Abstract
In an article previously published in Molecular Therapy, a high incidence of cancer formation was reported in mice transduced with adeno-associated viral (AAV) vector.1 Tumors from hepatectomized mice transduced with a self-complementary AAV (scAAV) vector containing a strong enhancer/promoter (CMV/beta-actin) but lacking a transgene or polyadenylation signal (“CBA-null,” Figure 1A) were more frequently associated with vector DNA than tumors in the control group that had been transduced with a conventional scAAV vector expressing a reporter gene.
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