Differences In Prostate Cancer Risk Research Articles

Genetic risk and likelihood of prostate cancer detection on first biopsy by ancestry.

Despite differences in prostate cancer risk across ancestry groups, relative performance of prostate cancer genetic risks scores (GRS) for positive biopsy prediction in different ancestry groups is unknown. This cross-sectional retrospective analysis examines the association between a polygenic hazard score (PHS290) and risk of prostate cancer diagnosis upon first biopsy in male veterans using 2-sided tests. Our analysis included 36 717 veterans (10 297 of African ancestry). Unadjusted rates of positive first prostate biopsy increased with higher genetic risk (low risk: 34%, high risk: 58%; P < .001). Among men of African ancestry, higher genetic risk was associated with increased prostate cancer detection on first biopsy (odds ratio = 2.18, 95% confidence interval = 1.93 to 2.47), but the effect was stronger among men of European descent (odds ratio = 3.89, 95% confidence interval = 3.62 to 4.18). These findings suggest that incorporating genetic risk into prediction models could better personalize biopsy decisions, although further study is needed to achieve equitable genetic risk stratification among ancestry groups.

MP55-16 FOCAL CRYOTHERAPY AND STEREOTACTIC BODY RADIOTHERAPY HAVE SIMILAR ONCOLOGIC AND FUNCTIONAL OUTCOMES IN TREATMENT OF LOW-TO-INTERMEDIATE UNILOBE PROSTATE CANCER

You have accessJournal of UrologyCME1 May 2022MP55-16 FOCAL CRYOTHERAPY AND STEREOTACTIC BODY RADIOTHERAPY HAVE SIMILAR ONCOLOGIC AND FUNCTIONAL OUTCOMES IN TREATMENT OF LOW-TO-INTERMEDIATE UNILOBE PROSTATE CANCER Ashley Monaco, Jessica Sommer, Chinyere Okpara, Jonathan Haas, Anthony Corcoran, and Aaron Katz Ashley MonacoAshley Monaco More articles by this author , Jessica SommerJessica Sommer More articles by this author , Chinyere OkparaChinyere Okpara More articles by this author , Jonathan HaasJonathan Haas More articles by this author , Anthony CorcoranAnthony Corcoran More articles by this author , and Aaron KatzAaron Katz More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000002634.16AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Minimal invasive treatment options such as focal cryotherapy (FC) and stereotactic body radiotherapy (SBRT) continue to evolve and grow in popularity. Comparative outcome data for these treatment options are sparse. This study compares oncologic and functional outcomes as well as complications following FC or SBRT for low-to-intermediate risk unilobe prostate cancer (PCa). METHODS: An IRB-approved database was reviewed for patients who underwent FC or SBRT for low-to-intermediate risk PCa as defined by D’Amico criteria. Patients with >1 year of follow-up, had prior PCa treatment, or PCa that was bilateral were excluded from this study. TF was defined as salvage treatment, a positive biopsy Gleason group (GG) of 2 or greater on post-treatment biopsy, or PCa metastasis. Functional outcomes were based on 2-year post treatment patient reported EPIC urinary, sexual, and bowel function surveys. Complications were categorized with the Clavien Dindo classification (CD). Descriptive statistics, univariate analyses, and Kaplan Meier curve were used to compare outcomes of SBRT and FC. P <0.05 was significant. RESULTS: 68 FC and 51 SBRT patients with a median age of 68 years (48-86) and a median follow-up time of 82 (14-135) months were included in this analysis. There was no difference in PCa risk (p=0.473), GG (p=0.2), or PSA (p=0.8) among the two cohorts at baseline. There was no difference between patients who experienced TF (19% vs. 18%; p=0.8; log-rank p=0.7), underwent salvage treatment (18% vs 18%; p=1.0), or had metastasis (2.9% vs. 9.8%; p=0.1) among FC and SBRT patients, respectively. At a minimum of 2-years post-treatment, urinary function (94 vs. 89; p=0.3), bowel function (96 vs. 96; p=0.4), and sexual function (50 vs. 32; p=0.6) were relatively similar among the FC and SBRT patients, respectively. 13 (19%) FC and 10 (20%) SBRT experienced treatment related complications (p=0.8) of which 4 (5.9%) FC and 6 (12%) were CD 1, 7 (10%) FC and 4 (7.8%) SBRT were CD 2, and 2 (2.9%) FC were CD 3A. CONCLUSIONS: Both FC and SBRT are associated with similar, excellent oncologic and functional outcomes 7-years following treatment. These results underscore the utility of FC and SBRT for management of unilobe low-to-intermediate risk PCa. Source of Funding: Department of Urology, NYU Langone Hospital – Long Island © 2022 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 207Issue Supplement 5May 2022Page: e944 Advertisement Copyright & Permissions© 2022 by American Urological Association Education and Research, Inc.MetricsAuthor Information Ashley Monaco More articles by this author Jessica Sommer More articles by this author Chinyere Okpara More articles by this author Jonathan Haas More articles by this author Anthony Corcoran More articles by this author Aaron Katz More articles by this author Expand All Advertisement PDF DownloadLoading ...

