Background
Men of African descent experience a disproportionately high prostate cancer mortality. Intratumoral inflammation was found to be associated with aggressive prostate cancer. We and others have shown that prostate tumors in African-American (AA) patients harbor a distinct immune and inflammation signature when compared with European-American (EA) patients. These observations suggest that inflammation could be a driver of aggressive disease in men of African descent, leading to the hypothesis that an anti-inflammatory drug like aspirin could prevent disease progression.
Methods
We examined the relationship between aspirin use and prostate cancer in the NCI-Maryland Prostate Cancer Case-Control Study consisting of 823 men with incident prostate cancer (422 AA and 401 EA) and 1034 population-based men without the disease diagnosis (486 AA and 548 EA).
Results
We observed a significant inverse association between regular aspirin use and prostate cancer among AA men. Stratification of AA patients by disease stage showed that daily and long-term (> 3 years) aspirin use significantly decreased the risk of advanced disease (adjusted odds ratios for T3/T4 disease: 0.35, 95% CI: 0.17 to 0.73 and 0.22, 95% CI: 0.08 to 0.60, respectively), but not early-stage disease (T1/T2). Regular aspirin use also reduced disease recurrence in AA men.
Conclusions
Regular aspirin use is associated with a decreased risk of advanced stage prostate cancer and increased disease-free survival in AA men.
Impact
Regular aspirin use before and after a prostate cancer diagnosis may prevent the development of aggressive disease in AA men who are at risk of a lethal malignancy.
Purpose
We use data from a community sample followed from ages 8 to 48. We focus on the main and risk-buffering effects of childhood and adolescent protective factors for predicting adulthood violence (official records and self reports).
Method
Males (N=436) from the Columbia County Longitudinal Study participated. The youth, their parents, and peers were first interviewed when the youth were age 8; the youth were later interviewed at ages 19, 30, and 48.
Results
Risk factors for adulthood violence included higher aggression and lower family socioeconomic status at ages 8 and 19. Protective factors included anxiety about behaving aggressively (ages 8 and 19), popularity (ages 8 and 19), family church attendance (age 8), lower negative family interactions (age 8), and higher educational aspirations (age 19). For youth with at least one risk factor, the sum of adolescent—but not childhood--protective factors reduced the likelihood of adulthood violence. The most critical adolescent risk-buffering protective factors were anxiety about behaving aggressively and educational aspirations.
Conclusions
Aggression and low family SES, even by age 8, place youth at risk for adulthood violence. Interventions to strengthen critical protective factors must continue into late adolescence to reduce the likelihood of adulthood violence among at-risk youth.
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