Lower Incidence Of Prostate Cancer Research Articles

Incretin-based drugs decrease the incidence of prostate cancer in type 2 diabetics: A pooling-up analysis.

Incretin-based drugs, a class of Antidiabetic medications (ADMs) used in the treatment of type 2 diabetes, may affect the incidence of prostate cancer (PCa). But real-world evidence for this possible effect is lacking. Therefore, the aim of this study is to assess the effect of incretin-based drugs on the incidence of PCa, including glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors. We searched PubMed, Embase, and Cochrane Library databases for eligible studies through September 2023. Two independent reviewers performed screening and data extraction. We used the Cochrane Handbook for Systematic Reviews and the Newcastle-Ottawa Scale (NOS) to assess the quality of included randomized controlled trials (RCTs) and cohort studies. We did a meta-analysis of available trial data to calculate overall risk ratios (RRs) for PCa. A total of 1238 articles were identified in our search. After screening for eligibility, 7 high-quality studies met the criteria for meta-analysis, including 2 RCTs and 5 cohort studies, with a total of 1165,738 patients. Compared with the control group, we found that incretin-based drugs reduced the relative risk of PCa by 35% (95% confidence interval (CI), 0.17-0.49; P = .0006). In subgroup analysis, the RR values for GLP-1 receptor agonists and DPP-4 inhibitors were 62% (95% CI, 0.45-0.85; P = .003) and 72% (95% CI, 0.46-1.12; P = .14), respectively. Incretin-based drugs are associated with lower incidence of prostate cancer and may have a preventive effect on prostate cancer in patients with type 2 diabetes.

Climate factors associated with cancer incidence: An ecological study covering 33 cancers from population-based registries in 37 countries

Cancer etiology is multifactorial, with climate change and environmental factors such as extreme weather events and ozone layer destruction potentially increasing cancer risk. Investigating climate factors with cancer incidence can provide valuable insights for prevention and future disease burden prediction. We conducted a population-based ecological study using data from the World Health Organization’s Cancer Incidence in Five Continents (CI5plus, 89 cancer registries from 1998 to 2012) and the Surveillance, Epidemiology, and End Results (SEER, 607 US counties from 2000 to 2018) Program. We tracked climate factors through satellite-based remote sensing, including green space, stratospheric ozone concentration, solar radiation, precipitation, and temperature. We performed linear panel regression models to estimate the effects of both long-term exposure, lag effect, and change rate of climate factors on cancer incidences. We adjusted for smoking prevalence, air pollution, and gross domestic product (GDP) per capita to account for potential confounding factors. Our study included more than 430 million underlying populations across 37 countries. Higher green space exposure (per 0.1-unit normalized difference vegetation index, NDVI) was associated with decreased incidence of lung cancer (up to 6.66 cases [95%CI 4.38–8.93] per 100,000) and prostate cancer (up to 10.84 cases [95% CI 7.73–13.95] per 100,000). Increased solar radiation was associated with a higher incidence of melanoma, but a lower incidence of prostate cancer. No evidence was found to suggest associations between temperature or precipitation and cancer incidence. However, a rapid increase in temperature was linked to higher incidences of corpus uteri cancer and melanoma. Long-term exposure and rapid changes in climate factors may influence changes in cancer incidence, particularly lung and prostate cancers. While some associations were supported by existing evidence (such as solar radiation and melanoma), further research is necessary to investigate the etiology of novel cancer risk factors.

Association between patient ethnicity and prostate cancer diagnosis following a prostate-specific antigen test: a cohort study of 730,000 men in primary care in the UK