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 [95% confidence interval (CI) 4.84–5.29] for men of European ancestry to 3.74 [95% CI 3.36–4.17] for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher [95% CI 2.14–2.22], and men of East Asian ancestry 0.73-times lower [95% CI 0.71–0.76], than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.

A Custom Genotyping Array Reveals Population-Level Heterogeneity for the Genetic Risks of Prostate Cancer and Other Cancers in Africa.

Although prostate cancer is the leading cause of cancer mortality for African men, the vast majority of known disease associations have been detected in European study cohorts. Furthermore, most genome-wide association studies have used genotyping arrays that are hindered by SNP ascertainment bias. To overcome these disparities in genomic medicine, the Men of African Descent and Carcinoma of the Prostate (MADCaP) Network has developed a genotyping array that is optimized for African populations. The MADCaP Array contains more than 1.5 million markers and an imputation backbone that successfully tags over 94% of common genetic variants in African populations. This array also has a high density of markers in genomic regions associated with cancer susceptibility, including 8q24. We assessed the effectiveness of the MADCaP Array by genotyping 399 prostate cancer cases and 403 controls from seven urban study sites in sub-Saharan Africa. Samples from Ghana and Nigeria clustered together, whereas samples from Senegal and South Africa yielded distinct ancestry clusters. Using the MADCaP array, we identified cancer-associated loci that have large allele frequency differences across African populations. Polygenic risk scores for prostate cancer were higher in Nigeria than in Senegal. In summary, individual and population-level differences in prostate cancer risk were revealed using a novel genotyping array. SIGNIFICANCE: This study presents an Africa-specific genotyping array, which enables investigators to identify novel disease associations and to fine-map genetic loci that are associated with prostate and other cancers.

Reduced risk of prostate cancer in a cohort of Lithuanian diabetes mellitus patients.

130 Background: An inverse association has been shown between diabetes and prostate cancer risk. The aim of this study was to determine whether type 2 diabetes mellitus (T2DM) and metformin is associated with prostate cancer risk. Methods: A retrospective cohort design was used to examine the relationship between diabetes and prostate cancer risk. The cohort was composed of male patients identified with diagnosis of T2DM in the National Health Insurance Fund database during 2000–2016. Cancer cases were identified by record linkage with the Lithuanian Cancer Registry which is a nationwide population-based cancer registry that contains personal and demographic information, as well as information on diagnosis of all people diagnosed with cancer in Lithuania since 1978. We calculated standardized incidence ratios (SIRs) for prostate cancers as a ratio of observed number of cancer case in people with diabetes diagnosis to the expected number of cancer cases in the underlying general population. Results: Overall, 68,449 males were diagnosed with diabetes in Lithuania between 2000 and 2016 were included in final cohort. 2,754 prostate cancers were observed versus 3,111.26 expected within a period of observation entailing an SIR of 0.89 (95% CI: 0.85–0.92). Significantly lower risk of prostate cancer was found in diabetic patients in all age groups, there were no differences in prostate cancer risk by time since diabetes diagnosis. Significantly lower risk of prostate cancer also was found in both metformin users and never-users groups, with higher risk reduction in metformin users (SIR 0.71, 95% CI: 0.68–0.75) than in T2DM patients never-users (SIR 0.88, 95% CI: 0.80–0.96). Conclusions: In the large population-based study we found significantly decreased risk of prostate cancer among men with T2DM. Our study suggests that metformin use in patients with T2DM may be associated with reduced risk of developing prostate cancer.

Geographic Differences in Baseline Prostate Inflammation and Relationship with Subsequent Prostate Cancer Risk: Results from the Multinational REDUCE Trial.

