In fact, assuming a more strong titer is associated with a more biologically important exposure, the lower risk of pharyngeal cancer associated with low HPV6 titer (OR = 1

In fact, assuming a more strong titer is associated with a more biologically important exposure, the lower risk of pharyngeal cancer associated with low HPV6 titer (OR = 1.5, 0.8C2.6) compared with a higher HPV6 titer (OR = 1.8, 1.0C3.2) is consistent with HPV6 being the etiologic agent. cancer (OR = 1.9, 1.0C3.6), suggesting that this cancer risk associated with HPV6 is independent of HPV16. There was no association between smoking and alcohol use and HPV6 serostatus. Further, the risk of pharyngeal cancer associated with heavy smoking was different among HPV6-seronegative (OR 3.1, 2.0C4.8) and HPV6-seropositive subjects (OR = 1.6, 0.7C3.5), while heavy drinking also appears to confer differing risk among HPV6-negative (OR 2.3, 1.5C3.7) and -positive subjects (OR = 1.3, 0.6C2.9). Conclusions: There may be interactions between positive serology and drinking and smoking, suggesting that this pathogenesis of human papillomavirus in HNSCC involves complex interactions with tobacco and alcohol exposure. (ICD-9) codes 141, 143-6, 148, and 161. All patients with carcinoma Dasatinib hydrochloride value of 0.05 was considered statistically significant.tpb -2pt results We studied 486 HNSCC cases and 548 controls (Table 1). Approximately three quarters of our study populace was male (74% of cases, 73% of controls). The mean age was 60 years of age for cases and 61 years of age for controls with the majority of the populace being white (92% of cases, 91% of controls). Table 1. Characteristics Dasatinib hydrochloride of HNSCC cases and controls = 548) (%)All cases (= 486)= 204)= 189)Larynx (= 93)(%)OR (95% CI)a(%)OR (95% CI)a(%)OR (95% CI)a(%)OR (95% CI)a 0.01) but weakly correlated to HPV titer of all other types (Spearman correlation coefficients ranged from 0.08 to 0.19), though the correlation between HPV11 and HPV18 was marginally significant (= 0.06). Among controls, HPV6 seropositivity was most common (14%) followed by HPV16 seropositivity (11%) and HPV18 seropositivity (8%). As shown in Table 3, controls with HPV16 seropositivity were significantly more likely to be seropositive for HPV6 (OR = 2.2, 95% CI 1.1C4.3), HPV11 (OR = 3.4, 1.4C8.0), and HPV18 (OR = 2.1, 1.0C4.8). Non-white controls were significantly more likely to be seropositive for HPV6 (OR = 2.5, 1.2C5.0) and HPV11 (OR = 3.2, 1.2C8.3), while heavy smokers were more likely to be seropositive for HPV6 (OR = 2.1, 1.2C3.5). Controls who were 60 years or older were less likely Tal1 to be HPV11 seropositive compared Dasatinib hydrochloride with those under 60 years of age (OR = 0.5, 0.2C1.0). Table 2. Spearman correlation between serology typesa among controls (= 548) 0.00010.17; = 0.00010.13; = 0.003HPV111.000.08; = 0.060.15; = 0.0004HPV181.000.12; = 0.007HPV161.00 Open in a separate window aCorrelations were evaluated using titer values. Table 3. Predictors of positive HPV6, 11, and 18 serology among controls (= 548) 0.05. aThe adjusted models include age, gender, race, drinking, smoking, and HPV16. Table 4 Dasatinib hydrochloride presents the crude and adjusted ORs for HPV6, HPV11, and HPV18 serology. The adjusted ORs controlled for smoking, drinking, and HPV16, though confounding by HPV16 serology, account for the majority of the difference between the crude and adjusted risk estimates. HPV6 seropositivity was associated with an increased risk of pharyngeal cancer (OR = 1.6, 1.0C2.5) while controlling for smoking, drinking, and HPV16. In fact, assuming a more strong titer is associated with a more biologically important exposure, the lower risk of pharyngeal cancer associated with low HPV6 titer (OR = 1.5, 0.8C2.6) compared with a higher HPV6 titer (OR = 1.8, 1.0C3.2) is consistent with HPV6 being the etiologic agent. Similarly, an increased risk of oral cancer was associated with high HPV6 titer (OR = 1.9, 1.1C3.4) but not low HPV6 titer, while controlling for smoking, drinking, and HPV16. Additionally, we investigated a possible synergistic effect of HPV6 and HPV16 seropositivity on HNSCC risk but found that the conversation was not significant (= 0.8). HPV11 and HPV18 seropositivity were not associated with risk for pharyngeal or oral malignancy, although the unadjusted models suggested some elevated risk for pharyngeal cancer that was not evident after adjustment.