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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Curr Drug ther. 2009 May 1;4(2):117–138. doi: 10.2174/157488509788185123

Figure 2. Strategies for development of CRAds.

Figure 2

Various deletions can be introduced at different locations (indicated by asterisk) to enable selective replication of Ad vectors in tumor cells [52, 74, 84, 86, 94]. Usually the function of protein encoded by the mutated gene is complemented in tumor cells but not in the normal cells. Expression of some of the critical genes of Ad (indicated with arrows) can be exogenously controlled by tumor-specific regulatory elements [109–112]. Ligation of defined 3′UTR or 5′UTR to the E1A gene can result in tumor selective stabilization or translation of E1A mRNA respectively [136, 137]. Such modifications allow tumor-specific replication of Ad vectors. Retention of E3 genes (E3B and E3-ADP) or overexpression of ADP (indicated by bold arrow) usually potentiates the efficacy of Ad vectors [91, 97]. The late transcription units that encode Ad structural proteins remain unmodified. ITR, Inverted terminal repeat. UTR, Untranslated region. E1A, E1B, E2, E3 and E4 are Ad early genes. L1, L2, L3, L4 and L5 are Ad late genes. Ψ, Ad packaging signal. VA, Virus-associated. ADP, Ad death protein.