Although cancer-related medical research has been developed for many years, pancreatic cancer is a highly lethal disease that is extremely difficult to detect and treat. Complete surgical resection is still the only chance of long-term disease-free survival. Unfortunately, 80% of patients will develop locally advanced or metastatic disease, which makes it impossible to perform resection after diagnosis. The majority of patients undergoing surgical treatment have only a slight improvement in survival rate, and almost all patients will relapse. Therefore, the treatment of pancreatic cancer has recently focused on multimodal treatment through surgery, chemotherapy and radiation. The development of pancreatic cancer-targeted drugs and chemotherapy only has a moderate impact on clinical outcomes, and has not changed its 5-year survival rate. Fortunately, the genetic and molecular mechanisms of pancreatic cancer are being quickly discovered and provide opportunities for new targeted therapies. Oncolytic virus (OV) therapy is currently one of the most promising targeted drugs for the treatment of pancreatic cancer.
Fig.1 Biologic features of pancreatic cancer. (Ryan, 2014)
Oncogenic transformation in the pancreas is currently considered to be a multistage process involving the accumulation of inherited and acquired mutations in specific cancer-related genes in precancerous tumors, following a multistep progression from preneoplastic to infiltrating carcinoma, characterized by an increased degree of morphological and cytological atypia. The most common situation is to start with activating mutations of the KRAS gene, followed by somatic mutations of one or more tumor suppressor genes TP53, p16/CDKN2A and SMAD4. About 10% of cases can be partially attributed to one of several germline mutations. The development of metastatic cancer requires both KRAS mutations and the deletion of tumor suppressor genes. Targeting these molecular pathways has become one of the methods of customizing oncolytic viruses and targeted therapies for pancreatic cancer.
OV itself has tumor selectivity and the ability to cause cancer cell lysis, and is becoming more and more popular in the treatment of many different forms of cancer. OV can prevent its binding and replication in normal cells through genetic engineering, and can add foreign genes that directly and/or indirectly cause cell death to selectively target tumor cells. These viruses usually also can replicate. Therefore, replication in tumor cells produces infectious progeny, which may further spread and kill the tumor mass. The efficacy of oncolytic viruses depends on direct tumor lysis, the ability of the virus to spread to surrounding cancer cells, and the ability of the virus to spread. At present, the main types of viruses used in the treatment of pancreatic cancer are the following:
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