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Article

Abrogation of the Postmitotic Checkpoint Contributes to Polyploidization in Human Papillomavirus E7-Expressing Cells

8 Jan 2009

Abstract excerpt

High-risk types of human papillomavirus (HPV) are considered the major causative agents of cervical carcinoma. The transforming ability of HPV resides in the E6 and E7 oncogenes, yet the pathway to transformation is not well understood. Cells expressing the oncogene E7 from high-risk HPVs have a high incidence of polyploidy, which has been shown to occur as an early event in cervical carcinogenesis and...

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PMID: 19129456
DOI: 10.1128/jvi.02149-08

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Abrogation of the Postmitotic Checkpoint Contributes to Polyploidization in Human Papillomavirus E7-Expressing CellsPMID 19129456Read ↗

p53-Independent Abrogation of a Postmitotic Checkpoint Contributes to Human Papillomavirus E6 -Induced PolyploidySemantic proximity Read ↗

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Centrosomes, Genomic Instability, and Cervical CarcinogenesisSemantic proximity Read ↗

Role of Cdk1 in the p53-Independent Abrogation of the Postmitotic Checkpoint by Human Papillomavirus E6Semantic proximity Read ↗

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Human Papillomavirus Type 16 E7 Oncoprotein Can Induce Abnormal Centrosome Duplication through a Mechanism Independent of Inactivation of Retinoblastoma Protein Family MembersSemantic proximity Read ↗

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