Self-reported Black Race Predicts Significant Prostate Cancer Independent of Clinical Setting and Clinical and Socioeconomic Risk Factors

Abstract

INTRODUCTION AND OBJECTIVE:

Studies have linked Black race to prostate cancer (PCa) risk but most fail to account for established risk factors such as 5-ARI use, prostate volume, socioeconomic status, and hospital setting. We assess whether Black race remains associated with PCa and Gleason ≥3+4 PCa, after adjusting for clinical setting and socioeconomic and clinical factors at prostate biopsy, with a focus on men aged 40–54 years, who may be excluded from current screening guidelines.

METHODS:

We recruited 564 men age 40–79 undergoing initial prostate biopsy for abnormal PSA or digital rectal examination (DRE) from three publicly funded and two private hospitals from 2009–2014. Univariate and multivariate analyses examined the associations between hospital type, race, West African Ancestry (WAA), clinical and sociodemographic risk factors with PCa diagnosis and Gleason ≥3+4 PCa. Given changes in PCa screening recommendations, we also assess the multivariate analyses for men age 40–54.

RESULTS:

Black and White men had similar age, BMI and prostate volume. Black men had higher PSA (8.10 ng/mL vs. 5.63 ng/mL) and PSA density (0.22 ng/mL/cm³ vs. 0.15 ng/mL/cm³, all p<0.001). Blacks had higher frequency of PCa (63.1% vs. 41.5%, p<0.001) and Gleason ≥3+4 PCa relative to Whites in both public (27.7% vs 11.6%, p<0.001) and private (48.4% vs 21.6%, p=0.002) settings. In models adjusted for age, first degree family history, prostate volume, 5-ARI use, hospital type, income, marital and educational status, Black race was independently associated with overall PCa diagnosis (OR =2.13, p =0.002). There was a significant multiplicative interaction with Black race and abnormal DRE for Gleason ≥3+4 PCa (OR =2.93, p =0.01). WAA was not predictive of overall or significant PCa among Black men. Black race (OR 5.66, p=0.02) and family history (OR 4.98, p=0.01) were independently positively associated with overall PCa diagnosis for men aged 40 to 54.

CONCLUSIONS:

Black race is independently associated with PCa and Gleason ≥3+4 PCa after accounting for clinical and socioeconomic risk factors including clinical setting and WAA, and has a higher odds ratio of PCa diagnosis in younger men. Further investigation into optimizing screening in Black men aged 40 to 54 is warranted.

Introduction:

In 2017, 161,360 estimated cases of prostate cancer (PCa) were diagnosed in the United States.[1] Men of high genetic West African ancestry face disparities in PCa incidence worldwide. As a corollary, several studies have demonstrated that US Black men have increased risk of PCa diagnosis on prostate biopsy relative to White men.[2] It is unclear whether this is predominantly attributable to socioeconomic or biologic factors.[3, 4]

Many have hypothesized that increased risk at biopsy is driven by poor access to care. To address this, a study in an equal access VA medical center showed that Black race is associated with PCa risk and higher grade PCa in men undergoing prostate biopsy, but could not account for socioeconomic factors.[5] In fact, several analyses that identify Black race as a biopsy risk factor are limited to clinical factors. [6–11] Yet, Black race is a social construct mirroring the interaction between genetics, clinical and non-clinical environmental factors. The inclusion of Black race in predictive risk calculators treats men of West African ancestry monolithically. Genetic West African ancestry, however, is heterogeneous, quantifiable and could hypothetically provide better prediction of PCa risk compared to self-reported race.

Given recent updates to screening guidelines that do not address screening in Black men,[12] our objectives are to determine if Black race remains an independent predictor of overall and clinically significant PCa on biopsy when adjusting for several established individual-level socioeconomic and biological factors. Secondarily we examine whether the adjusted association between PCa diagnosis and Black race is modified by younger age (40–54 years), and if genetic West African ancestry is associated with increased PCa diagnosis among self-reported Black men.

