CYP3A4-V, an A to G promoter variant associated with prostate cancer in African Americans, exhibits large differences in allele frequency between populations. Given that the African American population is genetically heterogeneous because of its African ancestry and subsequent admixture with European Americans, case-control studies with African Americans are highly susceptible to spurious associations. To test for association with prostate cancer, we genotyped CYP3A4-V in 1376 (2 N) chromosomes from prostate cancer patients and age- and ethnicity-matched controls representing African Americans, Nigerians, and European Americans. To detect population stratification among the African American samples, 10 unlinked genetic markers were genotyped. To correct for the stratification, the uncorrected association statistic was divided by the average of association statistics across the 10 unlinked markers. Sharp differences in CYP3A4-V frequencies were observed between Nigerian and European American controls (0.87 and 0.10, respectively; P<0.0001). African Americans were intermediate (0.66). An association uncorrected for stratification was observed between CYP3A4-V and prostate cancer in African Americans (P=0.007). A nominal association was also observed among European Americans (P=0.02) but not Nigerians. In addition, the unlinked genetic marker test provided strong evidence of population stratification among African Americans. Because of the high level of stratification, the corrected P-value was not significant (P=0.25). Follow-up studies on a larger dataset will be needed to confirm whether the association is indeed spurious; however, these results reveal the potential for confounding of association studies by using African Americans and the need for study designs that take into account substructure caused by differences in ancestral proportions between cases and controls.

OBJECTIVEData relating vitamin D status with indices of glucose homeostasis as manifested by A1C in the U.S. adult population are few.RESEARCH DESIGN AND METHODSWe examined the association between serum 25 hydroxyvitamin D [25(OH)D] and A1C levels in 9,773 adults (age ≥18 years old) participating in the 2003–2006 National Health and Nutrition Examination Survey. Multivariate linear regression analyzed the association after accounting for potential confounders.RESULTSSerum 25(OH)D levels were inversely associated with A1C levels in subjects age 35–74 years (P = 0.0045) and those who did not report a history of diabetes (P = 0.0282).CONCLUSIONSThese findings support a mechanistic link between serum vitamin D concentrations, glucose homeostasis, and the evolution of diabetes in a large segment of the U.S. adult population. Screening people with elevated A1C levels for vitamin D insufficiency should be considered.

SummaryThroughout biomedical research, there is growing interest in the use of ancestry informative markers (AIMs) to deconstruct racial categories into useful variables. Studies on recently admixed populations have shown significant population substructure due to differences in individual ancestry; however, few studies have examined Caribbean populations. Here we used a panel of 28 AIMs to examine the genetic ancestry of 298 individuals of African descent from the Caribbean islands of Jamaica, St. Thomas and Barbados. Differences in global admixture were observed, with Barbados having the highest level of West African ancestry (89.6% ± 2.0) and the lowest levels of European (10.2% ± 2.2) and Native American ancestry (0.2% ± 2.0), while Jamaica possessed the highest levels of European (12.4% ± 3.5) and Native American ancestry (3.2% ± 3.1). St. Thomas, USVI had ancestry levels quite similar to African Americans in continental U.S. (86.8% ± 2.2 West African, 10.6% ± 2.3 European, and 2.6% ± 2.1 Native American). Significant substructure was observed in the islands of Jamaica and St. Thomas but not Barbados (K=1), indicating that differences in population substructure exist across these three Caribbean islands. These differences likely stem from diverse colonial and historical experiences, and subsequent evolutionary processes. Most importantly, these differences may have significant ramifications for case-control studies of complex disease in Caribbean populations.

Background The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing the coronavirus disease 2019 (COVID-19) pandemic, has infected millions of people and caused hundreds of thousands of deaths. While COVID-19 has overwhelmed healthcare resources (e.g., healthcare personnel, testing resources, hospital beds, and ventilators) in a number of countries, limited research has been conducted to understand spatial accessibility of such resources. This study fills this gap by rapidly measuring the spatial accessibility of COVID-19 healthcare resources with a particular focus on Illinois, USA. Method The rapid measurement is achieved by resolving computational intensity of an enhanced two-step floating catchment area (E2SFCA) method through a parallel computing strategy based on cyberGIS (cyber geographic information science and systems). The E2SFCA has two major steps. First, it calculates a bed-to-population ratio for each hospital location. Second, it sums these ratios for residential locations where hospital locations overlap. Results The comparison of the spatial accessibility measures for COVID-19 patients to those of population at risk identifies which geographic areas need additional healthcare resources to improve access. The results also help delineate the areas that may face a COVID-19-induced shortage of healthcare resources. The Chicagoland, particularly the southern Chicago, shows an additional need for resources. This study also identified vulnerable population residing in the areas with low spatial accessibility in Chicago. Conclusion Rapidly measuring spatial accessibility of healthcare resources provides an improved understanding of how well the healthcare infrastructure is equipped to save people’s lives during the COVID-19 pandemic. The findings are relevant for policymakers and public health practitioners to allocate existing healthcare resources or distribute new resources for maximum access to health services.