Background: Prostate cancer incidence rates vary 25-fold worldwide. Differences in PSA screening are largely, but not entirely, responsible. We examined geographic differences in prevalence of histologic prostate inflammation and subsequent prostate cancer risk.Methods: Seven thousand nonHispanic white men were enrolled in the REduction by DUtasteride of prostate Cancer Events (REDUCE) trial from Europe (n = 4,644), North America (n = 1,746), South America (n = 466), and Australia/New Zealand (n = 144). Histologic inflammation in baseline negative prostate biopsies was classified as chronic (lymphocytes/macrophages) or acute (neutrophils). Multivariable logistic regression was used to examine associations between region and prostate inflammation, and between region and prostate cancer risk at 2-year biopsy.Results: Prevalence of prostate inflammation varied across region, with broadly similar patterns for acute and chronic inflammation. Relative to Europe, prevalence of acute inflammation was higher in North America [odds ratio (OR), 1.77; 95% confidence interval (CI), 1.51-2.08] and Australia/New Zealand (OR, 2.07; 95% CI, 1.40-3.06). Men from these regions had lower prostate cancer risk than Europeans at biopsy. Among North Americans, prevalence of acute inflammation was higher in Canada versus the United States (OR, 1.40; 95% CI, 1.07-1.83), but prostate cancer risk did not differ between these regions. Among Europeans, prevalence of acute inflammation was lower in Northern and Eastern (OR, 0.79; 95% CI, 0.65-0.97 and OR 0.62; 95% CI, 0.45-0.87, respectively), relative to Western Europe, and these men had higher prostate cancer risk at biopsy.Conclusions: Prevalence of histologic prostate inflammation varied by region. Geographic differences in prostate inflammation tracked inversely with geographic differences in prostate cancer risk.Impact: Characterization of premalignant prostate biology and the relationship with subsequent prostate cancer risk could inform prostate cancer prevention efforts. Cancer Epidemiol Biomarkers Prev; 27(7); 783-9. ©2018 AACR.

Differences in inherited risk among relatives of hereditary prostate cancer patients using genetic risk score.

Family history assigns equivalent risk to all relatives based upon the degree of relationship. Recent genetic studies have identified single nucleotide polymorphisms (SNPs) that can be used to calculate a genetic risk score (GRS) to determine prostate cancer (PCa) risk. We sought to determine whether GRS can stratify PCa risk among individuals in families considered to be at higher risk due their family history of PCa. Family members with hereditary PCa were recruited and genotyped for 17 SNPs associated with PCa. A GRS was calculated for all subjects. Analyses compared the distribution of GRS values among affected and unaffected family members of varying relationship degrees. Data was available for 789 family members of probands including 552 affected and 237 unaffected relatives. Median GRSs were higher among first-degree relatives compared to second- and third-degree relatives. In addition, GRS values among affected first- and second-degree relatives were significantly higher than unaffected relatives (P = 0.042 and P = 0.016, respectively). Multivariate analysis including GRS and degree of relationship demonstrated that GRS was a significant and independent predictor of PCa (OR 1.52, 95%CI 1.15-2.01). GRS is an easy-to-interpret, objective measure that can be used to assess differences in PCa risk among family members of affected men. GRS allows for further differentiation among family members, providing better risk assessment. While prospective validation studies are required, this information can help guide relatives in regards to the time of initiation and frequency of PCa screening.

Entacapone and prostate cancer in Parkinson's disease patients: A large Veterans Affairs healthcare system study

BackgroundAn increased incidence of prostate cancer was observed in Parkinson's disease (PD) patients treated with entacapone during a pre-approval randomized clinical trial; the relation has not been robustly investigated in the U.S. ambulatory setting. ObjectiveTo investigate whether entacapone is associated with prostate cancer and to assess whether the associations are correlated with advanced disease at the time of cancer diagnosis. MethodsUsing data from the Department of Veterans Affairs healthcare system, new-user cohorts were created of PD patients treated with add-on entacapone or add-on dopamine agonist/monoamine oxidase B inhibitors between January 2000 and December 2014. Patients were followed on-treatment for occurrence of prostate cancer, identified via linkage to the VA cancer registry. ResultsMean follow-up time was 3.1 and 4.0 years in the entacapone and control cohort, respectively. There were 17,666 subjects meeting study criteria (mean age, 74 (SD 8.6) years); the entacapone-treated group comprised 5,257 subjects. Twenty-three prostate cancer cases occurred in the entacapone cohort and ninety-seven in the control cohort. The overall incidence of prostate cancer was 1.8 per 1,000 person-years of risk. There was no difference in risk of prostate cancer between the cohorts for increased duration of entacapone intake (adjusted HR: 1.08; 95% confidence interval: 0.46–2.51 for cumulative exposure of ≥2 years). Time since starting drug therapy and cumulative dose (mg) also do not suggest a difference in prostate cancer risk between cohorts. ConclusionsProlonged therapy with entacapone was not associated with increased prostate cancer incidence; however, findings suggest a higher severity of prostate cancer.