Materials and Methods:

Patient recruitment

Following institutional review board approval, 940 consecutive men, age 40–79 presenting for biopsy for abnormal PSA or DRE were approached for an epidemiologic study evaluating the association between vitamin D status and prostate biopsy outcomes from 2009–2014.[13] Of this group, 21 men did not undergo biopsy, 355 were excluded because less than 10 cores were obtained (n=341) or for diagnosis of atypical small acinar proliferation (n=14). The remaining 564 participants were recruited from two private academic and three public (County, State and Veterans Administration) medical centers to ensure a socioeconomically and racially diverse sample.

All participants self-identified their race/ethnicity. We categorized men as non-Hispanic Black and non-Black since incidence rates of PCa are similar between US non-Hispanic Whites, Asians and Hispanics.[1] Overall, 287 Black and 277 non-Black men underwent initial prostate biopsy for elevated PSA, PSA velocity or suspicious digital rectal exam (DRE). Genetic West African ancestry was estimated from whole blood samples using a panel of 105 ancestry informative markers (AIMs).

Self-administered questionnaires confirmed demographic and medical history. [14] Histologicdiagnosis, DRE, and imaging reports were abstracted from electronic health records to determine disease stage according to American Joint Committee on Cancer TNM (tumor, node, metastasis) staging system.[15] Gleason grading was performed using 2005 ISUP Consensus guidelines.[16] The 2014 guidelines which converted more Gleason 3+3 to 3+4 were employed as early as 2013 at the academic medical centers. Clinically significant PCa was defined as Gleason ≥3+4.[17]

Prostate specific antigen was measured with a monoclonal radioimmunoassay (Hybritech, Inc., San Diego, CA) prior to prostatic manipulation/biopsy at each site. Prostate volume was estimated with transrectal ultrasonography using the prolate ellipsoid formula.[18]

Statistical Analysis

Self-reported race is a proxy for shared genetic and environmental factors which may interact to affect risk among patient groups. Commonly, environment includes diet, substance use, socioeconomic, demographic and neighborhood conditions, health seeking behaviors, and access to care. Demographic risk factors included self-reported race, age and marital status (married/living-as-married versus other statuses). Behavioral risk factors included alcohol (>10 beverages/week regularly) and cigarette smoking (>100 cigarettes/week ever). Socioeconomic risk factors included post-secondary education completion, annual household income in US dollars, and poverty (<$30,000/year annual income). Clinical setting was coded as public (County, State and VA) or private (academic centers).

Clinical risk factors included age, PSA, PSA density, prostate volume, BMI, PCa family history, suspicious digital rectal exam (DRE), 5-alpha-reductase inhibitor (ARI) use, and benign prostatic hyperplasia/lower urinary tract symptoms (BPH/LUTS) diagnosis. Genetic West African ancestry was included as a potential risk factor based on increased PCa incidence and mortality in men of West African ancestry (WAA). Percent WAA was coded on a continuous scale from 0–100% and converted to quartiles.

Student’s t-tests or Mann-Whitney U-tests were performed for continuous variables and χ² tests for categorical variables. For multivariate analyses, the main outcomes were overall and clinically significant (Gleason ≥3+4) PCa.[17]

We evaluated the risk of overall and Gleason ≥3+4 PCa in multivariable logistic regression models adjusted for several of the aforementioned risk factors using −2 log likelihood scores to maximize model fit. Covariates were excluded from final models for collinearity or p>0.15. Statistical analysis were two-sided with α=0.05 and performed using SPSS 24 (IBM Corporation 2016).

Results:

Patient Characteristics

Of 564 participants, 287 (50.9%) were non-Hispanic Black, 168 (29.8%) were non- Hispanic White, 82 (14.5%) were Hispanic, and 27 (4.8%) were from other racial groups. Blacks and non-Blacks had comparable median age (61.0 vs. 62.0 years, p=0.34) and BMI (27.5 vs. 27.1 kg/m², p=0.21) (Table 1). PSA (8.10 vs. 5.63 ng/mL, p<0.001) and PSA density (0.22 vs. 0.15 ng/mL/cm³, p<0.001) were higher in Blacks. Blacks had lower frequency of marriage (39.0% vs 72.2%, p<0.001) and were more

Table 1:

