RESUMO
OBJECTIVES: To examine the primary risk factor for oral cancer in the US, smoking and tobacco use, among the specific US states that experienced short-term increases in oral cancer incidence and mortality. METHODS: Population-based data on oral cancer morbidity and mortality in the US were obtained from the National Cancer Institute's (NCI) Surveillance, Epidemiology, and End Results (SEER) database for analysis of recent trends. Data were also obtained from the Centers for Disease Control and Prevention (CDC) Behavioral Risk Factor Surveillance System (BRFSS) to measure current and former trends of tobacco usage. To comprehensive measures of previous state tobacco use and tobacco-related policies, the Initial Outcomes Index (IOI, 1992-1993) and the Strength of Tobacco Control index (SoTC, 1999-2000) were also used for evaluation and comparison. RESULTS: Analysis of the NCI-SEER data confirmed a previous report of geographic increases in oral cancer and demonstrated these were state-specific, were not regional, and were unrelated to previously observed increases among females and minorities. Analysis of the CDC-BRFSS data revealed these states had relatively higher percentages of smokers currently, as well as historically. In addition, analysis of the IOI and SoTC indexes suggest that many factors, including cigarette pricing, taxes and home or workplace bans, may have had significant influence on smoking prevalence in these areas. Trend analysis of these data uncovered a recent and significant reversal in smoking rates that suggest oral cancer incidence and mortality may also begin to decline in the near future. CONCLUSION: Due to the rising costs of health care in the US and the limited resources available for health prevention efforts, it is essential to organize and direct more effective efforts by public health officials and epidemiologists, as well as funding from local, state and federal governments, to reduce and eliminate identified health disparities. This study provides evidence how these efforts may be directed to specific geographic areas, and towards the white males, previously thought to be unaffected by the increases in oral cancer among females and minorities.
RESUMO
BACKGROUND: Human 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. RESULTS: CAL27 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. CONCLUSION: Determining 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.
