Objective To investigate the association between genus β human papillomaviruses and the incidence of nonmelanocytic skin cancer in the general population. Design Population based case-control study. Setting New Hampshire, USA. Participants 2366 skin cancer cases and controls from the general population aged 25 to 74 years (663 squamous cell carcinoma, 898 basal cell carcinoma, 805 controls), with plasma samples tested for L1 antibodies to 16 genus β human papillomaviruses by multiplex serology. Main outcome measures Odds ratios for squamous cell carcinoma and basal cell carcinoma associated with seropositivity to β human papillomaviruses. Results Squamous cell carcinoma, but not basal cell carcinoma, cases had a higher prevalence of each of the individual β human papillomaviruses assayed compared with controls. The odds ratios for squamous cell carcinoma increased with the number of β types positive (odds ratio for one type positive 0.99 (95% confidence interval 0.74 to 1.33); two to three types positive 1.44 (1.03 to 2.01); four to eight types positive 1.51 (1.03 to 2.20); more than eight types positive 1.71 (1.12 to 2.62); P for trend (categorical)<0.001; P for trend (continuous) =0.003). With limited statistical power, the association was stronger among long term users of systemic glucocorticoids (odds ratio 3.21, 1.22 to 8.44) than among non-users (1.23, 0.97 to 1.55). Conclusions These findings support a relation between genus β human papillomavirus infection and the incidence of squamous cell carcinoma of the skin in the general population, as well as potential enhancement of risk by immunosuppression.
In early stage HPV-tumors, 3% cells were CD98+/BMI1+ compared to 6% in HPV+ tumors. In late stage, both HPV-and HPV+ tumors had 9% of CD98+/BMI1+ cells. We didn't have enough samples to evaluate the impact of smoking status. None of these comparisons was statistically significant after adjustment for multiple testing, based on a level of significance of 0.05. Conclusion: Contrary to our hypothesis, there were no differences in CD44, CD166, BMI1, or CD98 marker expression (either singly or combination) between HPV+ and HPV-patients. Currently, our results suggest that there is no significant difference in biology between CSCs in HPV+ compared to HPV-tumors. It is also possible that CSC numbers or biology do not play key roles in HPV-driven OPSCC, and other genetic or immune-based mechanisms underlie the more favorable biology of this subset of patients. Further studies including larger cohorts may provide a better understanding of the association between HPV infection and CSC biology.
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