Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive and highly lethal malignant tumor. Due to the difficulty in early diagnosis and limited treatment options, the 5-year survival rate is less than 10%. Traditional treatments such as surgery, chemotherapy, and radiotherapy have limited effects on PDAC, which is mainly attributed to its unique tumor microenvironment (TME), common gene mutations (such as KRAS, and TP53), and immunosuppressive properties. In recent years, with the advancement of molecular biology and genomics technologies, the molecular mechanisms of PDAC have been studied more deeply, revealing the gene mutations and regulatory networks associated with its pathogenesis. In particular, KRAS mutations have become an important research direction for targeted therapy. However, the effect of immunotherapy in PDAC is limited by the immune escape characteristics of TME. This article systematically summarizes the key gene mutations in PDAC and their regulatory mechanisms, including epigenetic regulation, microRNA, histone modification and other influencing factors. CRISPR-Cas9 shows great potential in correcting gene mutations and reshaping TME. In addition, combining immunotherapy with targeted drug delivery (such as nanotechnology) can improve the precision of treatment and reduce side effects. These advances provide a comprehensive reference for future personalized and effective treatment options for PDAC
Read full abstract