BackgroundBlack men have higher prostate-specific antigen (PSA) levels and higher prostate cancer incidence and mortality than White men, while Asian men tend to have lower prostate cancer incidence and mortality than White men. Much of the evidence comes from the USA, and information from UK populations is limited.MethodsThis retrospective cohort study used data on patients registered at general practices in England contributing to the Clinical Practice Research Datalink (CPRD) Aurum dataset. Those eligible were men aged 40 and over with a record of ethnicity and a PSA test result recorded between 2010 and 2017 with no prior cancer diagnosis.The aim was to assess the incidence of prostate cancer following a raised PSA test result in men from different ethnic groups. Additionally, incidence of advanced prostate cancer was investigated. Cancer incidence was estimated from multi-level logistic regression models adjusting for potential confounding factors.Results730,515 men with a PSA test were included (88.9% White). Black men and men with mixed ethnicity had higher PSA values, particularly for those aged above 60 years. In the year following a raised PSA result (using age-specific thresholds), Black men had the highest prostate cancer incidence at 24.7% (95% CI 23.3%, 26.2%); Asian men had the lowest at 13.4% (12.2%, 14.7%); incidence for White men was 19.8% (19.4%, 20.2%). The peak incidence of prostate cancer for all groups was in men aged 70–79. Incidence of prostate cancer diagnosed at an advanced stage was similar between Black and White men.ConclusionsMore prostate cancer was diagnosed in Black men with a raised PSA result, but rates of advanced prostate cancer were not higher in this group. In this large primary care-based cohort, the incidence of prostate cancer in men with elevated PSA levels increases with increasing age, even when using age-adjusted thresholds, with Black men significantly more likely to be diagnosed compared to White or Asian men. The incidence of advanced stage prostate cancer at diagnosis was similar for Black and White men with a raised PSA result, but lower for Asian men.

Effect of aspirin on incidence, recurrence, and mortality in prostate cancer patients: integrating evidence from randomized controlled trials and real-world studies.

Aspirin has been suggested to reduce the risk of cancer. However, previous studies have been inconsistent regarding the relationship between aspirin use and the risk of occurrence of prostate cancer (PCa). The purpose of this study was to assess the effect of aspirin on clinical outcomes in patients with PCa in a meta-analysis and to explore the possible dose-response relationship. A systematic literature search was conducted in 10 electronic databases and 4 registries. The combined relative risks (RRs) were calculated using a random-effects model with 95% confidence interval (CIs) to assess the effect of aspirin on the risk of PCa. Relevant subgroup analyses and sensitivity analyses were performed. The across studies results show that aspirin use associated with lower incidence of PCa (RR: 0.96, 95% CI: 0.95-0.98), and reduced mortality (RR: 0.88, 95% CI: 0.82-0.95). The results of the subgroup analysis indicated that both cohort and population studies in the Americas showed a reduction in PCa incidence and mortality with aspirin use. A linear correlation was observed between dosage/duration of aspirin use and its protective effect. Additionally, post-diagnosis aspirin use was associated with decreased risk of PCa mortality. This meta-analysis revealed an independent correlation between the use of aspirin and reductions in both the incidence and mortality rates of PCa. However, randomized controlled trials did not find any association between aspirin use and PCa. Furthermore, the impact of aspirin on PCa occurrence was found to be dependent on both dosage and duration.

Prostate cancer among South Asian men in the United Kingdom: A systematic review

Introduction: Rates of prostate cancer (PC) vary considerably between ethnic groups worldwide, and migratory studies have demonstrated the importance of both inherent and environmental influences. Healthcare systems also differ significantly worldwide, and comparisons of PC data between the United Kingdom and America have previously shown contradictory conclusions among ethnic groups. The South Asian population (SA) is the most predominant UK ethnic minority group. Aims: To systematically explore and critically analyse the available UK-based evidence regarding PC among SA men. Specifically, to review research that assesses the following factors: PC incidence, disease characteristics, treatment and survival outcomes. Results: The existing evidence suggests that UK SA men have a lower PC incidence and younger age at diagnosis, in comparison with White men in the United Kingdom. Contrasting evidence is presented in studies that separately analyse men originating from India, Pakistan and Bangladesh. There is insufficient and contradictory evidence regarding whether SA men show altered PC disease characteristics or have differential survival rates. The evidence is limited regarding PC treatment; however, this indicates that SA men are less frequently treated surgically compared to White men Conclusion: Further high-quality research is required focusing on accurate ethnicity allocation, analysis of separate SA origin countries, socio-economic adjustment, subgroup analysis of treatment in low-risk PC and identifying the support needs of SA minorities with PC. This will help to ensure that ethnic minorities with PC are appropriately diagnosed, counselled and treated Level of evidence: 3

Prostate cancer in transgender women: considerations for screening, diagnosis and management.

