Prostate cancer disproportionately affects racial and ethnic minority populations. Reasons for disparate outcomes among minority patients are multifaceted and complex, involving factors at the patient, provider, and system levels. Although advancements in our understanding of disease biology have led to novel therapeutics for men with advanced prostate cancer, including the introduction of biomarker-driven therapeutics, pivotal translational studies and clinical trials are underrepresented by minority populations. Despite attempts to bridge the disparities gap, there remains an unmet need to expand minority engagement and participation in clinical trials to better define the impact of therapy on efficacy outcomes, quality of life, and role of biomarkers in diverse patient populations. The IRONMAN registry (ClinicalTrials.gov identifier: NCT03151629 ), a global, prospective, population-based study, was borne from this unmet medical need to address persistent gaps in our knowledge of advanced prostate cancer. Through integrated collection of clinical outcomes, patient-reported outcomes, epidemiologic data, and biospecimens, IRONMAN has the goal of expanding our understanding of how and why prostate cancer outcomes differ by race and ethnicity. To this end, the Diversity Working Group of the IRONMAN registry has developed informed strategies for site selection, recruitment, engagement and retention, and trial design and eligibility criteria to ensure broad inclusion and needs awareness of minority participants. In concert with systematic strategies to tackle the complex levels of disparate care, our ultimate goal is to expand minority engagement in clinical research and bridge the disparities gap in prostate cancer care.
Background: Prenatal factors have been associated with risk of cancers later in life, although studies in men have largely been case–control and focused on birth size only. Methods: We used data from 5,845 men in the Health Professionals Follow-up Study (HPFS) to prospectively examine associations between several prenatal and perinatal factors and incident adult cancer risk. In 1994, mothers of participants reported information on characteristics and behaviors related to their pregnancy with their sons. We used multivariable Cox proportional hazards models to calculate HRs and 95% confidence intervals (CI) of associations between prenatal and perinatal risk factors and cancer risk. Results: During 20 years of follow-up, 1,228 incident cases of overall cancer were documented. Men with a birth weight of ≥4 kg had a 21% increased risk of overall cancer (HR, 1.21; 95% CI, 1.02–1.43) compared with those with a birth weight of 2.5 to 3.9 kg. Greater weight gain during pregnancy (>13.6 kg vs. 6.8–8.6 kg) was also associated with a higher risk of overall cancer (HR, 1.22; 95% CI, 1.02–1.46), and was stronger for men whose mothers had a prepregnancy BMI<21 kg/m2 (HR, 1.30; 95% CI, 1.00–1.67) compared with body mass index (BMI) ≥21 kg/m2 (HR, 1.14; 95% CI, 0.85–1.51). There was no association between maternal age and overall cancer risk. Conclusions: Higher birth weight and maternal weight gain are associated with increased cancer risk in adult men. Impact: Our findings support the hypothesis that the in utero environment plays a role in the etiology of cancer in middle and older adulthood.
Background: Racial disparities in prostate cancer incidence and mortality rates are considerable. We previously found in the Health Professionals Follow-up Study (HPFS) that African-American men had an 80% higher prostate cancer risk than White men. With 21 additional years of follow-up and four-fold increase in cases, we undertook a contemporary analysis of racial differences in prostate cancer incidence and mortality in HPFS. Methods: For 47,679 men, we estimated HRs and 95% confidence intervals (CI) for the association between race and risk of prostate cancer through 2016 using Cox proportional hazards regression. Multivariable models (mHR) were adjusted for lifestyle, diet, family history, and PSA screening collected on biennial questionnaires. Results: 6,909 prostate cancer cases were diagnosed in White, 89 in African-American, and 90 in Asian-American men. African-Americans had higher prostate cancer incidence (mHR = 1.31; 95% CI, 1.06–1.62) and mortality (mHR = 1.67; 95% CI, 1.00–2.78), and lower PSA screening prevalence than White men. The excess risk was greater in the pre-PSA screening era (HR = 1.68; 95% CI, 1.14–2.48) than the PSA screening era (HR = 1.20; 95% CI, 0.93–1.56). Asian-Americans had lower prostate cancer risk (mHR = 0.74; 95% CI, 0.60–0.92), but similar risk of fatal disease compared with white men. Conclusions: Racial differences in prostate cancer incidence and mortality in HPFS are not fully explained by differences in lifestyle, diet, family history, or PSA screening. Impact: Additional research is necessary to address the disproportionately higher rates of prostate cancer in African-American men.
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