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The p53 tumor suppressor pathway is impaired in more than 90% of cervical cancers and cancer‐derived cell lines as a result of infection by human papillomavirus (HPV). The HPV E6 oncoprotein forms complexes with p53 and promotes its degradation via ubiquitin‐dependent mechanism. In our study, we attempted to improve the clinical outcomes of this combined therapy by modifying the p53‐targeted adenovirus...
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