Demographic, clinical information and biopsy outcomes stratified by race

Continuous Variables	Black (N = 287)	Non-Black (N = 277)	p Value1
	Median [IQR]	Median [IQR]
Age, years	61.00 (56.00−66.00)	62.00 (57.00−66.00)	0.34
Body Mass Index, kg/m2	27.5 (24.4−31.7)	27.1 (24.4−29.8)	0.21
2Serum PSA, ng/mL	8.10 (5.60−16.10)	5.63 (4.20−10.00)	<0.001
Prostate volume, cm3	41.4 (30.0−59.0)	42.4 (28.6−62.1)	0.71
PSA density, ng/mL/cm3	0.22 (0.13−0.48)	0.15 (0.09−0.24)	<0.001
Free PSA, %	11.0 (8.4−20.4)	16.0 (9.5−21.3)	0.17
West African Ancestry, %	80.4 (70.4−86.4)	4.7(2.3−7.8)	<0.001
Annual Income (×1000)	$20 ($10−$30)	$30 ($10−$40)	<0.001
Categorical Variables	Black (N = 287 )	Non-Black (N = 277 )	p Value3
	N (%)	N (%)
Recruitment Site
· Cook County4	235 (81.9)	131 (47.3)	<0.001
· JBVAMC4	16 (5.6)	6 (2.1)
· UIC4	5 (1.7)	1 (0.4)
· Northwestern5	27 (9.4)	131 (47.3)
· U of Chicago5	4 (1.4)	8 (2.9)
Clinical Risk Factors
Abnormal DRE	95 (33.1)	85 (30.7)	0.56
Family History	45 (15.7)	61 (22.0)	0.05
5-ARI use (current)	33 (11.5)	34 (12.3)	0.78
History of Clinical BPH	106 (36.9)	126 (45.5)	0.04
Substance Use History
Alcohol use (>10 drinks per week regularly)	241 (84.0)	235 (84.8)|	0.69
Tobacco use (ever, >100cigs)	186 (64.8)	155 (56.0)	0.04
Sociodemographic Factors
High School Completed	116 (40.4)	159 (57.4)	<0.001
Married	112 (39.0)	200 (72.2)	<0.001

¹Using Mann-Whitney U-tests;

²PSA was doubled for 5-a-reductase inhibitor use;

³Using χ2 tests;

⁴bold type indicates p <0.05; Publicly funded sites;

⁵Privately funded sites

likely to be recruited from public hospitals (89.2% vs. 51.3% private, p<0.001). Rates of abnormal DRE and first-degree family history of PCa did not differ significantly between both groups (both p>0.05). Non-Blacks were more likely to have a BPH/LUTS diagnosis (45.5% vs. 36.9%, p=0.04) and less likely to have smoked (56.0% vs. 64.8%, p=0.04). There was no difference in alcohol use (p=0.69).

Sociodemographic Factors

Black men had lower socioeconomic status given lower post-secondary degree completion (40.4% vs. 57.4%, p<0.001), income (median $20k/yr vs. $30k/yr, p<0.001), and higher poverty (61.7% vs. 43.3%, p<0.001). However, within public sites, non- Blacks had higher frequency of poverty (84.0% vs. 65.0%, p<0.001) and tended towards decreased post-secondary degree completion (32.4% vs. 37.5%, p=0.31).

Prostate Biopsy and Cancer Outcomes

Blacks had higher frequency of overall PCa (63.1% vs. 43.5%, p<0.001), Gleason ≥3+4 (47.5% vs. 40.0%, p<0.001) and Gleason ≥4+4 disease (14.4% vs 9.6%, p=0.02; Table 2). Black men with PCa had higher clinical TNM tumor staging (p=0.01) and higher frequency of NCCN risk stratification ≥High (p=0.047).

