作者: Manel Cascallo , Alena Gros , Neus Bayo , Teresa Serrano , Gabriel Capella
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摘要: Deletion of viral functions that can be complemented by the specific phenotype tumor cells is a common strategy to design oncolytic viruses. For example, enhanced mRNA cytoplasmic export in phenocopies adenovirus E1B-55K function and renders mutants this protein selective. Also, an activated RB pathway complements E1A deleted produce In paper we demonstrate adenoviral mutant virus-associated I (VAI) VAII RNAs (Ad-VAdel) has oncotropism characterized 100-fold replication deficiency compared with wild-type normal unaffected ability replicate kill different types cells. This also displays active antitumoral activity vivo. contrast, less evident expressing inactive form VAI (Adsub719) because RNA expression upregulated. The translation promoted VA genes phenocopied activation signal transduction pathways, such as Ras pathway.