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Review
. 2018 Sep 4;8(9):a030387.
doi: 10.1101/cshperspect.a030387.

Prostate Cancer Disparities by Race and Ethnicity: From Nucleotide to Neighborhood

Affiliations
Review

Prostate Cancer Disparities by Race and Ethnicity: From Nucleotide to Neighborhood

Timothy R Rebbeck. Cold Spring Harb Perspect Med. .

Abstract

Prostate cancer (CaP) incidence, morbidity, and mortality rates vary substantially by race and ethnicity, with African American men experiencing among the highest CaP rates in the world. The causes of these disparities are multifactorial and complex, and likely involve differences in access to screening and treatment, exposure to CaP risk factors, variation in genomic susceptibility, and other biological factors. To date, the proportion of CaP that can be explained by environmental exposures is small and differences in the role factors play by race or ethnicity is poorly understood. In the absence of additional data, it is likely that environmental factors do not contribute greatly to CaP disparities. In contrast, CaP has one of the highest heritabilities of all major cancers and many CaP susceptibility genes have been identified. Some CaP loci, including the risk loci found at chromosome 8q24, have consistent effects in all racial/ethnic groups studied to date. However, replication of many susceptibility loci across race or ethnicity remains limited. It is likely that inequities in health care access strongly influences CaP disparities. CaP is a disease with a complex multifactorial etiology, and therefore any approach attempting to address racial/ethnic disparities in CaP must consider the many sources that influence risk, outcomes, and disparities.

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Figures

Figure 1.
Figure 1.
Depiction of disparities across the continuum of prostate cancer (CaP) progression from high-grade prostatic intraepithelial neoplasia (HGPIN) to prevalent (autopsy-detected) CaP, to clinically detected CaP, and CaP mortality. Chart reflects the ratio of rates for African Americans (AAs) compared with European Americans (EAs). Potential biomarkers acting at each stage in this continuum are depicted below the chart. PIA, Polysaccharide intercellular adhesin; PIN, prostatic intraepitheilial neoplasia; PTEN, phosphatase and tensin homolog; AR, androgen receptor.
Figure 2.
Figure 2.
Ratio of African American (AA) versus European American (EA) mortality rates by age group and year.
Figure 3.
Figure 3.
Framework for the definition of factors that underlie self-identified race or ethnicity that may influence prostate cancer (CaP) etiology and disparities.

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