Table 2:

Characteristics of biopsy outcomes and prostate cancer cases stratified by race

	Black	Non-Black
	(N =287)	(N =277)	p value1
	N (%)	N (%)
Biopsy Outcomes
Cancer on Biopsy	181 (63.1)	115 (41.5)	<0.001
≥ Gleason 3+4	86 (47.5)	46 (40.0)	<0.001
≥ Gleason 4+4	26 (14.4)	11 (9.6)	0.02
	Black cancer cases	Non-Black cancer cases	p value2
	(N =181)	(N =115)	-
	N (%)	N (%)	-
Clinical TNM Stage
T1c (N0/x, M0/x)	107 (59.1)	74 (64.3)	0.01
T2a (N0/x, M0/x)	26 (14.4)	18 (15.6)
T2b/c (N0/x, M0/x)	29 (16.0)	16 (13.9)
T3a (N0/x, M0/x)	2 (1.1)	1 (0.9)
T3b (N0/x, M0/x)	1 (0.6)	1 (0.9)
T4 (N0/x, M0/x)	1 (0.6)	0 (0)
N1	6 (3.3)	2 (1.7)
M1	14 (7.7)	4 (3.5)
NCCN Risk Strata
Very Low/Low	67 (37.0)	48 (41.7)	0.047
Intermediate	56 (30.9)	45 (39.1)
High/Very High/Metastatic	58 (32.0)	22 (19.1)
Prostate Biopsy Cores	Median (IQR)	Median (IQR)
Positive Cores	4.5 (2–8)	3 (2–6)	0.01
% Positive Cores	41.7 (16.7–66.7)	25.0(16.7 −50.0)	0.01

Note: TNM = Tumor, Node, Metastasis Staging System; NCCN = 2016 National Comprehensive Cancer Network prostate cancer Guidelines;

¹Using χ² test;

²Using Mann-Whitney U-test;

³bold type indicates p <0.05

Comparison of Prostate Biopsy Outcomes by Race, Stratified by Clinical Setting

Blacks had increased rates of Gleason ≥3+4 PCa relative to non-Blacks in both public (27.7% vs. 11.6%, p<0.001) and private (48.4% vs. 21.6%, p=0.002) settings. There was a significant positive association between Black race and NCCN ≥High-risk PCa in the private sites (40.9%) relative to non-Blacks (14.8%, p=0.01). Notably, private hospital patients were diagnosed with more Gleason ≥3+4 PCa than patients at public sites. This was significant among Blacks (48.4% vs. 27.7%, p=0.02) and non-Blacks (21.6% vs. 11.6%, p=0.03).

Overall PCa vs. Negative Biopsy

Multivariable logistic regressions for PCa vs. negative biopsy were adjusted for the aforementioned covariates from Table 1. Black race (OR 2.13, p=0.002), first-degree family history (OR 1.74, p=0.02), age (OR 1.04, p=0.02), and log_10-PSA (OR 4.32, p<0.001) were positively associated with PCa diagnosis. Prostate volume (OR 0.98, p<0.001), 5-ARI use (OR 0.38, p=0.004) and public site (OR 0.53, p=0.04) exhibited significant inverse associations with PCa diagnosis.

In post-hoc analysis, genetic WAA was not predictive of overall PCa diagnosis among Black men both as a continuous variable and in quartiles (all p>0.05).

Gleason ≥3+4 PCa vs. Gleason 3+3/Neqative Biopsy

For logistic regressions with Gleason ≥3+4 PCa as the outcome, Black race and abnormal DRE interact (OR 2.93, p=0.01) synergistically (Table 3). Age (OR 1.05, p=0.02), log₁₀-PSA (OR 13.09, p<0.001) and public site (OR 0.29, p=0.001) significantly predicted Gleason ≥3+4 PCa. Prostate volume (OR 0.98, p<0.001) and 5-ARI use (OR 0.32, p=0.02) were significantly inversely associated with Gleason ≥3+4 PCa.

