Highlights of This Issue

Abstract

African Americans (AAs) experience higher incidence and mortality of lung cancer compared with European Americans (EAs). Inflammation, which is associated with lung cancer, differs between AAs and EAs. Erickson and colleagues investigated whether the anti-inflammatory drug aspirin was associated with lung cancer risk and survival using data from the NCI-Maryland Case-Control Study. The study found aspirin use to be associated with a lower risk of non–small cell lung cancer among men only and provide evidence that the relationship between aspirin and lung cancer risk is confounded by body mass index. The study also found aspirin use to be associated with improved survival, but only among AAs. Aspirin use could be considered in chemoprevention among men and AAs.Using algorithms applied to electronic health record (EHR) and tumor registry data, this study by Pruitt and colleagues identified missed opportunities for cervical cancer prevention among diverse, under-insured, and uninsured women seen at an urban, integrated safety-net healthcare system. Analysis of clinical care pathways demonstrated multiple time points in the screening process to improve delivery of services. Other healthcare systems should harness their EHR data to conduct similar algorithm-driven analyses that can guide selection of evidence-based interventions for cervical cancer prevention.Circulating IGFBP-3 has been associated with prostate cancer (PCa) and preclinical studies have found that vitamin D regulates IGFBP-3 expression. Timpson and colleagues used a combination of observational and Mendelian randomization analyses to reassess relationships between IGFBP-3 and PCa and between inactive vitamin D(25(OH)D) and IGFBP-3. The study confirms IGFBP-3 as a risk factor for PCa but suggests that circulating inactive vitamin D (25(OH)D) is unlikely to be causally related to IGFBP-3. Findings do not preclude associations between 25(OH)D and IGFBP-3 in cancer tissues but urge a need for causal evidence if supplementation is to be justified at a population scale.Aspirin use has been associated with ovarian cancer risk, but the mechanism underlying this association remains unknown. Barnard and colleagues hypothesized that the mechanism may be the downregulation of prostaglandin synthesis and subsequent alteration of immune function. The authors estimated odds ratios for aspirin and nonaspirin nonsteroidal anti-inflammatory drugs and risk of ovarian cancer by high versus low expression of prostaglandin-related markers and tumor associated macrophage (TAM) markers. The study did not observe heterogeneity by prostaglandin-related markers but observed substantial differences by TAM infiltration. Future work should consider prostaglandin-independent mechanisms for the association between aspirin and ovarian cancer risk, including immune mechanisms.