Targeting PI3Kδ suppresses pancreatic cancer by dual disruption of fibrosis and immune evasion - PubMed
4 hours ago
- #PI3Kδ inhibition
- #pancreatic cancer fibrosis
- #tumor microenvironment reprogramming
- PI3Kδ is identified as a previously unrecognized driver of fibrosis in pancreatic ductal adenocarcinoma (PDAC).
- Inhibiting PI3Kδ reduces collagen deposition and enhances infiltration of activated CD8+ T cells, reprogramming the tumor microenvironment.
- PI3Kδ regulates lysophosphatidic acid (LPA) biosynthesis by controlling phosphatidylcholine-derived precursors in cancer cells and stromal fibroblasts.
- Co-inhibition of autotaxin and PI3Kδ amplifies stromal disruption and improves chemo-immunotherapy efficacy in preclinical PDAC models.
- PI3Kδ emerges as a central therapeutic target in PDAC, offering a dual-action strategy against stromal fibrosis and immune suppression.