Association Between Cervical Inflammatory Mediators and Prevalent Cervical Human Papillomavirus Infection.

PURPOSE: Inflammatory mediators are important regulators of immune response and can modulate the inflammation caused by viral infections, including human papillomavirus (HPV). In this study, we evaluated the association between cervical immune mediators, including chemokines, cytokines, and growth factors with HPV infections. MATERIALS AND METHODS: We used a nonmagnetic bead-based multiplex assay to determine 27 immune mediators in cervical secretions collected from 275 women in a prospective longitudinal cohort design. All the study participants were age 18 years or older, had a history of vaginal sexual intercourse, were not currently pregnant, and had no history of cervical disease or hysterectomy. RESULTS: The mean (±standard deviation) age of the participants was 41 (±8) years, and about half (51% [141/275]) were HPV-positive, of whom 7% (10/141) had low-risk HPV (lrHPV), 61% (86/141) had high-risk HPV (hrHPV), and 32% (45/141) had both lrHPV and hrHPV infections. Higher concentrations of some immune mediators were associated with HPV infections, including eotaxin, interferon-gamma, interleukin (IL)-1ß, IL-2, IL-4, IL-7, IL-8, IL-9, IL-10, IL-12p70, IL-13, IL-15, macrophage inflammatory protein (MIP)-1α, MIP-1ß, regulated upon activation normal T-cell expressed and secreted (RANTES), and tumor necrosis factor (TNF)-α and any HPV; IL-2, IL-4, IL-5, IL-7, IL-10, IL-12p70, and IL-13 and lrHPV; and eotaxin, interferon, IL-1B, IL-4, IL-7, IL-8, IL-9, IL-10, IL-13, IL-15, MIP-1α, MIP-1ß, RANTES, TNF-α concentrations, and hrHPV infections. Higher concentrations of granulocyte macrophage colony-stimulating factor, IL-1 receptor antagonist (IL-1Ra), and monocyte chemotactic protein-1 (MCP-1) were associated with reduced odds of any HPV, while IL-1Ra and MCP-1 were associated with reduced odds of hrHPV infections. CONCLUSION: Several chemokines, cytokines, and growth factors are associated with group-specific HPV infections in this population of women. These important findings contribute to the understanding of the immune response to HPV, cytokine profiles and their potential implications for cervical pathogenesis, and can guide future research in this field.

Cancers Attributable to Overweight and Obesity From 2012 to 2014 in Nigeria: A Population-Based Cancer Registry Study.

Background: Overweight and obesity are known risk factors for chronic diseases including cancers. In this study, we evaluated the age standardized incidence rates (ASR) and proportion of cancers attributable to overweight and obesity in Nigeria. Methods: We obtained incidence data from the databases of two population-based cancer registries (PBCRs) in Nigeria (Abuja and Enugu cancer registries), on cancer site for which there is established evidence of an association with overweight or obesity based on the International Agency for Research on Cancer (IARC) and the World Cancer Research Fund (WCRF) classification. We analyzed the data using population attributable fraction (PAF) for overweight or obesity associated cancers calculated using prevalence data and relative risk estimates in previous studies. Results: The two PBCRs reported 4,336 new cancer cases (ASR 113.9 per 100,000) from 2012 to 2014. Some 21% of these cancers were associated with overweight and obesity. The ASR for overweight and obesity associated cancers was 24.5 per 100,000; 40.7 per 100,000 in women and 8.2 per 100,000 in men. Overall, only 1.4% of incident cancers were attributable to overweight and obesity. The ASR of cancers attributable to overweight and obesity was 2.0 per 100,000. Postmenopausal breast cancer was the most common cancer attributable to overweight and obesity (n = 25; ASR 1.2 per 100,000). Conclusion: Our results suggest that a small proportion of incident cancer cases in Nigeria are potentially preventable by maintaining normal body weight. The burden of cancer attributed to overweight and obesity in Nigeria is relatively small, but it may increase in future.