Transgender individuals represent 0.55% of the US population, equivalent to 1.4 million transgender adults. In transgender women, feminisation can include a number of medical and surgical interventions. The main goal is to deprive the phenotypically masculine body of androgens and simultaneously provide oestrogen therapy for feminisation. In gender-confirming surgery (GCS) for transgender females, the prostate is usually not removed. Due to limitations of existing cohort studies, the true incidence of prostate cancer in transgender females is unknown but is thought to be less than the incidence among cis-gender males. It is unclear how prostate cancer develops in androgen-deprived conditions in these patients. Six out of eleven case reports in the literature presented with metastatic disease. It is thought that androgen receptor-mediated mechanisms or tumour-promoting effects of oestrogen may be responsible. Due to the low incidence of prostate cancer identified in transgender women, there is little evidence to drive specific screening recommendations in this patient subpopulation. The treatment of early and locally advanced prostate cancer in these patients warrants an individualised thoughtful approach with input from patients' reconstructive surgeons. Both surgical and radiation treatment for prostate cancer in these patients can profoundly impact the patient's quality of life. In this review, we discuss the evidence surrounding screening and treatment of prostate cancer in transgender women and consider the current gaps in our knowledge in providing evidence-based guidance at the molecular, genomic and epidemiological level, for clinical decision-making in the management of these patients.

MP58-20 USE OF LOW-VALUE PROSTATE-SPECIFIC ANTIGEN SCREENING AMONG YOUNG MEN WITH PRIVATE INSURANCE

You have accessJournal of UrologyCME1 May 2022MP58-20 USE OF LOW-VALUE PROSTATE-SPECIFIC ANTIGEN SCREENING AMONG YOUNG MEN WITH PRIVATE INSURANCE Jeffrey Vehawn, Suzanne Lange, Mouneeb Choudry, Jacob Ambrose, Benjamin Haaland, Jonathan Chipman, Heidi A. Hanson, and Brock O'Neil Jeffrey VehawnJeffrey Vehawn More articles by this author , Suzanne LangeSuzanne Lange More articles by this author , Mouneeb ChoudryMouneeb Choudry More articles by this author , Jacob AmbroseJacob Ambrose More articles by this author , Benjamin HaalandBenjamin Haaland More articles by this author , Jonathan ChipmanJonathan Chipman More articles by this author , Heidi A. HansonHeidi A. Hanson More articles by this author , and Brock O'NeilBrock O'Neil More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000002641.20AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Debate remains about the value of Prostate-specific antigen (PSA) based prostate cancer screening among men aged 55-69 (USPSTF Grade C). However, no professional society or guideline recommends PSA based prostate cancer screening in men younger than age 40. This study aims to understand the risk of PSA testing exposure in young men, and we hypothesize that substantial low-value testing occurs in this population. METHODS: We performed a retrospective analysis of claims data from the MarketScan database to identify men aged 18 to 39 without prostate cancer who received a PSA test from 2008 to 2017. For the primary analysis, men were required to be continuously in the database for least 5 years. Age groups were stratified to include: men less than 25, 25-29, 30-34, and 35-39 years.Secondary analysis did not limit subjects to those with 5 years of continuous data and explored the association of Charlson Comorbidity Index (CCI), lower urinary tract symptoms, erectile dysfunction, depression/anxiety, prostate cancer screening, infertility, and hypogonadism with PSA testing in young men. We used logistic regression to determine which of the factors were associated with PSA testing in young men. RESULTS: We identified claims for 40,164,773 adult men who met study criteria. Of these men, 3,230,748 were continuously in the Marketscan database for at least 5 years. The cumulative risk for receiving a PSA over 5 years for men under 40 is 2.5%. Stratified by age, men aged 35-39 are at highest risk. Logistic multivariable regression showed that, relative to all men between 18 and 40, patients in this age group who received a PSA were more likely to be diagnosed with hypogonadism (OR 20.55, 95% CI 20.39-20.71) or lower urinary tract symptoms (OR 9.34, 95% CI 9.26-9.41). Higher CCIs appeared to correlate with a decreased rate of PSA testing. This population was not significantly more likely to be diagnosed with infertility, depression, or anxiety. CONCLUSIONS: PSA screening for men under 40 is not uncommon, especially when associated with concomitant genitourinary symptoms. At a population level, this represents substantial low-value testing. Interventions aimed at clarifying the relationship between common urologic conditions and prostate cancer, the extremely low incidence of prostate cancer in this age group, and the lack of guidelines supporting this practice may help decrease low-value PSA testing. Source of Funding: Research reported in this publication was supported by the National Cancer Institute of the National Institutes of Health under Award Number K08CA234431. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health © 2022 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 207Issue Supplement 5May 2022Page: e1000 Advertisement Copyright & Permissions© 2022 by American Urological Association Education and Research, Inc.MetricsAuthor Information Jeffrey Vehawn More articles by this author Suzanne Lange More articles by this author Mouneeb Choudry More articles by this author Jacob Ambrose More articles by this author Benjamin Haaland More articles by this author Jonathan Chipman More articles by this author Heidi A. Hanson More articles by this author Brock O'Neil More articles by this author Expand All Advertisement PDF DownloadLoading ...

