Pancreatic ductal adenocarcinoma (PDAC) is one of the most common lethal-cancer related diseases, primarily characterised with rapid tumor progression, early metastasis, high recurrence and high resistance to therapeutic approaches and treatment. The disease has been found to be highly representative in the advanced stages and therefore has prevented early detection and treatment opportunities. Common mutations found in PDAC include KRAS, TP53, CDKN2A AND SMAD4 but there are not any novel targeted therapies available. Studies have demonstrated the immune microenvironment plays a significant role in tumor progression and the interactions between cancer and immune cells with the microenvironment can lead to immune evasion mechanisms.
Studies have demonstrated that PDAC has means to be able to enhance immune evasion by the recruitment of regulatory immune cells, immunosuppressive chemokines secretions including stromal cell-derived factor 1 as well as different cytokines such as interleukin (IL)-1, IL-6, IL-10, TGFß and cell-surface proteins such as programmed death-ligand 1 (PD-L1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA4). There has been evidence in which PD-L1 is found to be overexpressed in PDAC patients. In addition, cancer-associated fibroblast are known to modulate immune cells and tumor progression.
This Research Topic aims to highlight the impact and importance of studies focusing on the immune microenvironment in PDAC and how it may contribute to novel therapies and treatment. We welcome Original Research Articles, Review Articles and Systematic Reviews.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most common lethal-cancer related diseases, primarily characterised with rapid tumor progression, early metastasis, high recurrence and high resistance to therapeutic approaches and treatment. The disease has been found to be highly representative in the advanced stages and therefore has prevented early detection and treatment opportunities. Common mutations found in PDAC include KRAS, TP53, CDKN2A AND SMAD4 but there are not any novel targeted therapies available. Studies have demonstrated the immune microenvironment plays a significant role in tumor progression and the interactions between cancer and immune cells with the microenvironment can lead to immune evasion mechanisms.
Studies have demonstrated that PDAC has means to be able to enhance immune evasion by the recruitment of regulatory immune cells, immunosuppressive chemokines secretions including stromal cell-derived factor 1 as well as different cytokines such as interleukin (IL)-1, IL-6, IL-10, TGFß and cell-surface proteins such as programmed death-ligand 1 (PD-L1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA4). There has been evidence in which PD-L1 is found to be overexpressed in PDAC patients. In addition, cancer-associated fibroblast are known to modulate immune cells and tumor progression.
This Research Topic aims to highlight the impact and importance of studies focusing on the immune microenvironment in PDAC and how it may contribute to novel therapies and treatment. We welcome Original Research Articles, Review Articles and Systematic Reviews.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.