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Gene Therapy Eradicates Pancreatic Cancer in Preclinical Trial,Targeting System's Success in Mouse Model Reported in Cancer Cell

ung's team set out to address two obstacles to gene therapy for pancreatic cancer: lack of a targeted gene expression system that hits the cancer hard but spares normal tissue, and the need for an animal model that allows monitoring of tumor growth and metastasis without having to kill and dissect the animal.

They solved the monitoring problem by modifying two lines of pancreatic cancer to stably express firefly luciferace enzyme - the bioluminescent agent that lights up fireflies. This allowed live imaging of the mice to monitor cancer progression.

The researchers already had developed several components of the gene expression system. Led by first author Xiaoming Xie, Ph.D., a postdoctoral fellow and now instructor in Hung's department, the team used those components and pieces developed elsewhere to painstakingly build what became C-VISA-BikDD.

They used a gene-based targeting promoter called CCKAR known to be active in pancreatic cancer but not in healthy pancreatic tissue. The problem with pancreatic-cancer-specific gene promoters such as CCKAR, Hung says, is that they select narrowly for cancer cells but are not highly active once they get there. The success of gene therapy depends on efficient gene expression after delivery.

A system using a viral promoter such as CMV has the opposite problem: strong activity but indiscriminate delivery of the therapeutic gene to healthy tissue, which increases toxicity. The team's goal was to retain CCKAR's selectivity while boosting its activity to levels seen in CMV promoter-driven therapy.

To strengthen activity, the team added two key components: a regulatory gene sequence known as WPRE and the two-step transcriptional amplification system (TSTA) known to amplify activity of the prostate-specific antigen (PSA) promoter.

This enhanced C-VISA package increased gene activity levels by 67.6 percent to 287 percent over the CMV-driven therapy in three lines of pancreatic cancer. Lab exp
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