Low-value prostate cancer screening among young men with private insurance.

240 Background: Debate remains about the value of Prostate-specific antigen (PSA) based prostate cancer screening among men aged 55-69 (USPSTF Grade C). However, no professional society or guideline recommends PSA based prostate cancer screening in men younger than age 40. This study aims to understand the risk of PSA testing exposure in young men, and we hypothesize that substantial low-value testing occurs in this population. Methods: We performed a retrospective analysis of claims data from the MarketScan database to identify men aged 18 to 39 without prostate cancer who received a PSA test from 2008 to 2017. For the primary analysis, men were required to be continuously in the database for least 5 years. Age groups were stratified to include: men less than 25, 25-29, 30-34, and 35-39 years. Secondary analysis did not limit subjects to those with 5 years of continuous data and explored the association of Charlson Comorbidity Index (CCI), lower urinary tract symptoms, erectile dysfunction, depression/anxiety, prostate cancer screening, infertility, and hypogonadism with PSA testing in young men. We used logistic regression to determine which of the factors were associated with PSA testing in young men. Results: We identified claims for 40,164,773 adult men who met study criteria. Of these men, 3,230,748 were continuously in the Marketscan database for at least 5 years. The cumulative risk for receiving a PSA over 5 years for men under 40 is 2.5%. Stratified by age, men aged 35-39 are at highest risk (Table). Logistic multivariable regression showed that, relative to all men between 18 and 40, patients in this age group who received a PSA were more likely to be diagnosed with hypogonadism (OR 20.55, 95% CI 20.39-20.71) or lower urinary tract symptoms (OR 9.34, 95% CI 9.26-9.41). Higher CCIs appeared to correlate with a decreased rate of PSA testing. This population was not significantly more likely to be diagnosed with infertility, depression, or anxiety. Conclusions: PSA screening for men under 40 is not uncommon, especially when associated with concomitant genitourinary symptoms. At a population level, this represents substantial low-value testing. Interventions aimed at clarifying the relationship between common urologic conditions and prostate cancer, the extremely low incidence of prostate cancer in this age group, and the lack of guidelines supporting this practice may help decrease low-value PSA testing. Funding: Research reported in this publication was supported by the National Cancer Institute of the National Institutes of Health under Award Number K08CA234431. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.[Table: see text]

