Figure 2.

Schematic illustration of the molecular mechanisms of relevant immunotherapies for pancreatic cancer. (A) After binding to PD-1 or PD-L1, ICIs block the binding of tumor cells to T cells, thereby maintaining the tumor-killing activity of T cells and acting on pancreatic cancer. (B) Tumor antigens are delivered into patients in a variety of forms, such as autologous tumor cells, tumor-associated proteins or peptides, and dendritic cells as delivery vectors. After the vaccine enters the body, tumor antigens are phagocytosed by dendritic cells, which are then processed and presented to T cells to activate antigen-specific cytotoxic T cells, thereby killing pancreatic cancer. (C) The patient’s own immune cells were collected, genetically modified, and cultured in vitro, and then returned to the patient’s body to act on pancreatic cancer. (D) Oncolytic viruses replicate in tumor cells and can specifically infect and lyse tumor cells. In addition, the expression of viral antigens induces an antiviral immune response that can help destroy pancreatic cancer cells. 2E, Extracellular matrix-modified pancreatic cancer cells. Normally, pancreatic epithelial cells are surrounded by extracellular matrix (ECM), fibroblasts, and blood vessels to provide structural and nutritional support. However, during tumorigenesis, molecules such as tumor growth factors (such as TGF-β) or Hedgehog (SHH) activate intracellular signaling, leading cancer-associated fibroblasts to enhance ECM deposition. Forming a tumor microenvironment conducive to the growth and spread of pancreatic cancer. However, by blocking this pathway, it is possible to establish a more beneficial and healthy tumor microenvironment.