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All papers authored by John Doorbar

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2021 Maryam Khelil

ORCID

, Heather Griffin, Maaike C. G. Bleeker, Renske D. M. Steenbergen

ORCID

, Ke Zheng, Taylor Saunders-Wood, Sanne Samuels, Jossie Rotman

ORCID

, Wim Vos, Brendy E. van den Akker, Renée X. de Menezes, Gemma G. Kenter, John Doorbar

ORCID

, Ekaterina S. Jordanova

ORCID

Delta-Like Ligand–Notch1 Signaling Is Selectively Modulated by HPV16 E6 to Promote Squamous Cell Proliferation and Correlates with Cervical Cancer Prognosis

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2020 Aslam Shiraz, Robin Crawford, Nagayasu Egawa, Heather Griffin, John Doorbar

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The Early Detection of Cervical Cancer. The current and changing landscape of cervical disease detection

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2019 Heather Griffin, Hardeep Singh Mudhar, Paul Rundle, Aslam Shiraz, Radma Mahmood, Nagayasu Egawa

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, Wim Quint, Ian G. Rennie, John Doorbar

ORCID

Human papillomavirus type 16 causes a defined subset of conjunctival in situ squamous cell carcinomas

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John Doorbar

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, Heather Griffin

Refining our understanding of cervical neoplasia and its cellular origins

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Anne Hammer, Maurits Nc de Koning, Jan Blaakaer, Torben Steiniche, John Doorbar

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, Heather Griffin, Else Mejlgaard, Hans Svanholm, Wim Gv Quint, Patti E. Gravitt

Whole tissue cervical mapping of HPV infection: Molecular evidence for focal latent HPV infection in humans

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Isao Murakami, Nagayasu Egawa, Heather Griffin, Wen Yin, Christian Kranjec

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, Tomomi Nakahara

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ORCID

, John Doorbar

ORCID

Roles for E1-independent replication and E6-mediated p53 degradation during low-risk and high-risk human papillomavirus genome maintenance

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2017 Christian Kranjec

ORCID

, Christina Holleywood, Diane Libert, Heather Griffin, Radma Mahmood, Erin Isaacson, John Doorbar

ORCID

Modulation of basal cell fate during productive and transforming HPV-16 infection is mediated by progressive E6-driven depletion of Notch: HPV-16 E6, transforming viral infection and keratinocyte fate

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Nagayasu Egawa, Qian Wang, Heather M. Griffin, Isao Murakami

ORCID

, Deborah Jackson, Radma Mahmood, John Doorbar

ORCID

HPV16 and 18 genome amplification show different E4-dependence, with 16E4 enhancing E1 nuclear accumulation and replicative efficiency via its cell cycle arrest and kinase activation functions

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