Prostate cancer clinical trial completion: The role of geography

Background/aimsOne in five cancer clinical trials fails with another third failing to meet enrollment goals. Prior efforts to improve enrollment focus on patient facing interventions, but geographic factors such as regional cancer incidence may doom trials before they even begin. For these reasons, we examined associations of regional prostate cancer incidence with trial termination, and identified scientifically-underserved areas where future trials might thrive. MethodsWe merged US phase 2–3 prostate cancer clinical trial data from ClinicalTrials.gov with prostate cancer incidence data from statecancerprofiles.cancer.gov. We matched trial information from 293 closed and 560 active trials with incidence data for 2947 counties. Using multivariable logistic regression, we identified associations with trial termination. We identified ‘scientifically-underserved’ counties with the highest cancer incidence quintile (>61 annual cases) but lowest active trials quintile (0 or 1 trial). ResultsOf 293 closed trials, one in three was terminated (n = 96, 32.8%). On multivariable analysis, only lower regional prostate cancer incidence was associated with higher likelihood of premature trial termination (OR 0.98, 95% CI [0.96–0.99] for every 100 cases, p = 0.03). We identified 188 counties with >61 annual prostate cancer cases but 0 or 1 active trials, indicating potential scientifically-underserved areas. ConclusionsIn this novel study, we found prostate cancer trials in areas with low prostate cancer incidence were more likely to fail. We also identified scientifically-underserved areas where trials might thrive. Our findings provide a more nuanced understanding of clinical trial feasibility and upstream opportunities for improvement.

Factors Associated with Urethral and Bladder Neck Stricture After Transurethral Resection of the Prostate.

Introduction: Urethral and bladder neck stricture (U/BNS) is a complication that occurs in up to 9% of patients following transurethral resection of the prostate (TURP). The most relevant risk factors reported are prolonged surgical duration and prostatic volume. The purpose of this study is to analyze risk factors associated with the development of U/BNS following TURP. Materials and Methods: Case-control study. Population: patients who underwent TURP. Cases: patients with U/BNS following TURP, diagnosed between January 2010 and December 2018. We included patients with obstructive symptoms after TURP with clinical or radiographical evidence of U/BNS. Controls were patients who underwent TURP between January 2016 and December 2017, without evidence of stricture. Patients with history of pelvic fracture and previous U/BNS were excluded. We analyzed as risk factors age, prostatic volume, diabetes mellitus, previous use of transurethral catheter, urinary tract infection, bladder calculi, prostate cancer, previous TURP, resection time, resected volume during TURP, transoperative complications, and number of surgical procedures performed during the same event. We used chi-square or Mann-Whitney's U test for between-group comparison; association was established by odds ratios (ORs) and 95% confidence interval (CI), variables with p < 0.05 were included in the logistic regression. Results: We included 101 cases and 207 controls. Cases had lower incidence of prostate cancer, smaller prostates, less resection time during TURP, lower grams resected and prostate-specific antigen values than controls. History of transurethral catheter was more frequent in controls than cases (46% vs 29%, p = 0.004); there were no differences between groups in the other factors analyzed. On multivariate analysis, the use of a transurethral catheter was a protective factor against U/BNS (OR 0.16, 95% CI 0.064-0.442, p < 0.001). Conclusions: In this study, the use of urethral catheter before TURP is a protective factor against U/BNS.

Population-wide impacts of aspirin, statins, and metformin use on prostate cancer incidence and mortality

We evaluated the association between aspirin, statins, and metformin use and prostate cancer (PC) incidence and mortality using a large population-based dataset. 388,760 men who participated in national health screening program in Korea during 2002–2003 were observed from 2004 to 2013. Hazard ratios of aspirin, statins, and metformin use for PC incidence and PC mortality were calculated with adjustment for simultaneous drug use. Cumulative use of each drug was inserted as time-dependent variable with 2-year time windows. Aspirin use ≥ 1.5 year (per 2-year) was associated with borderline decrease in PC mortality when compared to non-users (adjusted hazard ratio [aHR] 0.71, 95% confidence interval [CI] 0.50–1.02). Statins use was not associated with either PC incidence or PC mortality. Metformin ever-use was associated with decreased PC incidence compared with non-diabetics (aHR 0.86, 95% CI 0.77–0.96). Diabetics who were not using metformin or using low cumulative doses had higher PC mortality than non-diabetics (aHR 2.01, 95% CI 1.44–2.81, and aHR 1.70, 95% CI 1.07–2.69, respectively). However, subjects with higher cumulative doses of metformin did not show increased PC mortality. In conclusion, metformin use was associated with lower PC incidence. Use of aspirin and that of metformin among diabetic patients were associated with lower PC mortality.

