br prostate cancer which might result in suboptimal cancer
prostate cancer, which might result in suboptimal cancer con-trol.14,15 An additional advantage of our analysis is that all patients were treated with RP, minimizing any potential confounding effect of differing treatment modalities.
The exact mechanisms underlying the link between low SES and advanced-stage prostate cancer are not entirely clear, although di-etary factors, obesity, environmental stressors, and differential screening practices/access to care have all been implicated.16-23 Previous studies have shown that chronic poverty can result in
4 - Clinical Genitourinary Cancer Month 2019
Samuel A. Weprin et al
Figure 1 (A) Postsurgical Cancer of the Prostate Risk Assessment (CAPRA-S) Risk Scores According to Income Quartile. (B) Rates of Adverse Pathology According to Income Quartile. CAPRA-S Scores and Rates of Adverse Pathology Are Inversely Associated With Income Level
food insecurity, ultimately resulting in overnutrition and obesity, a condition that might be further exacerbated by the lack of diversi-fied dietary choices in impoverished communities.22 Obesity, in turn, has been implicated in the development of high-grade tu-mors,17 as well as an increased risk of death from prostate cancer.24 Furthermore, low SES often results in chronic psychosocial stress, a condition thought to increase systemic beta-Nicotinamide and decrease immunity, conditions that might promote carcinogenesis.16,20 Finally, AA men in low-income communities might be less likely to undergo prostate cancer screening because of poor education, lack of access to health care, distrust of medical professionals, and beliefs regarding cancer fatalism.18,25 Although each of these factors likely contribute to the increased risk of aggressive cancers in impov-erished men, further study is clearly needed to elucidate the exact mechanisms linking poverty to advanced prostate cancer. Identifi-cation of these mechanisms might allow for targeted intervention in impoverished communities to decrease prostate cancer morbidity and mortality in these populations.
Figure 2 Scatterplot of Postsurgical Cancer of the Prostate Risk Assessment (CAPRA-S) Scores According to Income Level for Each Individual Patient; an Inverse Association Is Shown
Despite limited understanding of the mechanisms through which low SES increases the risk of adverse prostate cancers, there are clinical implications that can be gleaned from the current data. Our findings suggest that public health efforts to promote prostate cancer awareness and encourage prostate cancer screening might be especially beneficial in impoverished communities. Furthermore, tumors diagnosed in low SES individuals might be better managed with early, aggressive intervention as opposed to more conservative treatment modalities.
A primary limitation of our analysis is the use of census tract data as an estimate of median household income. Although previous studies have shown census tract data to correlate reasonably well with patient SES,8-10 census tract estimates are only a surrogate measure of individual household income. Furthermore, non-socioeconomic factors specific to a census tract could potentially influence prostate cancer severity. For example, a geographically isolated census tract with a paucity of health care facilities could result in more difficult access to care, delayed presentation of dis-ease, and inferior prostate cancer outcomes. As such, our findings linking low SES to adverse prostate cancer outcomes in AA men should be considered hypothesis-generating, and additional work is needed to confirm these findings.
Additional limitations include that we were unable to account for the effect of education level on the outcomes of interest. Low ed-ucation levels are common among men from socioeconomically disadvantaged neighborhoods and Lyon hypothesis lack of education likely works in concert with SES in predisposing patients to adverse prostate cancer outcomes.21,26 Because SES and education level are closely correlated, future study is needed to define the independent contribution of each of these factors in determining cancer-specific outcomes. Finally, this study used pathological outcomes as a proxy for the measurement of prostate cancer-specific mortality and longer follow-up is necessary before mortality data will be available in this cohort.