HPV16 E6 seropositivity and oropharyngeal cancer: Marker of exposure, risk, or disease?

Landy, Rebecca; Chaturvedi, Anil K.

doi:10.1016/j.ebiom.2020.103190

Cited by 2 publications

(2 citation statements)

References 10 publications

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“…[1][2][3][4] Despite the introduction of HPVdirected vaccines over ten years ago, the lack of their widespread distribution, uptake by the general population and availability continues to make HPV positive (HPV+) cancers prevalent. [4][5][6][7] Among ∼200 identied HPV strains, high-risk HPV16 and HPV18 are responsible for ∼75% of HPVassociated cervical cancers. [8][9][10][11] Current treatment strategies of HPV cancers include radiation therapy, 4 surgery, 12 chemotherapy, 13 monoclonal antibody (mAb) 14 and checkpoint blockade.…”

Section: Introductionmentioning

confidence: 99%

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

Ye,

Zhang,

Tao

et al. 2023

Chem. Sci.

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Section: Introductionmentioning

confidence: 99%

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

Ye,

Zhang,

Tao

et al. 2023

Chem. Sci.

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“…High-risk forms of HPV are causative in multiple cancers, including cervical, vaginal, oropharyngeal, and potentially a subset of prostate cancers [1][2][3][4] . Despite the introduction of HPVdirected vaccines over ten years ago, the lack of their widespread distribution, uptake by the general population and availability continues to make HPV positive (HPV+) cancers prevalent [4][5][6][7] . Among ~200 identified HPV strains, high-risk HPV16 and HPV18 are responsible for ~75% of HPV-associated cervical cancers [8][9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

Zhang

Tao

et al. 2023

Preprint

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Human papillomavirus (HPV) infections account for nearly all cervical cancer cases, which is the fourth most common cancer in women worldwide. High-risk variants, including HPV16, drive tumorigenesis in part by promoting the degradation of the tumor suppressor p53. This degradation is mediated by the HPV early protein 6 (E6), which recruits the E3 ubiquitin ligase E6AP and redirects its activity towards ubiquitinating p53. Targeting the protein interaction interface between HPV E6 and E6AP is a promising modality to mitigate HPV-mediated degradation of p53. In this study, we designed a covalent peptide inhibitor, termed reactide, that mimics the E6AP LXXLL binding motif by selectively targeting cysteine 58 in HPV16 E6 with quantitative conversion. This reactide provides a starting point in the development of covalent peptidomimetic inhibitors for intervention against HPV-driven cancers.

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HPV16 E6 seropositivity and oropharyngeal cancer: Marker of exposure, risk, or disease?

Cited by 2 publications

References 10 publications

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6

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