Living alone as a risk factor for cancer incidence, case-fatality and all-cause mortality: A nationwide registry study

Lack of social contacts has been associated with an increased risk of cancer mortality, but it is not known whether living alone increases the risk of cancer incidence or case fatality. We examined the association between living alone with cancer incidence, case-fatality and all-cause mortality in eight most common cancers. All patients with their first cancer diagnosis in 2000–2017 were identified from the nationwide Finnish Cancer Registry. Information on living arrangements was derived from Statistics Finland. The incidence analyses were conducted using Poisson regression. The total Finnish population served as the population at risk. Fine-Gray model was used to estimate case-fatality and Cox proportional regression model all-cause mortality. In men, we found an association between history of living alone and excess lung cancer incidence but living alone seemed to be associated with lower incidence of prostate cancer and skin melanoma. In women, living alone was more consistently associated with higher incidence of all studied cancers. Cancer patients living alone had an 11%–80% statistically significantly increased case-fatality and all-cause mortality in all studied cancers in men and in breast, colorectal and lung cancer in women. Living alone is consistently associated with increased cancer incidence risk in women but only in some cancers in men. Both men and women living alone had an increased risk of all-cause mortality after cancer diagnosis.

Oncological diseases in Klinefelter Syndrome: an overview.

Epidemiological studies have highlighted a higher incidence of morbidity and mortality among individuals with Klinefelter's Syndrome (KS), however, the relative impact of oncological diseases on KS subjects is still uncertain. While some malignancies (e.g., hematological and lung cancers) may show an increased prevalence in the KS population, only a few rare tumors (i.e., extragonadal germ cell tumors [GCTs] and male breast cancer [MBC]) seem to follow this trend. Additionally, hormonal and genetic determinants may be involved in the pathogenesis of neoplasia in KS, even if subjects affected by this syndrome generally show lower incidence of prostate cancer along with lower disease-specific mortality despite testosterone replacement therapy (TRT). This review deals with the pathophysiological and clinical aspects of neoplastic diseases occurring in KS.

Expression Patterns of ERα, ERβ, AR, SIRT1, SIRT2, and SIRT3 in Prostate Cancer Tissue and Normal Prostate Tissue

The purpose of this study was to examine the expression of estrogen receptor α (ERα) and β (ERβ), androgen receptor (AR), SIRT1, SIRT2 and SIRT3 in prostate cancer (PCa). From October 2010 to January 2015, 70 patients who had undergone radical prostatectomy following a PCa diagnosis were enrolled in our study. Normal prostate tissue (NPT) and prostate cancer tissues (PCAT) were separated, and the expression of each receptor in each tissue was analyzed with immunochemical staining. Univariate and multivariate analyses were performed to identify factors affecting the development of PCa. ERβ and AR were highly expressed in PCAT compared with NPT (p<0.05). SIRT2 was highly expressed in NPT and PCAT (p<0.05). Univariate and multivariate analyses showed that AR and SIRT2 affect PCa development. AR is a risk factor for PC, and SIRT2 is associated with a lower incidence of PCa.

Whole-exome Sequencing of Prostate Cancer in Sardinian Identify Recurrent UDP-glucuronosyltransferase Amplifications.

Globally, prostate cancer is the third most common cancer in the world, and the second most common cancer in men. However, rates for incidence and mortality vary considerably with race, ethnicity, and geography. Over 97 significantly mutated genes that have been identified in prostate cancer; however, a lack of genomic prostate cancer studies focusing on different racial and ethnic groups and racial mixing pose a serious challenge to universalize these findings. The Sardinian population is an isolated Mediterranean population that has a high frequency of centenarians and a much lower incidence of prostate cancer than found in males in mainland Europe. Here, we conducted a genomic prostate cancer study on a Sardinian cohort diagnosed with local prostate cancer. Our data reveals a low rate of ERG fusion in Sardinian prostate cancer. Interestingly, we identified a novel BTBD7-SLC2A5 fusion that occurred in 13% of the patients. We also found that the UGT2B4 on 4q13.2 was amplified in 20% of the Sardinian patients but rarely amplified in patients of other population. These observations underscore the importance of the inter-population molecular heterogeneity of prostate cancer. In addition, we examined the expression of UGT2B4 in 497 prostate cancer patients derived from The Cancer Genome Atlas database. We found that high expression of UGT2B4 was associated with low-grade prostate cancer and upregulation of UGT2B4 in tumors was associated with upregulation of metabolism pathways such as 'de novo' IMP biosynthetic process, glutamine and monocarboxylic acid metabolism. These data provide insight into clinical relevance and functional mechanism of UGT2B4. Further understanding functional mechanism of UGT2B4 amplification and BTBD7-SLC2A5 fusion will aid in developing drugs to benefit the prostate cancer patients.