Table 3:

Binary logistic regressions for Black race versus overall prostate cancer and Gleason ≥3+4 prostate cancer diagnosis

Multivariable Logistic Regression for Cancer on Biopsy vs. Negative Biopsy			Multivariable Logistic Regression for Gleason ≥3+4 Prostate Ca vs. Gleason 3+3/Negative Biopsy
Covariates	Odds Ratio (95% C.l.)	p value	Covariates	Odds Ratio (95% C.l.)	p value
Black race	2.13 (1.33–3.40)	0.002	Black race X Abnormal DRE	2.93 (1.31–6.53)	0.009
Abnormal DRE (yes)	1.14 (0.74–1.76)	0.57	Black race X Normal DREa	1.14 (0.56–2.32)	0.72
-	-	-	Non-Black race X Abnormal DREa	0.86 (0.39–1.94)	0.72
-	-	-	Non-Black race X Normal DREa (ref)	1	-
1st degree Fam Hx (yes)	1.74 (1.07–2.83)	0.02	1st degree Fam Hx (yes)	1.48 (0.86–2.56)	0.16
Age, years	1.04 (1.01–1.07)	0.02	Age, years	1.05 (1.01–1.08)	0.02
Log(PSA), ng/ml	4.32 (2.29–8.14)	<0.001	Log(PSA), ng/ml	13.09 (6.06–28.27)	<0.001
Publicly funded site (yes)	0.53 (0.28–0.98)	0.04	Publicly funded site (yes)	0.29 (0.14–0.60)	0.001
High School completion (yes)	1.17 (0.74–1.84)	0.49	High School completion (yes)	0.84 (0.48–1.48)	0.55
Prostate volume, cm3	0.98 (0.97–0.99)	<0.001	Prostate volume, cm3	0.98 (0.97–0.99)	<0.001
5-ARI use (yes, ≥6 months)	0.38 (0.19–0.74)	0.004	5-ARI use (yes, ≥6 months)	0.32 (0.12–0.85)	0.02
Married (yes)	0.86 (0.56–1.33)	0.81	Married (yes)	0.61 (0.36–1.03)	0.06
Annual Income < $30K/year	1.1 (0.67–1.78)	0.72	Annual Income < $30K/year	1.15 (0.64–2.06)	0.63

Note: Bolded variables have a p-value < 0.05.

Abnormal DRE had a stronger association with Gleason ≥3+4 PCa among Blacks. Black men with abnormal DREs had ~2.5x the frequency of Gleason ≥3+4 PCa compared to non-Black men (49.5% vs. 18.8%, Figure 1).Again in analyses limited to self-reported Blacks, percent WAA coded as a continuous variable and WAA quartiles were not predictive of Gleason ≥3+4 PCa among Blacks (all p>0.05).

Figure 1:

Race and abnormal rectal examination and frequency of Gleason ≥3+4 prostate cancer.

PCa on Biopsy for Men Aged <55

Adjusted multivariable logistic regressions for PCa vs. negative biopsy were stratified by age <55 years. Black race (OR 5.66, 95% Cl:1.38–23.16, p=0.02), family history (OR 4.98, 95% CI:1.39–17.87, p=0.01, and log10-PSA (OR 7.12, 95% CI:1.29–39.2, p=0.02)were independently associated with overall PCa diagnosis for men aged 40–54. For men ≥55 years, Black race (OR 2.18, p=0.001) and log₁₀-PSA (OR 2.36, p=0.002) were independently associated with overall PCa. Family history was not significant (OR 1.43, p=0.16).

Discussion:

It remains unclear why PCa is more common and more lethal among Black men compared to non-Black counterparts. Black race remains independently associated with overall and Gleason ≥3+4 PCa after accounting for clinical setting, socioeconomic and clinical factors at time of prostate biopsy, and has a higher effect estimate for men under 55. Although self-reported Black race is correlated with PCa risk and degree of WAA, genetic WAA was not associated with PCa diagnosis among Blacks. Notable features of our study include substantial recruitment from publicly funded hospitals (69.9%) and socioeconomic diversity within Black and non-Black groups, allowing for more comprehensive assessment of the influence of healthcare access, marriage, education and income.[8, 10]

Few studies have demonstrated the effect of Black race on initial prostate biopsy outcome while comprehensively accounting for both socioeconomic and clinical risk factors. One study found that Black race was not associated with increased PCa risk after adjusting for literacy,[19] but was likely underpowered (n=212) and did not include individual-level socioeconomic factors. Gaines et al demonstrated increased odds of PCa on biopsy among Black men in an equal-access healthcare system, however, failed to control for sociodemographic variables and 5-ARI use.[5]

Our study corroborates the negative associations of marriage with PCa diagnosis on univariate analysis,[20] however it was not significant in multivariate models. For unmarried men, patient navigation and a medical home model may be beneficial. Similarly, 5-ARI use had negative associations with PCa diagnosis on both univariate and multivariate models. [21, 22] Given the over-representation of Black men in our cohort, 5-ARI chemoprevention trials may be of benefit in Black men given their increased odds of overall and clinically significant PCa.

