxygenase-2 CPS Capsular polysaccharides CRC Colorectal cancer CREB cAMP response element-binding protein CRISPR Clustered regularly interspaced short palindromic repeats CTL Cytotoxic T lymphocyte CTLA-4 Cytotoxic T lymphocyte antigen-4 CXCL C-X-C motif chemokine ligand CXCR C-X-C motif chemokine receptor CYP2E1 Cytochrome P450 2E1 DAT Desaminotyrosine DC Dendritic cell DCA Deoxycholic acid DHA Docosahexaenoic acid DNA Deoxyribonucleic acid EcN E

Unlike genetic mutations, the reversibility and plasticity of epigenetic changes provide a unique molecular foundation for the rapid adaptation of tumor cells to therapeutic stress, while also creating critical therapeutic windows [4]

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