Presenting Pattern and Treatment Modalities of Prostate Cancer in Nicrh

Objective: The aim was to describe the clinicopathological presentation of prostate cancer and the treatment modality in patients seen in Uro-oncology department of National Institute of Cancer Research &amp; Hospital (NICRH), Bangladesh.&#x0D; Methods: Data were collected prospectively from all patients with diagnosed prostate cancer and managed in Uro-oncology department of NICRH from January 2016 to December 2017. Patient’s age, clinical presentation, prostate specific antigen(PSA) level, mode of diagnosis, Gleason sum score, stage of the disease at presentation and modality of treatment were recorded and analyzed.&#x0D; Results: There were 407 cases of histologically proven prostate cancer. Mean patient age was 69 years. About 87% presented as diagnosed prostate cancer. Twenty one(5%) patient presented with features of metastasis with unknown primary , we confirmed after prostate biopsy. About 77% of patients had a serum PSA above 20 ng/ml. Gleason sum score was 8 or more in 46% of patients. Metastases were found at the time of presentation in 85% of patients. Ten (2.5%) patients underwent radical radiotherapy, while two patients had radical prostatectomy. Most (68%) of the 347 patients who required androgen deprivation therapy had surgical orchiectomy.&#x0D; Conclusion: Bangladesh appear to be having a low incidence of prostate cancer, but a larger proportion of advanced and high grade cancers in comparison to the UK and USA. Although genetic differences may exist, a dietary or an environmental factor is more likely to be the cause for these changes. The protective effect of this factor appears to wane as South Asians emigrate and live in UK and USA.&#x0D; Bangladesh Journal of Urology, Vol. 21, No. 2, July 2018 p 56-61

Risk of prostate cancer in men with HIV/AIDS: a systematic review and meta-analysis.

Although previous studies have shown a decreased incidence of prostate cancer in men with HIV/AIDS, the consensus has not been reached. Our aim is to conduct a systematic review and meta-analysis to assess the risk of prostate cancer among people with HIV/AIDS. We systematically searched PubMed, Web of Science, Embase, and Cochrane Library until March 2020. Cohort studies were included if they compared the prostate cancer risk between people with HIV/AIDS and uninfected controls or the general population. The summary standardized incidence ratio (SIR) and 95% confidence interval (CI) were calculated using a random-effects model. A total of 27 studies were included for analysis, with more than 2780 males with HIV/AIDS developing prostate cancer. The results showed that HIV infection was associated with a decreased risk of prostate cancer incidence (SIR, 0.76; 95% CI, 0.64-0.91; P = 0.003), with significant heterogeneity (P < 0.001; I2 = 91.6%). A range of sensitivity analyzes did not significantly change the results. Our study shows that people with HIV/AIDS have a lower incidence of prostate cancer compared with the general population. However, significant heterogeneity exists among the included studies. Further prospective studies with better designs are needed to elucidate the association between HIV infection and prostate cancer.

Sedentary Behavior and Prostate Cancer: A Systematic Review and Meta-Analysis of Prospective Cohort Studies.

