ArticleInfectious agents and cancer2007
High risk HPV types 18 and 16 are potent modulators of oral squamous cell carcinoma phenotypes in vitro.
Article in Infectious agents and cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- The role and diagnostic value of deregulated miRNAs in cervical cancer.Discover oncology · 2025Review
- Human papillomavirus, human immunodeficiency virus, and esophageal squamous cell carcinoma in South Africa: a study of prevalence, co-infection, and risk factors.Frontiers in oncology · 2025Article
- Understanding and treating HPV-associated oropharyngeal carcinoma: insights from a MedNewsWeek Keynote lecture by Dr Theodoros N. Teknos and literature review.Therapeutic advances in medical oncology · 2025Review
- Oncogenic and Stemness Signatures of the High-Risk HCMV Strains in Breast Cancer Progression.Cancers · 2022Article
- Article
- In Vitro Organotypic Systems to Model Tumor Microenvironment in Human Papillomavirus (HPV)-Related Cancers.Cancers · 2020Review
- Human papillomavirus 16 (HPV16) enhances tumor growth and cancer stemness of HPV-negative oral/oropharyngeal squamous cell carcinoma cells via miR-181 regulation.Papillomavirus research (Amsterdam, Netherlands) · 2015Article
- Human Papilloma Virus Associated Squamous Cell Carcinoma of the Head and Neck.Journal of sexually transmitted diseases · 2015Review
- Screening and detection of human papillomavirus (HPV) high-risk strains HPV16 and HPV18 in saliva samples from subjects under 18 years old in Nevada: a pilot study.BMC oral health · 2012Article
- Role of viruses in oral squamous cell carcinoma.Oncology reviews · 2012Review
- Article
- Folic acid supplementation increases survival and modulates high risk HPV-induced phenotypes in oral squamous cell carcinoma cells and correlates with p53 mRNA transcriptional down-regulation.Cancer cell international · 2012Article
- Differential impact of IL-10 expression on survival and relapse between HPV16-positive and -negative oral squamous cell carcinomas.PloS one · 2012Article
- High-risk human papillomavirus (HPV) screening and detection in healthy patient saliva samples: a pilot study.BMC oral health · 2011Article
- Cranberry and grape seed extracts inhibit the proliferative phenotype of oral squamous cell carcinomas.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- Analysis of primary risk factors for oral cancer from select US states with increasing rates.Tobacco induced diseases · 2010Article
- Analysis of oral cancer epidemiology in the US reveals state-specific trends: implications for oral cancer prevention.BMC public health · 2008Article
- Research enrichment: evaluation of structured research in the curriculum for dental medicine students as part of the vertical and horizontal integration of biomedical training and discovery.BMC medical education · 2008Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman papillomavirus (HPV) has been confirmed as the primary etiological factor that transforms cervical epithelia into cancer. The presence of HPV in oral cancers suggests that HPV may play a similar role in transforming the oral epithelia. A high degree of variability in the prevalence of HPV in oral cancers has been found, however, raising questions regarding its role in the transformation and development of oral cancers. The goal of this study was to test our hypothesis that high-risk HPV strains HPV16 and HPV18 will alter the phenotype of transformed oral squamous cell carcinoma cell lines, CAL27, SCC-15 and SCC-25 in vitro.
resultsCAL27 cells transfected with HPV18, HPV16, as well as HPV16/18 co-transfectants, demonstrated significant increases in proliferation, adhesion and cell spreading compared with non-transfected controls. These observed differences were correlated with a small level of increased cell survival. SCC-15 cells, however, displayed a differential response to HPV transfection, with only HPV18-transfectants demonstrated changes to proliferation. Interestingly, SCC-25 cells displayed a more complex response, with HPV16-induced increases in cell proliferation, viability and cell spreading, while HPV18- and 16/18-transfectants exhibited reduced adhesion and proliferation.
conclusionDetermining the potential of specific high-risk HPV strains to alter phenotypic behaviors of already transformed oral carcinomas is a critical step in providing more accurate prognosis and treatment options for oral cancer patients. The identification of differential responses to specific HPV strains among oral cancers suggests a more significant, complex and multifactorial role of HPV, not only in transforming, but also in modulating, the phenotype and treatment responsiveness of precancerous and cancerous oral lesions. This study provides some of the first evidence to help identify the important molecular markers for pathways that could be used to determine the most effective and appropriate treatment plans for oral cancer patients with concomitant oral HPV infections.
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Registered trials
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