ArticleCancer research2009
Nitric oxide induces early viral transcription coincident with increased DNA damage and mutation rates in human papillomavirus-infected cells.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 97 citations in OpenAlex.
- Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model.International journal of molecular sciences · 2026Review
- Global impact of air pollution on cancer: causal evidence and health inequities across regions from 1990 to 2021.BMC cancer · 2025Article
- Inflammation in Penile Squamous Cell Carcinoma: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Article
- High-risk human papillomavirus infection and cervical cytopathology: relationship with cervical nitric oxide levels.Virology journal · 2024Article
- Dysregulation of base excision repair factors associated with low tumor immunogenicity in head and neck cancer: implication for immunotherapy.Therapeutic advances in medical oncology · 2024Article
- Nitric Oxide: Physiological Functions, Delivery, and Biomedical Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Genetic Modulation of HPV Infection and Cervical Lesions: Role of Oxidative Stress-Related Genes.Antioxidants (Basel, Switzerland) · 2023Article
- The role of viruses in cancer development versus cancer therapy: An oncological perspective.Cancer medicine · 2023Review
- Inflammation in Urological Malignancies: The Silent Killer.International journal of molecular sciences · 2023Review
- Expression of HPV-16 E6 and E7 oncoproteins altersFrontiers in cellular and infection microbiology · 2023Article
- Strategies of Pathogens to Escape from NO-Based Host Defense.Antioxidants (Basel, Switzerland) · 2022Review
- Lactoferrin as a Human Genome "Guardian"-An Overall Point of View.International journal of molecular sciences · 2022Review
- IFN-γ activates the tumor cell-intrinsic STING pathway through the induction of DNA damage and cytosolic dsDNA formation.Oncoimmunology · 2022Article
- Causes and Consequences of HPV Integration in Head and Neck Squamous Cell Carcinomas: State of the Art.Cancers · 2021Review
- Nitric oxide and viral infection: Recent developments in antiviral therapies and platforms.Applied materials today · 2021Review
- MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors.PLoS pathogens · 2021Article
- Article
- Oxidative stress markers in patient-derived non-cancerous cervical tissues and cells.Scientific reports · 2020Article
- Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) in Oropharyngeal Cancer Associated with EBV and HPV Coinfection.Viruses · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
High-risk human papillomavirus (HPV) infections are necessary but insufficient causes of cervical cancers. Other risk factors for cervical cancer (e.g., pregnancy, smoking, infections causing inflammation) can lead to high and sustained nitric oxide (NO) concentrations in the cervix, and high NO levels are related to carcinogenesis through DNA damage and mutation. However, the effects of NO exposure in HPV-infected cells have not been investigated. In this study, we used the NO donor DETA-NO to model NO exposure to cervical epithelium. In cell culture media, 24-hour exposure to 0.25 to 0.5 mmol/L DETA-NO yielded a pathologically relevant NO concentration. Exposure of cells maintaining episomal high-risk HPV genomes to NO increased HPV early transcript levels 2- to 4-fold but did not increase viral DNA replication. Accompanying increased E6 and E7 mRNA levels were significant decreases in p53 and pRb protein levels, lower apoptotic indices, increased DNA double-strand breaks, and higher mutation frequencies when compared with HPV-negative cells. We propose that NO is a molecular cofactor with HPV infection in cervical carcinogenesis, and that modifying local NO cervical concentrations may constitute a strategy whereby HPV-related cancer can be reduced.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.