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Updated: May 14, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage
Published on: February 15, 2020
Oxidative stress and HPV carcinogenesis.
1Laboratory of Virology, Regina Elena, Italian National Cancer Institute, Via delle Messi d'Oro 156, 00158 Rome, Italy. demarco@ifo.it
High-risk human papillomavirus (HR-HPV) causes cancer, but oxidative stress (OS) may also play a role. This review explores how OS interacts with HR-HPV infection to promote cancer development, highlighting underexplored areas for future research.
Area of Science:
- Oncology
- Virology
- Biochemistry
Background:
- High-risk human papillomavirus (HR-HPV) is a potent carcinogen, but cancer development is rare.
- Co-factors are necessary for HR-HPV infection to lead to neoplastic transformation.
- Oxidative stress (OS) is an underexplored co-factor in HR-HPV-driven carcinogenesis.
Purpose of the Study:
- To summarize data on the specific interaction between OS and HR-HPV in cancer initiation and progression.
- To review experimental evidence supporting OS's role in viral infection and integration.
- To highlight unexplored aspects of OS and HR-HPV interplay.
Main Methods:
- Literature review of experimental data and indirect evidence.
- Discussion of the roles of nitric oxide (NO) and inducible nitric oxide synthase (iNOS).
- Analysis of OS/HPV cooperation in cancer metabolism adaptation.
Main Results:
- OS may directly interact with molecular stages of HR-HPV-induced neoplasia.
- OS and HPV-induced genomic instability can independently contribute to cancer.
- NO/iNOS exhibit anti-apoptotic and pro-angiogenetic effects relevant to OS/HPV cooperation.
Conclusions:
- OS is a significant, underexplored co-factor in HR-HPV carcinogenesis.
- Further research into OS-HPV interactions is needed to understand cancer development.
- Investigating OS interplay may reveal novel approaches for cancer prevention and treatment.
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