African Ancestry Gradient Is Associated with Lower Systemic F 2

Context. Low levels of systemic F2-isoprostanes (F2-IsoP) increase the risk of diabetes and weight gain and were found in African Americans. Low F2-IsoPs could reflect an unfavorable metabolic characteristic, namely, slow mitochondrial metabolism in individuals with African ancestry. Objective. To examine differences in plasma F2-IsoPs in three groups with a priori different proportion of African ancestry: non-Hispanic Whites (NHWs), US-born African Americans (AAs), and West African immigrants (WAI). Design. Cross-sectional study. Setting. Georgia residents recruited from church communities. Participants. 218 males and females 25–74 years of age, who are self-identified as NHW (n=83), AA (n=56), or WAI (n=79). Main Outcome Measure(s). Plasma F2-IsoPs quantified by gas chromatography-mass spectrometry. Results. After adjustment for age, gender, obesity, and other comorbidities, WAI had lower levels of plasma F2-IsoP than AA (beta-coefficient = −9.8, p<0.001) and AA had lower levels than NHW (beta-coefficient = −30.3, p<0.001). Similarly, among healthy nonobese participants, F2-IsoP levels were lowest among WAI, followed by AA, and the highest levels were among NHW. Conclusion. Plasma F2-IsoPs are inversely associated with African ancestry gradient. Additional studies are required to test whether optimization of systemic F2-IsoP levels can serve as means to improve race-specific lifestyle and pharmacological intervention targeted to obesity prevention and treatment

Influence of obesity-related risk factors in the aetiology of glioma

BACKGROUND: Obesity and related factors have been implicated as possible aetiological factors for the development of glioma in epidemiological observation studies. We used genetic markers in a Mendelian randomisation framework to examine whether obesity-related traits influence glioma risk. This methodology reduces bias from confounding and is not affected by reverse causation. METHODS: Genetic instruments were identified for 10 key obesity-related risk factors, and their association with glioma risk was evaluated using data from a genome-wide association study of 12,488 glioma patients and 18,169 controls. The estimated odds ratio of glioma associated with each of the genetically defined obesity-related traits was used to infer evidence for a causal relationship. RESULTS: No convincing association with glioma risk was seen for genetic instruments for body mass index, waist-to-hip ratio, lipids, type-2 diabetes, hyperglycaemia or insulin resistance. Similarly, we found no evidence to support a relationship between obesity-related traits with subtypes of glioma-glioblastoma (GBM) or non-GBM tumours. CONCLUSIONS: This study provides no evidence to implicate obesity-related factors as causes of glioma

Capturing emergency dispatch address points as geocoding candidates to quantify delimited confidence in residential geolocation

Abstract Background In response to citizens’ concerns about elevated cancer incidence in their locales, US CDC proposed publishing cancer incidence at sub-county scales. At these scales, confidence in patients’ residential geolocation becomes a key constraint of geospatial analysis. To support monitoring cancer incidence in sub-county areas, we presented summary metrics to numerically delimit confidence in residential geolocation. Results We defined a concept of Residential Address Discriminant Power (RADP) as theoretically perfect within all residential addresses and its practical application, i.e., using Emergency Dispatch (ED) Address Point Candidates of Equivalent Likelihood (CEL) to quantify Residential Geolocation Discriminant Power (RGDP) to approximate RADP. Leveraging different productivity of probabilistic, deterministic, and interactive geocoding record linkage, we simultaneously detected CEL for 5,807 cancer cases reported to North Carolina Central Cancer Registry (NC CCR)- in January 2022. Batch-match probabilistic and deterministic algorithms matched 86.0% cases to their unique ED address point candidates or a CEL, 4.4% to parcel site address, and 1.4% to street centerline. Interactively geocoded cases were 8.2%. To demonstrate differences in residential geolocation confidence between enumeration areas, we calculated sRGDP for cancer cases by county and assessed the existing uncertainty within the ED data, i.e., identified duplicate addresses (as CEL) for each ED address point in the 2014 version of the NC ED data and calculated ED_sRGDP by county. Both summary RGDP (sRGDP) (0.62–1.00) and ED_sRGDP (0.36–1.00) varied across counties and were lower in rural counties (p < 0.05); sRGDP correlated with ED_sRGDP (r = 0.42, p < 0.001). The discussion covered multiple conceptual and economic issues attendant to quantifying confidence in residential geolocation and presented a set of organizing principles for future work. Conclusions Our methodology produces simple metrics – sRGDP – to capture confidence in residential geolocation via leveraging ED address points as CEL. Two facts demonstrate the usefulness of sRGDP as area-based summary metrics: sRGDP variability between counties and the overall lower quality of residential geolocation in rural vs. urban counties. Low sRGDP for the cancer cases within the area of interest helps manage expectations for the uncertainty in cancer incidence data. By supplementing cancer incidence data with sRGDP and ED_sRGDP, CCRs can demonstrate transparency in geocoding success, which may help win citizen trust

