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On the other hand, this scenario fulfills two requirements for oncolytic virus infection in tumor cells: inactivation of tumor suppressors and presence of oncoproteins, also the requirements to engage malignancy. Several of these oncogenes have a negative impact on the main interferon antiviral defense, the double-stranded RNA-activated protein kinase (PKR), which helps viruses to spontaneously target tumor cells instead of normal cells. This review is focused on the negative impact of overexpression of oncogenes on conventional and targeted therapy and their positive impact on viral oncolysis due to their ability to inhibit PKR-induced translation blockage, allowing virion release and cell death. <\/jats:p>","DOI":"10.4137\/bic.s33378","type":"journal-article","created":{"date-parts":[[2016,7,28]],"date-time":"2016-07-28T23:18:18Z","timestamp":1469747898000},"page":"BIC.S33378","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":25,"title":["Oncogenes: The Passport for Viral Oncolysis through PKR Inhibition"],"prefix":"10.4137","volume":"8","author":[{"given":"Janaina","family":"Fernandes","sequence":"first","affiliation":[{"name":"NUMPEX-BIO, Campus Xer\u00e9m, Federal University of Rio de Janeiro, Duque de Caxias, Rio de Janeiro, Brazil."},{"name":"Institute for Translational Research on Health and Environment in the Amazon Region\u2013-INPeTAm, 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