A prevailing mantra has been that disparate prostate biopsy outcomes among Blacks are driven by poor health care access. Although healthcare access may contribute to health disparities, we find that rates of overall and Gleason ≥3+4 PCa on biopsy are higher for Blacks in both public and private sites. Understandably, treatment at a public site may not reflect barriers to access and could be a result of patient preference. Still, univariate analysis (data not shown) revealed that in public sites, Black race was positively associated with Gleason ≥3+4 PCa, despite the fact that non-Blacks in public hospitals were more socioeconomically disadvantaged than Blacks (poverty 84.0% vs. 65.0%, p<0.001). This suggests that socioeconomics and clinical setting alone cannot explain racial disparities in PCa incidence. To adjust for the impact of marked delays in care in our multivariable regressions, we limited serum PSA to <10ng/ml and found similar associations between Gleason ≥3+4 and Black race (OR 2.50, p=0.01), public site (OR 0.22, p<0.001), logi₁₀-PSA (OR 5.93, p=0.02), abnormal DRE (OR 1.72, p=0.09) and family history (OR 1.91, p=0.046).

While different SES and clinical factors may explain racial disparities in prostate cancer risk, it is increasingly recognized that these disparities also have a molecular basis.

Racial differences have been found in the frequency of risk alleles and specifically of; variants in genes regulating androgen biosynthesis and metabolism. Altered expression of growth factors, inflammatory and apoptotic genes, and ethnic variation in the frequency of alleles that may be associated with PCa risk have also been implicated.[23, 24]

Ancestry informative markers are increasingly utilized to quantify the dynamics of risk and disease prevalence between genetically and ethnically distinct populations.

Because men of West African ancestry have the highest PCa incidence and mortality rates globally, genetic WAA could hypothetically predict PCa diagnosis among American Blacks. On multivariate analysis of overall and Gleason ≥3+4 PCa diagnosis, WAA was not independently associated with cancer among Black men. However, it is known that locus-specific WAA is associated with increased PCa risk.[25] Although WAA alone is not predictive, increased frequency of PCa-associated risk alleles or increased exposure to environmental risk factors and certain gene-environment interactions might increase PCa risk in Black men. Put differently, Blacks with the highest degree of WAA did not have increased odds of PCa diagnosis compared to Blacks at the lowest WAA quartiles, thereby disputing potential use of genetic West African ancestry as a substitute for Black race in PCa predictive models. The resulting disparity in PCa diagnosis is likely driven by gene-environment interactions which are most comprehensively captured by the self- reported Black race variable.

In regressions for Gleason ≥3+4 PCa diagnosis model with the highest −2 log likelihood score included an interaction term between abnormal DRE and Black race (Table 3). Figure 1 shows that Black men with normal DRE have a higher proportion of significant PCa than their non-Black counterparts with an abnormal DRE. Furthermore Blacks with an abnormal DRE have more than double the proportion of significant PCa. This suggests that Black race is intimately linked with higher odds of significant PCa diagnosis and suggests a greater significance of DRE in screening Black men.

The ongoing controversy in PSA screening has intensified with revision of the USPSTF guidelines on PCa screening.[12, 26, 27] In men under 55, Black race was associated with a 5.7-fold increased odds of overall PCa (p=0.02). This effect size closely rivals a ten-fold increase in logi₁₀-PSA (OR 7.12, p=0.02). Black men are at high risk for PCa at early ages, and studies optimizing screening strategies for Black men under 55 are needed. Significantly, we demonstrate the persistence of an independent association ofBlack race with prostate biopsy outcomes in more fully adjusted models accounting for clinical features, individual level socioeconomic factors, and clinical setting.