BackgroundSelenium status is inversely associated with the incidence of prostate cancer. However, supplementation trials have not indicated a benefit of selenium supplementation in reducing cancer risk. Polymorphisms in the gene encoding selenoprotein 15 (SELENOF) are associated with cancer incidence/mortality and present disproportionately in African Americans. Relationships among the genotype of selenoproteins implicated in increased cancer risk, selenium status, and race with prostate cancer were investigated.MethodsTissue microarrays were used to assess SELENOF levels and cellular location in prostatic tissue. Sera and DNA from participants of the Chicago‐based Adiposity Study Cohort were used to quantify selenium levels and genotype frequencies of the genes for SELENOF and the selenium‐carrier protein selenoprotein P (SELENOP). Logistic regression models for dichotomous patient outcomes and regression models for continuous outcome were employed to identify both clinical, genetic, and biochemical characteristics that are associated with these outcomes.ResultsSELENOF is dramatically reduced in prostate cancer and lower in tumors derived from African American men as compared to tumors obtained from Caucasians. Differing frequency of SELENOF polymorphisms and lower selenium levels were observed in African Americans as compared to Caucasians. SELENOF genotypes were associated with higher histological tumor grade. A polymorphism in SELENOP was associated with recurrence and higher serum PSA.ConclusionsThese results indicate an interaction between selenium status and selenoprotein genotypes that may contribute to the disparity in prostate cancer incidence and outcome experienced by African Americans.

Background Social determinants of prostate cancer survival and their relation to racial/ethnic disparities thereof are poorly understood. We analyzed whether census tract-level socioeconomic status (SES) at diagnosis is a prognostic factor in men with prostate cancer and helps explain racial/ethnic disparities in survival. Methods We used a retrospective cohort of 833 African-American and white, non-Hispanic men diagnosed with prostate cancer at four Chicago-area medical centers between 1986 and 1990. Tract-level concentrated disadvantage (CD), a multi-dimensional area-based measure of SES, was calculated for each case using 1990 U.S. census data. Its association with prostate cancer-specific survival was measured using Cox proportional hazard models adjusted for case and tumor characteristics, treatment, and healthcare system (private sector vs. Veterans Administration [VA]). Results Tract-level CD associated with an increased risk of death from prostate cancer (highest vs. lowest quartile, hazard ratio [HR] = 2.37, p < .0001). However, the association was observed in the private sector and not in the VA (per 1 standard deviation [SD] increase, HR = 1.33, p < .0001 and HR = 0.93, p = .46, respectively). The multivariate HR for African Americans before and after accounting for tract-level CD was 1.30 (p = .0036) and 0.96 (p = .82), respectively. Conclusion Census tract-level SES is a social determinant of prostate-specific mortality and helps account for racial/ethnic disparities in survival. An equal-access healthcare system may moderate this association. Impact This study identifies a potential pathway for minimizing disparities in prostate cancer control. The findings need confirmation in a population-based study.

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This study evaluated how prostatic levels of antioxidants relate to plasma levels and self-reported usual dietary intake. Definition of these relations may aid in interpreting studies of antioxidant exposure and prostate cancer risk. Between July 1996 and April 1997, plasma and prostatic tissue levels of tocopherols, carotenoids, and retinol were measured in 47 men undergoing radical prostatectomy or transurethral prostatectomy at Loyola University Medical Center, Maywood, Illinois, and an affiliate hospital. Dietary intake was measured by using a 122-item version of the Block Health Habits and History Questionnaire, and correlations were assessed with Pearson's coefficients. Prostatic levels of tocopherols and carotenoids (but not retinol) were significantly correlated with plasma levels (r= 0.31-0.56, p < 0.05-0.0001); the strongest correlations were associated with lycopene, beta-carotene, and gamma-tocopherol (0.56, 0.54, and 0.52, respectively; p < 0.0001). Relative concentrations of tocopherols and carotenoids in prostate tissue were proportionate to those in plasma. No correlation between prostatic levels and reported dietary intake was observed (r = -0.09 to 0.16, p < not significant). Adjustment for energy intake, body mass index, and serum lipids did not impact these relations. These results suggest that plasma levels of tocopherols and carotenoids better reflect prostatic exposure than self-reported usual dietary intake.