Genetic Hitchhiking and Population Bottlenecks Contribute to Prostate Cancer Disparities in Men of African Descent.

Prostate cancer incidence and mortality rates in African and African American men are greatly elevated compared with other ethnicities. This disparity is likely explained by a combination of social, environmental, and genetic factors. A large number of susceptibility loci have been reported by genome-wide association studies (GWAS), but the contribution of these loci to prostate cancer disparities is unclear. Here, we investigated the population structure of 68 previously reported GWAS loci and calculated genetic disparity contribution statistics to identify SNPs that contribute the most to differences in prostate cancer risk across populations. By integrating GWAS results with allele frequency data, we generated genetic risk scores for 45 African and 19 non-African populations. Tests of natural selection were used to assess why some SNPs have large allele frequency differences across populations. We report that genetic predictions of prostate cancer risks are highest for West African men and lowest for East Asian men. These differences may be explained by the out-of-Africa bottleneck and natural selection. A small number of loci appear to drive elevated prostate cancer risks in men of African descent, including rs9623117, rs6983267, rs10896449, rs10993994, and rs817826. Although most prostate cancer-associated loci are evolving neutrally, there are multiple instances where alleles have hitchhiked to high frequencies with linked adaptive alleles. For example, a protective allele at 2q37 appears to have risen to high frequency in Europe due to selection acting on pigmentation. Our results suggest that evolutionary history contributes to the high rates of prostate cancer in African and African American men.Significance: A small number of genetic variants cause an elevated risk of prostate cancer in men of West African descent. Cancer Res; 78(9); 2432-43. ©2018 AACR.

Abstract 4962: Geographic disparities in prevalence of baseline prostate inflammation and prostate cancer risk: Results from a multinational trial

Abstract Introduction: Prostate cancer incidence rates vary 25-fold worldwide. The distribution of lifestyle factors also varies by geographic region and these factors may impact prostate inflammation, which is inversely associated with prostate cancer risk in the REduction by DUtasteride of prostate Cancer Events (REDUCE) trial. Herein, we examined geographic differences in the prevalence of histological prostate inflammation and geographic differences in prostate cancer risk using REDUCE, a multinational trial of men with a negative baseline prostate biopsy. Methods: We conducted a retrospective analysis of data from 7,213 men with a negative baseline prostate biopsy in REDUCE from Europe (n=4,802), North America (n=1,796), South America (n=467), and Australia/New Zealand (n=148). Histological inflammation was classified as chronic (lymphocytes, macrophages) or acute (neutrophils) by central review of negative baseline prostate biopsies. Logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI) for associations between geographic region and prostate inflammation, and between geographic region and prostate cancer risk at trial-mandated repeat biopsy, adjusting for potential confounders. To avoid confounding by race, analyses were restricted to white men. Results: Chronic and acute prostate inflammation was detected in 77% and 15% of men, respectively. Relative to Europeans, North Americans and Australians/New Zealanders were more likely to have acute prostate inflammation in the negative biopsy (OR 1.74; 95% CI 1.48-2.05 and OR 2.04; 95% CI 1.38-3.02, respectively), while South Americans were less likely to have acute inflammation (OR 0.42; 95% CI 0.28-0.61). Among North Americans, Canadians were more likely to have acute prostate inflammation than men from the United States (OR 1.40; 95% CI 1.07-1.83). Among Europeans, the prevalence of acute inflammation was lower in Northern, Southern and Eastern Europe, relative to Western Europe (OR 0.79; 95% CI 0.65-0.97, OR 0.84; 95% CI 0.66-1.07 and OR 0.62; 95% CI 0.45-0.87, respectively), with similar results for chronic inflammation. Regions with higher prevalence of prostate inflammation had lower prostate cancer risk at 2-year biopsy, including North America (OR 0.87; 95% CI 0.71-1.07) and Australia/New Zealand (OR 0.48; 95% CI 0.24-0.95), relative to Europe. Conversely, regions with lower prevalence of prostate inflammation had higher prostate cancer risk at 2-year biopsy, including Northern and Eastern Europe (OR 1.30; 95% CI 1.05-1.62 and OR 1.74; 95% CI 1.29-2.35, respectively), relative to Western Europe. Conclusions: Geographic disparities in the prevalence of prostate inflammation is a potential biologic mechanism contributing to global differences in prostate cancer incidence rates. Citation Format: Emma H. Allott, Sarah Markt, Lauren E. Howard, Adriana C. Vidal, Daniel M. Moreira, Ramiro Castro-Santamaria, Gerald L. Andriole, Lorelei A. Mucci, Stephen J. Freedland. Geographic disparities in prevalence of baseline prostate inflammation and prostate cancer risk: Results from a multinational trial [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4962. doi:10.1158/1538-7445.AM2017-4962

