MmuPV1 E7 promotes phenotypes associated with "high-risk" HPV infection in mouse keratinocytes. [PDF]
Duxbury KR +6 more
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Diagnosis, Management, and Follow-Up of Human Papillomavirus Type 16 (HPV-16) Lesions in the Oral Cavity. [PDF]
Patel M +3 more
europepmc +1 more source
The membrane-associated ubiquitin ligase MARCHF8 degrades MHC-I in HPV-positive head and neck cancer for immune evasion. [PDF]
Khalil MI +16 more
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HPV, APOBEC3B, and the origins of breast cancer: a narrative review and perspectives on novel mechanisms. [PDF]
Liu ZY, Chen R.
europepmc +1 more source
Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses. [PDF]
Collins CD +3 more
europepmc +1 more source
Efficacy and Safety of PHPV Fusion Factor Vaginal Gel (PHPV®) in Clearing Cervical Persistent High-Risk Human Papillomavirus Infection: A Randomized Controlled Clinical Trial. [PDF]
Yan L +6 more
europepmc +1 more source
Oncogenic HPV types identified in Paleolithic and Chalcolithic human genome sequencing data from Ust'-Ishim and Ötzi. [PDF]
Yazigi JB +6 more
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Papillomavirus E6 and E7 proteins and their cellular targets
Frontiers in Bioscience, 2008The mucosal human papillomaviruses (HPVs) infect human genital and oral epithelial cells and cause lesions ranging in severity from benign to malignant. HPV associated malignancies include cervical and other anogenital cancers as well as a subpopulation of head and neck cancers.
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The human papillomavirus E7 protein as a transforming and transactivating factor
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1993The HPV proteins encoded by the early viral genes, including E6 and E7, are thought to subvert the normal regulatory pathways of infected cells to accommodate viral replication. Mechanistically some of this is accomplished by protein-protein interactions between viral proteins and a number of key cellular regulatory proteins that include tumor ...
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Interactions of the human papillomavirus E7 protein with cell cycle regulators
Seminars in Cancer Biology, 1996Human papillomavirus (HPVs) critically depend on the cellular machinery for the replication of their genome. Viral replication is restricted to the differentiated strata of the skin that are normally growth arrested. Hence, the HPVs have developed strategies to subvert cellular growth regulatory pathways and are able to uncouple cellular proliferation ...
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