ArticleCarcinogenesis2014
Tobacco exposure results in increased E6 and E7 oncogene expression, DNA damage and mutation rates in cells maintaining episomal human papillomavirus 16 genomes.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Elevated Prevalence of Oral HPV Infection Among Females with Periodontitis: A Cross-Sectional Study.Oral health & preventive dentistry · 2026Article
- Global burden and projections of cervical cancer attributable to unsafe sex and smoking, 1990-2034.PloS one · 2026Article
- Curcumin attenuates smoking and drinking activated NF-κB/IL-6 inflammatory signaling axis in cervical cancer.Cancer cell international · 2024Article
- Oral and periodontal manifestation related during human papilloma virus infections: Update on early prognostic factors.Heliyon · 2024Review
- Prevalence of human papillomavirus infection and associated factors among women attending cervical cancer screening in setting of Addis Ababa, Ethiopia.Scientific reports · 2024Article
- Risk factors for the development of cervical cancer: analysis of the evidence.Frontiers in oncology · 2024Review
- The oral microbiome and oral and upper gastrointestinal diseases.Journal of oral microbiology · 2024Review
- Association between human papillomavirus and oral cancer: a literature review.International journal of clinical oncology · 2023Review
- HPV and Cervical Cancer: A Review of Epidemiology and Screening Uptake in the UK.Pathogens (Basel, Switzerland) · 2023Review
- Review
- Article
- Interplay between Epstein-Barr virus infection and environmental xenobiotic exposure in cancer.Infectious agents and cancer · 2021Review
- Relationship between the prevalence of oral human papillomavirus DNA and periodontal disease (Review).Biomedical reports · 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
- The Preventive Effect of Dietary Antioxidants on Cervical Cancer Development.Medicina (Kaunas, Lithuania) · 2020Review
- Chemopreventive Role of Apigenin against the Synergistic Carcinogenesis of Human Papillomavirus and 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone.Biomedicines · 2020Article
- Oxidative stress markers in patient-derived non-cancerous cervical tissues and cells.Scientific reports · 2020Article
- Significance of HPV16 Viral Load Testing in Anal Cancer.Pathology oncology research : POR · 2020Article
- High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.Cancers · 2020Review
- The Preventive Effect of Dietary Antioxidants Against Cervical Cancer Versus the Promotive Effect of Tobacco Smoking.Healthcare (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
High-risk human papillomavirus (HR-HPV) infections are necessary but insufficient agents of cervical and other epithelial cancers. Epidemiological studies support a causal, but ill-defined, relationship between tobacco smoking and cervical malignancies. In this study, we used mainstream tobacco smoke condensate (MSTS-C) treatments of cervical cell lines that maintain either episomal or integrated HPV16 or HPV31 genomes to model tobacco smoke exposure to the cervical epithelium of the smoker. MSTS-C exposure caused a dose-dependent increase in viral genome replication and correspondingly higher early gene transcription in cells with episomal HPV genomes. However, MSTS-C exposure in cells with integrated HR-HPV genomes had no effect on genome copy number or early gene transcription. In cells with episomal HPV genomes, the MSTS-C-induced increases in E6 oncogene transcription led to decreased p53 protein levels and activity. As expected from loss of p53 activity in tobacco-exposed cells, DNA strand breaks were significantly higher but apoptosis was minimal compared with cells containing integrated viral genomes. Furthermore, DNA mutation frequencies were higher in surviving cells with HPV episomes. These findings provide increased understanding of tobacco smoke exposure risk in HPV infection and indicate tobacco smoking acts more directly to alter HR-HPV oncogene expression in cells that maintain episomal viral genomes. This suggests a more prominent role for tobacco smoke in earlier stages of HPV-related cancer progression.
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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.