Prostate cancer is the second most common cancer in men worldwide, and sedentary behavior is widespread, yet reviews and meta-analyses summarizing the role of sedentary behavior as a potential risk factor for prostate cancer are scarce. We searched PubMed, Web of Science, and Cochrane databases for relevant articles up to January 2019. We pooled maximally adjusted risk estimates in a random effects model and performed meta-regression meta-analysis, assessed heterogeneity and publication bias using I², funnel plots, and Egger and Begg tests, and conducted sensitivity analyses and influence diagnostics. Data from 12 prospective cohort studies including a total of 30,810 prostate cancer cases were analyzed. We found no statistically significant association between high versus low sedentary behavior and prostate cancer incidence [RR = 1.07; 95% confidence interval (CI), 0.99-1.16; P = 0.10]. We noted that adjustment for body mass index (BMI) modified the relation of sedentary behavior to prostate cancer, particularly aggressive cancer. Sedentary behavior was related to a statistically significant increased risk of aggressive prostate cancer in analyses not adjusted for BMI (RR = 1.21; 95% CI, 1.03-1.43), whereas no association was apparent in BMI-adjusted analyses (RR = 0.98; 95% CI, 0.90-1.07), and the difference between those summary risk estimates was statistically significant (P difference = 0.02). Sedentary behavior is not independently associated with prostate cancer. However, prolonged sedentary behavior may be related to increased risk of aggressive prostate cancer through a mechanism involving obesity. This finding represents a potentially important step toward considering sedentary behavior as a modifiable behavioral risk factor for aggressive prostate cancer.

High dietary fat intake lowers serum equol concentration and promotes prostate carcinogenesis in a transgenic mouse prostate model

BackgroundConsumption of diet high in soy products is suggested to contribute to lower prostate cancer incidence in Asian men. But little has been known about the influences of dietary patterns on gut microbiota and microbiota-mediated isoflavone metabolism. Here, we determined the influences of western pattern diet on prostate carcinogenesis, gut microbiota and microbiota-mediated equol metabolism using a transgenic adenocarcinoma of mouse prostate (TRAMP) model.MethodsWe mimicked the western pattern diet using a high fat diet (HFD). TRAMP mice were fed with either control diet (CD) or HFD. At the age of 24 weeks, mice were orally administered daidzein over a 4-day period, and then sacrificed. The serum daidzein and equol were analyzed by ultra high performance liquid chromatography. Fecal microbiome was analyzed with fecal 16S rRNA pyrosequencing, and prostate was dissected and performed with histopathology.ResultsHFD could promote prostate carcinogenesis in TRAMP mice (p = 0.045). The daidzein showed no significant differences between CD and HFD groups, while equol was significantly decreased in HFD group (p = 0.019). Fecal microbiotas differed between the two groups, 21 microbial phylotypes were increased and 11 phylotypes were decreased in abundance in HFD group, including decreased abundance of equol-producing bacterium Adlercreutzia (0.08% vs. 0.27%).ConclusionsHFD may promote prostate carcinogenesis through adversely affecting equol-producing bacterium. Further functional validations are required to ascertain the mechanism of those HFD-responsive bacteria in carcinogenesis.

Role of Estrogen in Androgen-Induced Prostate Carcinogenesis in NBL Rats.

Androgens are thought to cause prostate cancer, but the underlying mechanisms are unclear. Data from animal studies suggest that for androgens to cause prostate cancer, they must be aromatized to estrogen and act in concert with estrogen metabolites. We tested the hypothesis that androgen-receptor and estrogen receptor-mediated effects of androgen and estrogen are necessary, as well as genotoxicity of estrogen metabolites. NBL rats were treated with androgenic and estrogenic compounds for 16-75weeks through slow-release silastic implants or pellets. Testosterone alone induced cancer in the prostate of 37% of rats. 5α-Dihydrotestosterone, which cannot be converted to estradiol or testosterone, did not cause a significant prostate cancer incidence (4%). Addition of estradiol to 5α-dihydrotestosterone treatment did not markedly enhance prostate cancer incidence (14%), unlike adding estradiol to testosterone treatment which induced a 100% tumor incidence. Testosterone plus estradiol treatment induced a DNA adduct detectable by 32P-postlabeling, oxidative DNA damage (8-hydroxyguanosine), and lipid peroxidation at the site within the prostate where this treatment causes cancers, preceding later cancer formation. The non-estrogenic 4-hydroxy metabolite of estradiol, when combined with testosterone, induced prostatic dysplasia within 16weeks and, after long-term treatment, a very low incidence of prostate cancer (21%). When an estrogen that cannot be hydroxylated (2-fluoroestradiol) was added to this combined treatment with testosterone and 4-hydroxyestradiol, dysplasia frequency after 16weeks was doubled. These results strongly support the hypothesis, but additional definitive studies are needed which may identify new targets to interfere with these mechanisms that are clinically feasible in humans.