Pancreatic cancer is a type of malignant tumor that begins in the pancreas of the human body. The pancreas, an organ with a length of 6 inches long gland, lies among the stomach, the spleen, and small intestine. It has two main functions: releasing insulin or glucagon into the blood and producing digestive enzymes released into the small intestine. Common symptoms of pancreatic cancer include losing weight, unusual back pain, yellow skin, or dark urine. Till now, a wide variety of types of pancreatic cancers, such as pancreatic exocrine tumors and pancreatic neuroendocrine tumors (PNETs), have been identified and broadly studied. Among them, adenocarcinoma has become the most common pancreatic exocrine tumor. More than 90% of patients with pancreatic cancer have this cancer type. Moreover, many reports have shown that pancreatic cancer is aggressive with a 5-year survival rate of 10%, and is associated with a poor prognosis in the clinic. The main treatment modalities for pancreatic cancer are surgery, chemotherapy, as well as radiotherapy.
Many researchers have revealed that the pancreatic tumor microenvironment (TME) is associated with immune modulation and chemotherapy resistance. Normally, the development of pancreatic cancer is the inevitable result of the interaction among inflammatory cells, mediators, pancreatic stellate cells (PSCs), and the extracellular matrix (ECM). Pancreatic cancer cells can produce a range of growth factors, like TGFβ-1, FGF2, or PDGF to promote PSC proliferation and improve ECM accumulation. In this condition, PSCs and ECM will further contribute to the chemotherapy resistance by actively capturing target drugs in the cytoplasm and limiting T-cells accumulation near pancreatic cancer cells. ECM can also increase fluid pressure in the tumor tissue, cause vascular dysfunction, and increase hypoxia in the tumor. As a consequence, the desmoplastic reaction in pancreatic cancer has been treated as an attractive target for cancer immunotherapy and drug development.
Currently, immune checkpoint therapy has revolutionized cancer treatment and has been considered as a new strategy to improve patients’ outcomes in pancreatic cancer. In general, immune checkpoint therapy is designed to induce or promote the activation of enough immune responses to kill tumor cells. To do this, a number of immune checkpoint molecules, such as cytotoxic T lymphocyte antigen 4 (CTLA-4), programmed cell death 1 (PD-1), as well as programmed cell death ligand 1 (PD-L1), have been treated as switches that control the initiation of the immune response. Nowadays, a series of immune checkpoint inhibitors (ICIs) have been generated for creating a heterogeneous tumor that can return to immune surveillance to avoid suppressing or evading immune responses. Till now, two anti-CTLA-4-antibodies have been approved and used for the treatment of pancreatic cancer. Moreover, numerous data have suggested that CTLA-4-based immune checkpoint therapy plays an important role in improving tumor regression, immune response rate, as well as overall survival progression.
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