Two Novel Susceptibility Loci for Prostate Cancer in Men of African Ancestry.

Prostate cancer incidence is 1.6-fold higher in African Americans than in other populations. The risk factors that drive this disparity are unknown and potentially consist of social, environmental, and genetic influences. To investigate the genetic basis of prostate cancer in men of African ancestry, we performed a genome-wide association meta-analysis using two-sided statistical tests in 10 202 case subjects and 10 810 control subjects. We identified novel signals on chromosomes 13q34 and 22q12, with the risk-associated alleles found only in men of African ancestry (13q34: rs75823044, risk allele frequency = 2.2%, odds ratio [OR] = 1.55, 95% confidence interval [CI] = 1.37 to 1.76, P = 6.10 × 10−12; 22q12.1: rs78554043, risk allele frequency = 1.5%, OR = 1.62, 95% CI = 1.39 to 1.89, P = 7.50 × 10−10). At 13q34, the signal is located 5’ of the gene IRS2 and 3’ of a long noncoding RNA, while at 22q12 the candidate functional allele is a missense variant in the CHEK2 gene. These findings provide further support for the role of ancestry-specific germline variation in contributing to population differences in prostate cancer risk.

Racial differences in prostate cancer risk in young HIV-positive and HIV-negative men: a prospective cohort study.

African American men have the highest incidence of prostate cancer among ethnic groups, and racial disparity is highest in younger men. Prostate cancer prevalence is rising in HIV-infected men due to improved survival on antiretroviral therapies, yet little is known about racial differences in prostate cancer risk by HIV-infection status and age. This is a prospective cohort study of prostate cancer risk in 2,800 HIV-infected and -uninfected men who have sex with men (MSM) aged 40-70 years (22% African American) who were enrolled in the multicenter AIDS cohort study from 1996 to 2010. Poisson regression models were used to examine associations between race and HIV-infection status and prostate cancer risk among men aged 40-70, 40-55, and 56-70 years. Among men aged 40-70 years, incidence rates (IR) per 100,000 person-years were 169 among all men and 276 among African American HIV-infected men. Prostate cancer risk was similar by HIV-infection status (IRR 1.0, 95% CI 0.55-1.82), but nearly threefold higher in African Americans compared to non-African Americans in adjusted models (IRRs 2.66 and 3.22, 95% CIs 1.36-5.18 and 1.27-8.16 for all or HIV-infected men, respectively). Racial disparity in prostate cancer risk was greatest in African American men aged 40-55 years (adjusted IRR 3.31, 95% CI 1.19-9.22). Prostate cancer risk showed associations with family history of prostate cancer (p=0.001), but not heavy smoking, androgen supplement use, or HIV-related factors. Among MSM, African American HIV-positive and HIV-negative men aged 40-55 years have threefold increased risk of young-onset prostate cancer compared to non-African American men, highlighting the need to make informed decisions about screening in this population.

Prostate Cancer and Socioeconomic Status in the Finnish Randomized Study of Screening for Prostate Cancer.

