Neighborhood social and built environments have been recognized as important contexts in which health is shaped. We review the extent to which these neighborhood factors have been addressed in population-level cancer research, with a scan of the literature for research that focuses on specific social and/or built environment characteristics and association with outcomes across the cancer continuum, including incidence, diagnosis, treatment, survivorship, and survival. We discuss commonalities and differences in methodologies across studies, current challenges in research methodology, and future directions in this research area. The assessment of social and built environment factors in relation to cancer is a relatively new field, with 82% of 34 reviewed papers published since 2010. Across the wide range of social and built environment exposures and cancer outcomes considered by the studies, numerous associations were reported. However, the directions and magnitudes of association varied, due in large part to the variation in cancer sites and outcomes being studied, but also likely due to differences in study populations, geographical region, and, importantly, choice of neighborhood measure and geographic scale. We recommend that future studies consider the life course implications of cancer incidence and survival, integrate secondary and self-report data, consider work neighborhood environments, and further develop analytical and statistical approaches appropriate to the geospatial and multilevel nature of the data. Incorporating social and built environment factors into research on cancer etiology and outcomes can provide insights into disease processes, identify vulnerable populations, and generate results with translational impact of relevance for interventionists and policy makers.
IntroductionBreast cancers are increasingly recognized as heterogeneous based on expression of receptors for estrogen (ER), progesterone (PR), and human epidermal growth factor receptor 2 (HER2). Triple-negative tumors (ER-/PR-/HER2-) have been reported to be more common among younger women, but occurrence of the spectrum of breast cancer subtypes in adolescent and young adult (AYA) women aged between 15 and 39 years is otherwise poorly understood.MethodsData regarding all 5,605 AYA breast cancers diagnosed in California during the period 2005 to 2009, including ER and PR status (referred to jointly as hormone receptor (HR) status) and HER2 status, was obtained from the population-based California Cancer Registry. Incidence rates were calculated by subtype (triple-negative; HR+/HER2-; HR+/HER2+; HR-/HER2+), and logistic regression was used to evaluate differences in subtype characteristics by age group.ResultsAYAs had higher proportions of HR+/HER2+, triple-negative and HR-/HER2+ breast cancer subtypes and higher proportions of patients of non-White race/ethnicity than did older women. AYAs also were more likely to be diagnosed with stage III/IV disease and high-grade tumors than were older women. Rates of HR+/HER2- and triple-negative subtypes in AYAs varied substantially by race/ethnicity.ConclusionsThe distribution of breast cancer subtypes among AYAs varies from that observed in older women, and varies further by race/ethnicity. Observed subtype distributions may explain the poorer breast cancer survival previously observed among AYAs.
Hair morphogenesis takes place through reciprocal epithelial and mesenchymal signaling; however, the mechanisms controlling signal exchange are poorly understood. Laminins are extracellular proteins that play critical roles in adhesion and signaling. Here we demonstrate the mechanism of how laminin-511 controls hair morphogenesis. Dermal papilla (DP) from laminin-511 mutants showed developmental defects by E16.5, including a failure to maintain expression of the key morphogen noggin. This maintenance was critical as exogenous introduction of noggin or sonic hedgehog (Shh) produced downstream from noggin was sufficient to restore hair follicle development in lama5 −/− (laminin-511-null) skin. Hair development required the 1 integrin binding but not the heparin binding domain of laminin-511. Previous studies demonstrated that Shh signaling requires primary cilia, microtubule-based signaling organelles. Laminin-511 mutant DP showed decreased length and structure of primary cilia in vitro and in vivo. Laminin-511, but not laminin-111, restored primary cilia formation in lama5 −/− mesenchyme and triggered noggin expression in an Shh-and PDGF-dependent manner. Inhibition of laminin-511 receptor 1 integrin disrupted DP primary cilia formation as well as hair development. These studies show that epithelial-derived laminin-511 is a critical early signal that directs ciliary function and DP maintenance as a requirement for hair follicle downgrowth.[Keywords: Laminin; primary cilium; basement membrane; integrin; hair] Supplemental material is available at http://www.genesdev.org.
Background Previous studies documented racial/ethnic and socioeconomic disparities in survival after Hodgkin lymphoma (HL) among adolescents and young adults (AYAs), but did not consider the influence of combined-modality treatment and health insurance. Methods Data for 9,353 AYA patients aged 15–39 when diagnosed with HL during 1988–2011 were obtained from the California Cancer Registry. Using multivariate Cox proportional hazards regression, we examined the impact of socio-demographic characteristics (race/ethnicity, neighborhood socioeconomic status (SES), and health insurance), initial combined-modality treatment, and subsequent cancers on survival. Results Over the 24-year study period, we observed improvements in HL-specific survival by diagnostic period and differences in survival by race/ethnicity, neighborhood SES and health insurance for a subset of more recently diagnosed patients (2001–2011). In multivariable analyses, HL-specific survival was worse for Blacks than Whites with early-stage (Hazard Ratio (HR): 1.68; 95% Confidence Interval (CI): 1.14, 2.49) and late-stage disease (HR: 1.68; 95% CI: 1.17, 2.41) and for Hispanics than Whites with late-stage disease (HR: 1.58; 95% CI: 1.22, 2.04). AYAs diagnosed with early-stage disease experienced worse survival if they also resided in lower SES neighborhoods (HR: 2.06; 95% CI: 1.59, 2.68). Furthermore, more recently diagnosed AYAs with public health insurance or who were uninsured experienced worse HL-specific survival (HR: 2.08; 95% CI: 1.52, 2.84). Conclusion Our findings identify several subgroups of HL patients at higher risk for HL mortality. Impact Identifying and reducing barriers to recommended treatment and surveillance in these AYAs at much higher risk of mortality is essential to ameliorating these survival disparities.
Both individual- and contextual-level SES influence overall survival of men with prostate cancer. Additional research is needed to identify the mechanisms underlying these robust associations.
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