Abstract

Background: Due to advances in viral design, oncolytic adenoviruses have emerged as a promising approach for treatment of human cancer. Development of this technology is impeded by two major obstacles: one being poor tropism, and another being a lack of specificity for cancerous cells. It has become possible to target these viruses to preferentially infect cancer cells by modifying the fiber protein of the viral capsid, making a serotype 5/3 chimera, thereby changing tropism. It is also now possible to render the replication of the virus conditional with tumor selective expression of the E1A gene using promoters that are active in cancer cells but not in normal tissue, such as the CXCR4 promotor region.

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