Prostate cancer (PC) screening remains controversial. We investigated whether screening reduces the difference in prostate cancer risk by socioeconomic status (SES). In 1996-2011, a total of 72,139 men from the Finnish Randomized Study of Screening for Prostate Cancer were analyzed. Outcome measures were PC incidence, mortality, and participation in screening. SES indicators were educational level, income, and home ownership status (data obtained from the Statistics Finland registry). The mean duration of follow-up was 12.7 years. Higher SES was associated with a higher incidence of low- to moderate-risk PC but with a lower risk of advanced PC. Higher education was associated with significantly lower PC mortality in both control and screening arms (risk ratio=0.48-0.69; P<0.05). Higher income was also associated with lower PC mortality but only in the control arm (risk ratio=0.45-0.73; P<0.05). There were no significant differences in SES gradient by arm (Pinteraction=0.33 and Pinteraction=0.47 for primary vs. secondary education and primary vs. tertiary education, respectively; Pinteraction=0.65 and Pinteraction=0.09 for low vs. intermediate income and low vs. high income, respectively; and Pinteraction=0.27 among home ownership status strata). Substantial gradients by SES in PC incidence and mortality were observed in the control arm. Higher SES was associated with overdiagnosis of low-risk PC and, conversely, lower risk of incurable PC and lower PC mortality. Special attention should be directed toward recruiting men with low SES to participate in population-based cancer screening.

Racial differences in prostate inflammation: results from the REDUCE study.

Prostate cancer (PC) risk differs between races, and we previously showed prostate inflammation in benign prostate tissue was linked with a lower future PC risk. However, whether prostate tissue inflammation varies by race is unknown. We analyzed baseline acute and chronic prostate inflammation by race in REDUCE, a 4-year, multicenter, placebo-controlled study where all men had a negative prostate biopsy prior to enrollment. We included 7,982 men with standardized central pathology review to determine the presence or absence of chronic or acute inflammation in baseline prostate biopsy tissue. Logistic regression was used to compare prostate inflammation by race, adjusting for confounders. Of 7,982 men, 7,271 were white (91.1%), 180 (2.3%) black, 131 (1.6%) Asian, 319 (4.0%) Hispanic and 81 (1%) unknown. A total of 78% had chronic and 15% had acute inflammation. On multivariable analysis relative to white men, black men were less likely (OR = 0.65, 95%CI: 0.41-1.03, p = 0.07) and Asian men more likely to have acute inflammation (OR = 1.74, 95%CI: 1.14-2.65, p = 0.001). Hispanic men had similar levels of acute inflammation as white men. Chronic inflammation did not significantly differ across races. We identified racial differences in acute inflammation, particularly in Asian men, in benign prostate tissue that inversely mirrored population-level data on PC race disparity. As we showed in REDUCE that acute inflammation is linked with lower future PC risk, if validated in future studies, these data suggest racial differences in prostatic acute inflammation may contribute in part to race differences in PC risk, especially among Asian men.

The Effect of Start and Stop Age at Screening on the Risk of Being Diagnosed with Prostate Cancer

We investigated the effect of age and number of screens on the risk of prostate cancer diagnosis. Since 1995 the Göteborg randomized population based prostate cancer screening trial has invited men biennially for prostate specific antigen testing, until the upper age limit of 70 years. Men with a prostate specific antigen above the threshold of 2.5 ng/ml were recommended further evaluation including 10-core biopsy (sextant before 2009). The present study comprises 9,065 men born between 1930 and 1943 (1944 excluded due to different screening algorithm). Complete attendees were defined as men who accepted all screening invitations (maximum 3 to 9 invitations). The cumulative incidence of prostate cancer was calculated using standard methods. Of the 3,488 (38%) complete attendees 667 were diagnosed with prostate cancer (followup 1995 to June 30, 2014). At age 70 years there was no significant difference in prostate cancer risk among those who started screening at the age of 52 (9 screens), 55 (7 screens) or 60 (5 screens) years. However, the cumulative risk of prostate cancer diagnosis increased dramatically with age, and was 7.9% at age 60, 15% at age 65 and 21% at age 70 for men who had been screened 4 or more times. There was no clear association between risk of prostate cancer and the number of screens. Starting screening at an early age appears to advance the time of prostate cancer diagnosis but does not seem to increase the risk of being diagnosed with the disease. Age at termination of screening is strongly associated with the risk of being diagnosed with prostate cancer.

Distinct Genomic Alterations in Prostate Tumors from African American Men

Distinct Genomic Alterations in Prostate Tumors from African American Men

Racial/ethnic differences in lifestyle-related factors and prostate cancer risk: the Multiethnic Cohort Study.