Application of mutagen sensitivity assay in a glioma case-control study

Few risk factors for glioma have been identified other than ionizing radiation. The alkylating agent acrylamide is a compound found in both occupational and the general environment and identified as one of the forty known or suspected neurocarcinogens in animal models. The mutagen sensitivity assay (MSA) has been used to indirectly show reduced DNA repair capacity upon exposure to ionizing radiation in those with glioma compared to controls. In this study, MSA was used to assess its applicability to a glioma case-control study and to test the hypothesis that subjects with glioma may have lower DNA repair capacity after exposure to selected potential human neurocarcinogens (i.e. acrylamide), compared to controls. Approximately 50 case and 50 control subjects were identified from a clinic-based study that investigated environmental risk factors for glioma, who completed an exposure survey, and had frozen immortalized lymphocytes available. A total of 50 metaphase spreads were read and reported for each participant. The association of case-control status with MSA for acrylamide, i.e. breaks per spread, was examined by multivariable logistic regression models. The mean number of breaks per slide was similar between hospital-based controls and cases. In addition, case-control status or exposure categories were not associated with the number of breaks per spread. Although the MSA has been shown as a useful molecular epidemiology tool for identifying individuals at higher risk for cancer, our data do not support the hypothesis that glioma patients have reduced DNA repair capacity in response to exposure to acrylamide. Further research is needed before the MSA is utilized in large-scale epidemiological investigations of alkylating agents. Keywords: DNA repair, Assay interaction, Acrylamid

Distinctions in Breast Tumor Recurrence Patterns Post-Therapy among Racially Distinct Populations

<div><p>Background</p><p>Clinical studies have revealed a higher risk of breast tumor recurrence in African-American (AA) patients compared to European-American (EA) patients, contributing to the alarming inequality in clinical outcomes among the ethnic groups. However, distinctions in recurrence patterns upon receiving hormone, radiation, and/or chemotherapy between the races remain poorly characterized.</p><p>Methods</p><p>We compared patterns and rates (per 1000 cancer patients per 1 year) of recurrence following each form of treatment between AA (n = 1850) and EA breast cancer patients (n = 7931) from a cohort of patients (n = 10504) treated between 2005–2015 at Northside Hospital in Atlanta, GA.</p><p>Results</p><p>Among patients who received any combination of adjuvant therapy, AA displayed higher overall rates of recurrence than EA (p = 0.015; HR: 1.699; CI: 1.108–2.606). Furthermore, recurrence rates were higher in AA than EA among stage I (p = 0.031; HR: 1.736; CI: 1.052–2.864) and T1 classified patients (p = 0.003; HR: 2.009; CI: 1.263–3.197). Interestingly, among patients who received neoadjuvant chemotherapy, AA displayed higher rates of local recurrence than EA (p = 0.024; HR: 7.134; CI: 1.295–39.313).</p><p>Conclusion</p><p>Our analysis revealed higher incidence rates of recurrence in AA compared to EA among patients that received any combination of adjuvant therapy. Moreover, our data demonstrates an increased risk of tumor recurrence in AA than EA among patients diagnosed with minimally invasive disease. This is the first clinical study to suggest that neoadjuvant chemotherapy improves breast cancer recurrence rates and patterns in AA.</p></div

AA exhibit lower survival duration than EA among recurrent breast cancer patients.

<p>(<b>A</b>) Survival time from first recurrence episode until death was compared between AA and EA breast cancer patients. Log-rank analysis was conducted to determine statistical differences between the racial groups. AA exhibited a non-significant lower survival time than EA (p = 0.231). (<b>B</b>) The mean time (days) until death was compared between AA and EA breast cancer patients displaying distant recurrence. AA died notably sooner than EA patients (p = 0.015). A t-test was performed to determine significant differences between the racial groups.</p