Addressing differences in cancer: a framework for synergistic programming in cancer prevention and control.

Background: Cancer remains a leading cause of death worldwide and continues to disproportionately impact certain populations. Several frameworks have been developed that illustrate the multiple determinants of cancer. Expanding upon the work of others, we present an applied framework for cancer prevention and control designed to help clinicians, as well as public health practitioners and researchers, better address differences in cancer outcomes. Methods: The framework was developed by the Cancer Prevention and Control Research Network's Health Behaviors Workgroup. An initial framework draft was developed based on workgroup discussion, public health theory, and rapid literature review on the determinants of cancer. The framework was refined through interviews and focus groups with Federally Qualified Health Center providers (n=2) and cancer patients (n=2); participants were asked to provide feedback on the framework's causal pathways, completeness, and applicability to their work and personal life. Results: The framework provides an overview of the relationships between sociodemographic inequalities, social and structural determinants, and key risk factors associated with cancer diagnosis, survivorship, and cancer morbidity and mortality across the lifespan. The framework emphasizes how health-risk behaviors like cigarette smoking interact with psychological, psychosocial, biological, and psychosocial risk factors, as well as healthcare-related behavior and other chronic diseases. Importantly, the framework emphasizes addressing social and structural determinants that influence health behaviors to reduce the burden of cancer and improve health equity. Aligned with previous theory, our framework underscores the importance of addressing co-occurring risk factors and disease states, understanding the complex relationships between factors that influence cancer, and assessing how multiple forms of inequality or disadvantage intersect to increase cancer risk across the lifespan. Conclusions: This paper presents an applied framework for cancer prevention and control to address cancer differences. Because the framework highlights determinants and factors that influence cancer risk at multiple levels, it can be used to inform the development, implementation, and evaluation of interventions to address cancer morbidity and mortality.

Cervical cytomegalovirus reactivation, cytokines and spontaneous preterm birth in Kenyan women.

Genital cytomegalovirus (CMV) reactivation is common during the third trimester of pregnancy. We hypothesized that cervical CMV shedding may increase risk of spontaneous preterm birth (sPTB) through the release of inflammatory cytokines in the cervix. We conducted a nested case-control analysis to determine the relationship between CMV shedding and sPTB using data and samples from a prospective cohort study in western Kenya. Women who delivered between 28 + 0 and 33 + 6 weeks gestation were matched by gestational age at sample collection to controls who delivered ≥ 37 + 0 weeks. Levels of CMV DNA and interleukin (IL)-1 beta (ß), IL-6, IL-8 and tumor necrosis factor (TNF)-α were measured in cervical swabs. We used conditional logistic regression to assess relationships between CMV shedding, cervical cytokine levels and sPTB. Among 86 cases and 86 matched controls, cervical CMV levels were not significantly associated with sPTB [odds ratio (OR) = 1·23, 95% confidence interval (CI) = 0·59-2·56], but were significantly associated with higher levels of cervical IL-6 (ß = 0·15, 95% CI = 0·02-0·29) and TNF-α (ß = 0·14, 95% CI = 0·01-0·27). In univariate analysis, higher odds of sPTB was associated with higher cervical IL-6 levels (OR = 1·54, 95% CI = 1·00-2·38), but not with other cervical cytokines. In this cohort of Kenyan women, we did not find a significant association between cervical CMV shedding and sPTB before 34 weeks.