Evidence map›Paper›PMID 18001474›Full record

ArticleInfectious agents and cancer2007

High risk HPV types 18 and 16 are potent modulators of oral squamous cell carcinoma phenotypes in vitro.

Nicole Reddout, Todd Christensen, Anthony Bunnell, Dayne Jensen, Devin Johnson, Susan O'Malley, Karl Kingsley

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Nicole ReddoutDepartment of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Todd ChristensenDepartment of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Anthony BunnellDepartment of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Dayne JensenDepartment of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Devin JohnsonDepartment of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Susan O'Malley *Department of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.
Karl Kingsley *Department of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Identifiers

PMID18001474
PMCPMC2206007

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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.