I can understand that we all can not have the same opinions, and
HPV is a difficult virus to understand, there are so many different research findings, I am not suggesting that there is no cancer in which only the
HPV is involved, I know that this does happend , but oral cancer is on the whole a multifactorial disease and the number who get cancer of the only
HPV is incredibly small number, so small that it is difficult to statement as statistics or draw conclusions, there are many adoption from all sides
http://www.merckmanuals.com/home/sec18/ch216/ch216c.htmlhttp://www.springerlink.com/content/870485v71w88nw67Tobacco, alcohol, and human papillomavirus (
HPV) are major risk factors for head and neck cancer (HNC), but it is unclear whether there are two distinct HNC risk groups, one associated with
HPV and the other with tobacco/alcohol. Because
HPV-positive HNC are clinically distinct from
HPV-negative cases in treatment response and with more favorable prognoses, determining whether these differences result from infection alone or in association with other HNC risk factors is important for developing future therapeutic strategies. Incident cases of HNC (n = 201) and age-gender frequency-matched controls (n = 324) were recruited to assess anti-
HPV VLP (virus like particles) antibodies 16, 18, 31, and 33. Multivariate logistic regression and stratified analyses were used to calculate adjusted odds ratios (OR).
HPV-seronegative and seropositive/heavy tobacco users had similar increased adjusted risks of HNC (
HPV-seronegative OR = 2.6, 1.4�5.0;
HPV-seropositive OR = 2.3, 1.1�4.8), as did
HPV-seronegative (OR = 4.3, 2.1�9.1) versus
HPV-seropositive/heavy alcohol users (OR = 3.9, 1.6�9.4). Similar
HPV/tobacco/alcohol risk profiles also were seen in oropharyngeal and oral cavity tumor sites. Our finding that tobacco/alcohol use increased the risk of HNC in both
HPV-seropositive and
HPV-seronegative individuals is consistent with the observation that
HPV infection is not a sufficient cause of HNC but requires the accumulation of additional cellular changes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917346/CONCLUSIONS:
HPV16 E6 and E7 alone are not sufficient for invasive growth. However, the synergistic activity of H-Ras and E6 was sufficient to result in invasive growth.
Our findings also suggest that
HPV related carcinogenesis is a multi-step process. We have found that expression of
HPV viral oncogenes alone is not sufficient to permit metastatic growth. This result supports the clinical finding that not all patients with persistent
HPV infection develop cancer. It is likely that at least one additional cellular mutation in the presence of
HPV oncogenes is required for metastatic growth. E6 transgenic mouse data also support these findings. In one study, only 14% of mice that overexpressed E6 developed malignant tumors, suggesting that E6 is not sufficient to induce tumor growth by itself. Chromosomal analysis of the tumors that developed in these mice indicated that they exhibited other genetic alterations compared to the surrounding tissue10. The fact that H-Ras synergizes with E6 to result in invasive growth may shed light into what other cellular pathways need to be altered to result in invasive tumorigenic growth. H-Ras activation is a downstream event of growth factor signaling34. Growth factor receptor overexpression is common in HNSCCA35. Although H-Ras mutations have not been reported in
HPV related HSCCA, it is possible that alterations like growth factor overexpression or other components of the growth factor signaling cascade could synergize with
HPV oncogenes to allow invasive growth.
