Rates Of Prostate Cancer In Men Research Articles

Reclassification of prostate cancer risk using sequentially identified SNPs: Results from the REDUCE trial.

Although the clinical validity of risk-associated single nucleotide polymorphisms (SNPs) for assessment of disease susceptibility has been consistently established, risk reclassification from increasing numbers of implicated risk-associated SNPs raises concern that it is premature for clinical use. Our objective is to assess the degree and impact of risk reclassification with the increasing number of SNPs. A total of 3239 patients from the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial were included. Four genetic risk scores (GRSs) were calculated based on sets of sequentially discovered prostate cancer (PCa) risk-associated SNPs (17, 34, 51, and 68 SNPs). Pair-wise correlation coefficients between sets of GRSs increased as more SNPs were included in the GRS: 0.80, 0.86, and 0.95 for 17 versus 34 SNPs, 34 versus 51 SNPs, and 51 versus 68 SNPs, respectively. Using a GRS of 1.5 as a cutoff for higher versus lower risk, reclassification rates of PCa risk decreased: 14.11%, 12.04%, and 8.15% for 17 versus 34 SNPs, 34 versus 51 SNPs, and 51 versus 68 SNPs, respectively. Evolving GRSs, nevertheless, provide a tool for further refining risk assessment. When all four sequential GRSs were considered, the detection rates of PCa for men whose GRSs were consistently <1.5, reclassified, and consistently ≥1.5 were 20.8%, 29.67%, and 39.26%, respectively (Ptrend = 1.12 × 10-8 ). In comparison, the detection rates of PCa in men with negative or positive family history were 23.75% and 31.78%, respectively. Risk assessment using currently available SNPs is justified. Multiple GRS values from evolving sets of SNPs provide a valuable tool for better refining risk.

Prevalence of incidental prostate cancer: A systematic review of autopsy studies.

Prostate cancer screening may detect nonprogressive cancers, leading to overdiagnosis and overtreatment. The potential for overdiagnosis can be assessed from the reservoir of prostate cancer in autopsy studies that report incidental prostate cancer rates in men who died of other causes. We aimed to estimate the age-specific incidental cancer prevalence from all published autopsy studies. We identified eligible studies by searches of Medline and Embase, forward and backward citation searches and contacting authors. We screened the titles and abstracts of all articles; checked the full-text articles for eligibility and extracted clinical and pathology data using standardized forms. We extracted mean cancer prevalence, age-specific cancer prevalence and validity measures and then pooled data from all studies using logistic regression models with random effects. The 29 studies included in the review dated from 1948 to 2013. Incidental cancer was detected in all populations, with no obvious time trends in prevalence. Prostate cancer prevalence increased with each decade of age, OR = 1.7 (1.6–1.8), and was higher in studies that used the Gleason score, OR = 2.0 (1.1–3.7). No other factors were significantly predictive. The estimated mean cancer prevalence increased in a nonlinear fashion from 5% (95% CI: 3–8%) at age <30 years to 59% (95% CI: 48–71%) by age >79 years. There was substantial variation between populations in estimated cancer prevalence. There is a substantial reservoir of incidental prostate cancer which increases with age. The high risk of overdiagnosis limits the usefulness of prostate cancer screening.What’s new?Before symptoms of prostate cancer manifest clinically, many men die of other causes. Yet, prostate screening, particularly in older men, frequently turns out positive, resulting in overdiagnosis and overtreatment. This meta-analysis of published autopsy studies shows that incidental prostate cancer increases with age and with the use of sensitive screening strategies, especially in older men. Among men whose prostate cancers are designated “favorable-risk,” active surveillance and subsequent biopsy can result in reclassification with higher-grade cancer, purely by chance. The potential for the detection of clinically irrelevant, incidental prostate cancer is high, indicating a need for improved screening strategies.

Prostate volume as an independent predictor of prostate cancer in men with PSA of 10–50 ng ml−1

Prostate volume (PV) has been shown to be associated with prostate cancer (PCa) detection rates in men with a prostate-specific antigen (PSA) in the 'grey zone' (2.0-10.0 ng ml(-1)). However, the PSA 'grey zone' in Asian men should be higher because the incidence of PCa in Asian men is relatively low. Therefore, we evaluated the association between PV and PCa detection rates in men with PSAs measuring 10-50 ng ml(-1). Men who underwent a 13-core prostatic biopsy with PV documentation participated in the study. A multivariate stepwise regression was used to evaluate whether the PV at time of prostate biopsy could predict the risk of PCa. The rates of PCa among men in different PSA ranges, stratified by PV medians (<60 and ≥60 ml), were calculated. There were 261 men included in the final analysis. PV was the strongest predictor of PCa risk (odds ratio, 0.02; P<0.001) compared to other variables. The PCa rates in men with PVs measuring <60 and ≥60 ml in the 10-19.9 ng ml(-1) PSA group were 40.6% and 15.1%, respectively, while the rates for men with PSAs measuring 20-50 ng ml(-1) were 65.1% and 26.8%. PV is an independent predictor of PCa in men with PSA measuring 10-50 ng ml(-1). In clinical practice, particularly for those countries with lower incidences of PCa, PV should be considered when counselling patients with PSAs measuring 10-50 ng ml(-1) regarding their PCa risks.

No high-risk human papillomavirus infection in prostate cancer tissues

To the Editor, Although human papillomavirus (HPV) has been associated with the development of specifi c cancers, its role as an aetiological agent of prostate cancer (PCa) is still the subject of debate. Therefore, we read with great interest the article by Dr Aghakhani and co-workers in which they reported the detection of high-risk (HR)-HPV DNA in 13 of 104 (12.5%) PCa and 8 of 104 (7.7%) benign prostatic hyperplasia (BPH) formalin-fi xed paraffi n-embedded tissue specimens [1]. Prior to this article, other investigators had reported higher rates of PCa in men with a history of exposure to HPV [2] and HPV associated with at least a subset of prostate carcinomas [3], while others had found no HPV DNA in PCa tissue [4], with most studies having limited power. Recently we investigated the presence of 14 HRHPV types in prostatic biopsy specimens from 61 Russian patients with PCa and 14 men with BPH (mean age 71.4 and 74.9 y, respectively) using an in-house PCR; only men with abnormal digital rectal examination (DRE) results and serum prostate specifi c antigen (PSA) levels above 4 ng/ml were included in the study. We found no association with PCa: no viral DNA was found in the BPH cases and HPV-16 and HPV-33 DNA were detected in only 3.3% and 1.6%, respectively, of PCa cases. To avoid sampling errors resulting in the taking of no malignant tissue by biopsy, we later sought to determine the presence of 14 HR-HPV types using the validated GP5 /6 assay [5], used worldwide. A total of 80 PCa tissue specimens obtained by taking the 4 histopathologically most suspect slides out of 20 archival paraffi n tissues from Dutch men who had undergone a radical prostatectomy (mean age 61 y, preoperative PSA 13 ng/ml) were investigated (this was supported by a European Urological Scholarship Programme Clinical Fellowship 2007 to Dr Vitaly Smelov); all samples were negative. Our recent data based on HR-HPV DNA detection indeed corroborate the conclusions of Aghakhani and colleagues that this transient most common sexually transmitted viral infection has no major role in the development of PCa [1]. However, men still represent an important source for the transmission of HPV: we need to focus on lowering HPV transmission between sexual partners and the role of male transmission of HPV in the development of other cancers [6].