Abstract
Conditionally replicating adenoviruses (CRAds) represent a potent approach for treatment of neoplastic diseases. Replication of CRAds can be restricted to cancer cells in two different ways: limit the expression of viral E1A to tumor tissues with tumor-specific promoters or engineer deletions in genes critical for viral replication in normal cells but not in tumor cells. Gene therapy applications are usually based on Ad serotype 5, which binds to the coxsackie- adenovirus receptor (CAR). However, expression of CAR is frequently dysregulated in many types of advanced cancers. Substituting the knob domain of Ad5 with the corresponding domain of serotype 3 allows CAR-independent binding and entry through the Ad3 receptor, which is expressed to high degree on ovarian cancer cells.
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