Epigenetic-immune landscape of pancreatic ductal adenocarcinoma: From tumor biology to multimodal treatment in the surgical setting

Figure 1 Epigenetic reprogramming and immune microenvironment crosstalk in pancreatic ductal adenocarcinoma. Major epigenetic alterations, including DNA methylation, histone modifications, non-coding RNAs, and chromatin remodeling, interact with immune components in the pancreatic tumor microenvironment. These epigenetic events may regulate chemokine expression, antigen presentation, immune checkpoint activity, macrophage polarization, myeloid-derived suppressor cell recruitment, Treg accumulation, and cytotoxic T-cell dysfunction. PD-L1: Programmed death-ligand 1; CTLA-4: Cytotoxic T-lymphocyte-associated protein 4; CXCL9/CXCL10: C-X-C motif chemokine ligand 9/10; CCL2: C-C motif chemokine ligand 2; IL-10: Interleukin-10; TAM: Tumor-associated macrophage; MDSC: Myeloid-derived suppressor cell; Treg: Regulatory T cell; NK: Natural killer.