Older age, African ancestry, and family history of prostate cancer are well-established risk factors for prostate cancer, and all are non-modifiable. Various lifestyle factors have been examined in relation to prostate cancer risk, including diet, obesity, and physical activity; however, none of them has been consistently related to risk. In the Multiethnic Cohort Study, we investigated whether lifestyle-related factors are associated with prostate cancer risk and whether such factors explain the racial/ethnic differences in risk. During a mean follow-up of 13.9 years, 7,115 incident cases were identified among 75,216 white, African-American, Native Hawaiian, Japanese American, and Latino men. Cox proportional hazards models were used to calculate relative risks (RRs) and 95 % confidence intervals (95 % CIs) for prostate cancer. Among selected lifestyle-related factors including body mass index, height, education, physical activity, and intakes of alcohol, calcium, legumes, lycopene, and selenium, only smoking (RR for current (≥20 cigarettes/day) vs. never smoking = 0.72; 95 % CI 0.63-0.83) and history of diabetes (RR for yes vs. no = 0.78; 95 % CI 0.72-0.85) were significantly associated with prostate cancer risk. Compared to whites, the risk of incident prostate cancer was twofold higher in African-Americans and 16 % higher in Latinos. Additional adjustment for a history of PSA testing did not change the results. The findings suggest that racial/ethnic differences in prostate cancer risk are not explained by the lifestyle factors examined and that underlying genetic factors may be involved.

Testosterone therapy and cancer risk

To determine if testosterone therapy (TT) status modifies a man's risk of cancer. The Urology clinic hormone database was queried for all men with a serum testosterone level and charts examined to determine TT status. Patient records were linked to the Texas Cancer Registry to determine the incidence of cancer. Men accrued time at risk from the date of initiating TT or the first office visit for men not on TT. Standardised incidence rates and time to event analysis were performed. In all, 247 men were on TT and 211 did not use testosterone. In all, 47 men developed cancer, 27 (12.8%) were not on TT and 20 (8.1%) on TT. There was no significant difference in the risk of cancer incidence based on TT (hazard ratio [HR] 1.0, 95% confidence interval [CI] 0.57-1.9; P = 1.8). There was no difference in prostate cancer risk based on TT status (HR 1.2, 95% CI 0.54-2.50). There was no change in cancer risk overall, or prostate cancer risk specifically, for men aged >40 years using long-term TT.

Prostate cancer and occupational exposure to whole-body vibration in a national population-based cohort study.

Following preliminary evidence from observational studies, we test the potential relationship between whole-body vibration (WBV) and prostate cancer in a cohort study. WBV exposure was assigned based on occupation in 1991 and 1,107,700 participants were followed for incident prostate cancer until the end of 2003. Adjusted hazard rate ratios (HRs) were calculated using Cox proportional hazards modeling. 17,922 incident prostate cancer cases were observed. WBV-exposed men in Natural and Applied Sciences Occupations had a 37% elevated risk of prostate cancer (95% CI 1.09-1.72) and WBV-exposed men in Trades, Transport, and Equipment Operators Occupations had a 9% reduced risk (95% CI 0.86-0.97). Independent of WBV exposure, small but significant differences in risk were seen for several occupational categories. We found no consistent relationship between WBV and prostate cancer. Further research could focus on other exposures or specific occupations in the studied categories to determine what may be contributing to the observed differences in prostate cancer risk.

Patterns of meat intake and risk of prostate cancer among African-Americans in a large prospective study

Given the large racial differences in prostate cancer risk, further investigation of diet and prostate cancer is warranted among high-risk groups. The purpose of this study was to examine the association between type of meat intake and prostate cancer risk among African-American men. In the large, prospective NIH-AARP Diet and Health Study, we analyzed baseline (1995-1996) data from African-American participants, aged 50-71years. Incident prostate cancer cases (n=1,089) were identified through 2006. Dietary and risk factor data were ascertained by questionnaires administered at baseline. Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) within intake quantiles. Neither white nor processed meat intake was associated with prostate cancer, regardless of meat-cooking method. Red meats cooked at high temperatures were associated with an increased risk of prostate cancer (HR=1.18, 95% CI=1.00-1.38 and HR=1.22, 95% CI=1.03-1.44, for the upper two intake tertiles). Intake of the heterocyclic amine (HCA), 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline (DiMeIQx) was positively associated with prostate cancer (HR=1.30; 95% CI=1.05-1.61, p=0.02). No associations were observed for intake of other HCAs. Red meats cooked at high temperatures were positively associated with prostate cancer risk among African-American men. Further studies are needed to replicate these findings.