Renal cell carcinoma (RCC) is one of the top 10 cancers in the United States. This study assessed RCC health disparities in American Indians/Alaska Natives (AIs/ANs) and Hispanic Americans (HAs) focusing on advanced-stage and mortality. RCC patients’ data were obtained from the National Cancer Database (NCDB) and Arizona Cancer Registry (ACR). Logistic and Cox regression analyses were performed to ascertain the effect of race/ethnicity on stage and mortality, adjusting for neighborhood socioeconomic factors, rural/urban residence pattern, and other factors. In both data sets, AIs/ANs had significantly increased odds of advanced-stage RCC in the unadjusted model, but not in adjusted models. Mexican Americans had higher odds of advanced-stage compared to non-Hispanic Whites in NCDB (OR 1.22, 95% CI: 1.11–1.35) and ACR (OR 2.02, 95% CI: 1.58–2.58), even after adjusting for neighborhood characteristics. AIs/ANs did not show increased mortality risk in NCDB after adjusting for neighborhood characteristics, while the association remained significant in ACR (HR 1.33, 95% CI: 1.03–1.72). The great risk of all-cause and RCC-specific mortality was observed in U.S.-born Mexican Americans in Arizona (HR 3.21, 95% CI: 2.61–3.98 and sub-distribution HR 2.79, 95% CI: 2.05–3.81). RCC disparities in AIs/ANs is partially explained by neighborhood factors, but not in HAs.
The objective of this article is to call for integrating biological pathways of social experiences in the concept model of cancer disparities and social determinants of health (SDH) fields. Black, Indigenous, and People of Color (BIPOC) populations experience more negative outcomes across the cancer continuum. Social conditions are instrumental in better understanding the contemporary and historical constructs that create these patterns of disparities. There is an equally important body of evidence that points to the ways that social conditions shape biological pathways. To date, these areas of research are, for the most part, separate. This paper calls for a bridging of these two areas of research to create new directions for the field of cancer disparities. We discuss inflammation, epigenetic changes, co-morbidities, and early onset as examples of the biological consequences of social conditions that BIPOC populations experience throughout their lifespan that may contribute to disproportionate tumorigenesis and tumor progression.
Introduction: Breast cancer continues to be the leading form of cancer among women in the United States. Additionally, disparities across the breast cancer continuum continue to increase for women of historically marginalized populations. The mechanism driving these trends are unclear, however, accelerated biological age may provide key insights into better understanding these disease patterns. Accelerated age measured by DNA methylation using epigenetic clocks is to date the most robust method for estimating accelerated age. Here we synthesize the existing evidence on epigenetic clocks measurement of DNA methylation based accelerated age and breast cancer outcomes.Methods: Our database searches were conducted from January 2022 to April 2022 and yielded a total of 2,908 articles for consideration. We implemented methods derived from guidance of the PROSPERO Scoping Review Protocol to assess articles in the PubMed database on epigenetic clocks and breast cancer risk.Results: Five articles were deemed appropriate for inclusion in this review. Ten epigenetic clocks were used across the five articles demonstrating statistically significant results for breast cancer risk. DNA methylation accelerated age varied by sample type. The studies did not consider social factors or epidemiological risk factors. The studies lacked representation of ancestrally diverse populations.Discussion: DNA methylation based accelerated age as captured by epigenetic clocks has a statistically significant associative relationship with breast cancer risk, however, important social factors that contribute to patterns of methylation were not comprehensively considered in the available literature. More research is needed on DNA methylation based accelerated age across the lifespan including during menopausal transition and in diverse populations. This review demonstrates that DNA methylation accelerated age may provide key insights for tackling increasing rates of U.S. breast cancer incidence and overall disease disparities experienced by women from minoritized backgrounds.
Background: Obesity, classified by body mass index (BMI), is associated with higher postmenopausal breast cancer (BCa) risk. Yet, the associations between abdominal visceral (VAT) and subcutaneous adipose tissue (SAT) with BCa are unclear. Methods: We assessed BCa associations with abdominal VAT and SAT in a prospective cohort of postmenopausal women without a history of cancer and with 27 years follow-up (N = 9950), during which all new cancers were adjudicated. Dual-energy x-ray absorptiometry scans assessed adiposity at baseline, year 3, and year 6. Competing-risks multivariable sub-hazard ratios (SHR), with adjustments for sociodemographic, behavioral, reproductive, and anthropometric characteristics, were estimated for baseline and time-dependent associations between VAT, SAT, and incident BCa. Results: Participants averaged 63.3 ± 7.4 years of age and a BMI of 28.20 ± 5.72 kg/m2 at baseline. The models included 738 incident BCa case patients (N = 593 invasive; N = 145 in situ). Baseline VAT and SAT area were associated with statistically significantly increased BCa risk, by 36% and 19%, respectively. Increasing VAT/SAT ratio was associated with an 8% increase in incident BCa. Time-dependent models produced similar results. VAT and VAT/SAT associated BCa risk was highest for African American/Black women, although not statistically significantly different from other groups. Quartiles (Q) of VAT/SAT were also explored; the SHR for Q4 compared with Q1 was 1.49 (95% CI = 1.18 to 1.87). Conclusion: Higher abdominal VAT and SAT are associated with an increased risk of postmenopausal BCa, and VAT/SAT may provide a distinctive risk estimate. Potential racial and ethnic differences require replication in a larger sample (Women’s Health Initiative; NCT00000611; https://clinicaltrials.gov/study/NCT00000611).
American Indians/Alaska Natives (AI/AN) and Hispanic Americans (HA) have higher kidney cancer incidence and mortality rates compared to non-Hispanic Whites (NHW). Herein, we describe the disparity in renal cell carcinoma (RCC) surgical treatment for AI/AN and HA and the potential association with mortality in Arizona. A total of 5111 stage I RCC cases diagnosed between 2007 and 2016 from the Arizona Cancer Registry were included. Statistical analyses were performed to test the association of race/ethnicity with surgical treatment pattern and overall mortality, adjusting for patients’ demographic, healthcare access, and socioeconomic factors. AI/AN were diagnosed 6 years younger than NHW and were more likely to receive radical rather than partial nephrectomy (OR 1.49 95% CI: 1.07–2.07) compared to NHW. Mexican Americans had increased odds of not undergoing surgical treatment (OR 1.66, 95% CI: 1.08–2.53). Analysis showed that not undergoing surgical treatment and undergoing radical nephrectomy were statistically significantly associated with higher overall mortality (HR 1.82 95% CI: 1.21–2.76 and HR 1.59 95% CI: 1.30–1.95 respectively). Mexican Americans, particularly U.S.-born Mexican Americans, had an increased risk for overall mortality and RCC-specific mortality even after adjusting for neighborhood socioeconomic factors and surgical treatment patterns. Although statistically not significant after adjusting for neighborhood-level socioeconomic factors and surgical treatment patterns, AI/AN had an elevated risk of mortality.