Limitations

There are limitations for generalizability in this cross-sectional study. Pathologic review was not centralized across sites which led to earlier adoption of ISUP 2014 guidelines at the private centers and higher rates of clinically significant PCa diagnosis. We cannot rule out the possibility that our results stem from a selection bias. Black men have known increased PCa mortality rate, frequently have delays in time to prostate biopsy in public health systems, and harbor higher degrees of medical mistrust and we are unable to assess their affect on provider referral patterns. We did assess the indications for prostate biopsy and found that the majority of Black and non-Black men were referred for elevated PSA at a similar proportion. Non-Black men were more often referred for abnormal DRE only or for elevated PSA velocity only relative to Blacks. Overall, our population was similar to external populations in terms of age and clinical risk factors, but cannot exclude the possibility of residual confounding.[5, 7] Though we evaluate established socioeconomic risk factors, we lack PCa screening history and several individual (e.g. health literacy, diet) and neighborhood-associated factors (e.g. food access, crime). Race is a social construct and was self-reported. Given the heterogeneity of genetic West African ancestry among Blacks, race becomes less of a biological phenomenon, and instead serves as a proxy for shared environmental risk factors and their interaction with genetics.

Conclusions:

Black race is independently associated with increased odds of clinically significant PCa on initial biopsy after adjusting for clinical, behavioral and socioeconomic risk factors, and is a significant predictor of PCa diagnosis in younger men. Further investigation into optimizing screening in Black men aged 40–54 is warranted. Future discussions about the role of socioeconomic factors should not discount the biological and genetic underpinnings of PCa disparities.

Table 4.

: Binary logistic regressions for age < 55 years

Cancer on Biopsy vs. Negative Biopsy			Gleason ≥3+4 Prostate Ca vs. Gleason 3+3/Negative Biopsy
Covariates	Odds Ratio (95% C.l.)	p value	Covariates	Odds Ratio (95% C.l.)	p value
Black race	2.13 (1.33–3.40)	0.002	Black race x Abnormal DRE	2.93 (1.31–6.53)	0.009
Abnormal DRE (yes)	1.14 (0.74–1.76)	0.57	Black race x Normal DREa	1.14 (0.56–2.32)	0.72
-	-	-	Non-Black race x Abnormal DREa	0.86 (0.39–1.94)	0.72
-	-	-	Non-Black race x Normal DREa(ref)	1	-
1st degree Fam Hx (yes)	1.74 (1.07–2.83)	0.02	1st degree Fam Hx (yes)	1.48 (0.86–2.56)	0.16
Age, years	1.04 (1.01–1.07)	0.02	Age, years	1.05 (1.01–1.08)	0.02
Log(PSA), ng/ml	4.32 (2.29–8.14)	<0.001	Log(PSA), ng/ml	13.09 (6.06-28.27)	<0.001
Publicly funded site (yes)	0.53 (0.28–0.98)	0.04	Publicly funded site (yes)	0.29 (0.14–0.60)	0.001
High School completion (yes)	1.17 (0.74–1.84)	0.49	High School completion (yes)	0.84 (0.48–1.48)	0.55
Prostate volume, cm3	0.98 (0.97–0.99)	<0.001	Prostate volume, cm3	0.98 (0.97–0.99)	<0.001
5-ARI use (yes, ≥6 months)	0.38 (0.19–0.74)	0.004	5-ARI use (yes, ≥6 months)	0.32 (0.12–0.85)	0.02
Married (yes)	0.86 (0.56–1.33)	0.81	Married (yes)	0.61 (0.36–1.03)	0.06
Annual Income < $30K/year	1.1 (0.67–1.78)	0.72	Annual Income < $30K/year	1.15 (0.64–2.06)	0.63

Note: Bolded variables have a p-value < 0.05.

Highlight.

• Black race remains associated with new PCa diagnosis after adjusting for clinical and socioeconomic risk factors

• Black race is a significant predictor of PCa diagnosis in men under 55 years

• West African Ancestry does not predict significant PCa among self-reported Blacks