BackgroundWe investigated whether age influences the predictiveness of genetic risk score (GRS) for prostate cancer (PCa) in a Chinese hospital-based biopsy cohort.MethodsWe included consecutive patients who underwent prostate biopsies in two tertiary centers between 2012 and 2014. GRS was calculated using 24 PCa-associated genetic variants and its predictiveness was assessed by area under curve (AUC).ResultsOf 1120 men tested, 724 with prostate-specific antigen (PSA) < 20 ng/ml were selected for further analysis. Patients were divided into 3 groups by age cutoffs at 60 and 70 years. GRS significantly predicted PCa for all patients (AUC: 0.561; 95% CI: 0.514–0.609) and was an independent predictor in multivariate analysis for the 60–70 year-olds (AUC: 0.612, 95% CI: 0.541–0.684), but not for patients aged < 60 years or ≥70 years. For PCa with Gleason score ≥7, GRS discriminative ability was 0.582 (95% CI=0.527–0.637) for all patients, and 0.647 (95% CI: 0.541–0.684) for the 60–70 year-old group.ConclusionGRS significantly increased clinical prediction of PCa and high-grade disease in Chinese men aged 60–70 years, which implies that men in this age group would benefit most from genetic testing.
The [-2]proPSA (p2PSA) and its derivatives, the p2PSA-to-free PSA ratio (%p2PSA), and the Prostate Health Index (PHI) have greatly improved discrimination between men with and without prostate cancer (PCa) in prostate biopsies. However, little is known about their performance in cases where a digital rectal examination (DRE) and transrectal ultrasonography (TRUS) are negative. A prospective cohort of 261 consecutive patients in China with negative DRE and TRUS were recruited and underwent prostate biopsies. A serum sample had collected before the biopsy was used to measure various PSA derivatives, including total prostate-specific antigen (tPSA), free PSA, and p2PSA. For each patient, the free-to-total PSA ratio (%fPSA), PSA density (PSAD), p2PSA-to-free PSA ratio (%p2PSA), and PHI were calculated. Discriminative performance was assessed using the area under the receiver operating characteristic curve (AUC) and the biopsy rate at 91% sensitivity. The AUC scores within the entire cohort with respect to age, tPSA, %fPSA, PSAD, p2PSA, %p2PSA, and PHI were 0.598, 0.751, 0.646, 0.789, 0.814, 0.808, and 0.853, respectively. PHI was the best predictor of prostate biopsy results, especially in patients with a tPSA of 10.1–20 ng ml−1. Compared with other markers, at a sensitivity of 91%, PHI was the most useful for determining which men did not need to undergo biopsy, thereby avoiding unnecessary procedures. The use of PHI could improve the accuracy of PCa detection by predicting prostate biopsy outcomes among men with a negative DRE and TRUS in China.
Herein, we aimed to examine whether the association of body mass index (BMI) with prostate cancer (PCa) at biopsy differs according to genetic susceptibility.In a multicenter prospective cohort including 1120 men undergoing diagnostic prostate biopsy in China, we evaluated the interaction between BMI and genetic risk score (GRS) comprising 24 PCa-associated single nucleotide polymorphisms (SNPs), as well as a GRS consisting of 7 SNPs derived from an East-Asian population. The genetic risk was defined as low, intermediate, or high when GRS fell in the first, second, and third tertiles, respectively.We observed a significant interaction between BMI and PCa GRS (Pinteraction = 0.047), suggesting that the predictive value of BMI on PCa was strongly modified by genetic susceptibility. In men with high genetic risk, BMI was an independent predictor of PCa (odds ratio [OR] = 1.167, P = 0.008) after adjusting for conventional risk factors. The relationship between BMI and PCa risk diminished (P = 0.990) in men with low genetic risk. The interaction was more pronounced with the East-Asian GRS (Pinteraction = 0.032), suggesting that the overall GRS interaction most likely occurs through genetic susceptibility in the East-Asian population.Our results suggest that the predictive effect of BMI on the PCa risk is strongly modified by individual genetic susceptibility. The association is more positive among men with high genetic risk for PCa.
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