Prostate Cancer Risk Research Articles

A Comparison of Prostate Cancer Screening Information Quality on Standard and Advanced Versions of ChatGPT, Google Gemini, and Microsoft Copilot: A Cross-Sectional Study.

Artificially Intelligent (AI) chatbots have the potential to produce information to support shared prostate cancer (PrCA) decision-making. Therefore, our purpose was to evaluate and compare the accuracy, completeness, readability, and credibility of responses from standard and advanced versions of popular chatbots: ChatGPT-3.5, ChatGPT-4.0, Microsoft Copilot, Microsoft Copilot Pro, Google Gemini, and Google Gemini Advanced. We also investigated whether prompting chatbots for low-literacy PrCA information would improve the readability of responses. Lastly, we determined if the responses were appropriate for African-American men, who have the worst PrCA outcomes. The study used a cross-sectional approach to examine the quality of responses solicited from chatbots. The study did not include human subjects. Eleven frequently asked PrCA questions, based on resources produced by the Centers for Disease Control and Prevention (CDC) and the American Cancer Society (ACS), were posed to each chatbot twice (once for low literacy populations). A coding/rating form containing questions with key points/answers from the ACS or CDC to facilitate the rating process. Accuracy and completeness were rated dichotomously (i.e., yes/no). Credibility was determined by whether a trustworthy medical or health-related organization was cited. Readability was determined using a Flesch-Kincaid readability score calculator that enabled chatbot responses to be entered individually. Average accuracy, completeness, credibility, and readability percentages or scores were calculated using Excel. All chatbots were accurate, but the completeness, readability, and credibility of responses varied. Soliciting low-literacy responses significantly improved readability, but sometimes at the detriment of completeness. All chatbots recognized the higher PrCA risk in African-American men and tailored screening recommendations. Microsoft Copilot Pro had the best overall performance on standard screening questions. Microsoft Copilot outperformed other chatbots on responses for low literacy populations. AI chatbots are useful tools for learning about PrCA screening but should be combined with healthcare provider advice.

Impact of Genomic Classifiers on Risk Stratification and Treatment Intensity in Patients With Localized Prostate Cancer : A Systematic Review.

Tissue-based genomic classifiers (GCs) have been developed to improve prostate cancer (PCa) risk assessment and treatment recommendations. To summarize the impact of the Decipher, Oncotype DX Genomic Prostate Score (GPS), and Prolaris GCs on risk stratification and patient-clinician decisions on treatment choice among patients with localized PCa considering first-line treatment. MEDLINE, EMBASE, and Web of Science published from January 2010 to August 2024. Two investigators independently identified studies on risk classification and treatment choice after GC testing for patients with localized PCa considering first-line treatment. Relevant data extracted by 1 researcher and overread by a second. Risk of bias (ROB) was assessed in duplicate. Ten studies reported risk reclassification after GC testing. In low ROB observational studies, very low- or low-risk patients with PCa were more likely to have their risk levels classified as the same or lower (GPS, 100% to 88.1%; Decipher, 87.2% to 82.9%; Prolaris, 76.9%). However, 1 randomized trial found that GC testing with GPS reclassified 34.5% of very low-risk and 29.4% of low-risk patients to a higher risk category. Twelve observational studies indicated that treatment decisions after GC testing either remained unchanged or slightly favored active surveillance. In contrast, analyses from a single randomized trial found fewer choices for active surveillance after GPS testing. Heterogeneity in screening patterns, risk-determination cutoffs, pathology, and clinical practices. Studies on treatment choice were moderate to high ROB. Although GC tests do not consistently influence risk classification or treatment decisions, the differences observed between observational and randomized studies highlight a need for well-designed trials to explore the role of GC tests in patients with newly diagnosed PCa considering first-line treatment. U.S. Department of Veterans Affairs. (PROSPERO: CRD42022347950).

Prostate-specific antigen screening at low thresholds of men with pathogenic BRCA1/2 variants.

Men with pathogenic BRCA1/2 variants are at higher risk of prostate cancer We included men with likely pathogenic/pathogenic (LP/P) variants in BRCA1/2 in a prostate-specific antigen (PSA) screening program after cascade germline testing since 2014. PSA was tested yearly and an age-specific low PSA threshold for biopsy was used, to determine if a low PSA threshold for biopsy is justified for men with pathogenic BRCA1/2 variants. From 2014 to 2023 a total of 340 men were included in the program. We report demographics, clinical characteristics, and treatment outcomes at 7 years. The cumulative incidence of a primary biopsy was 37% (95CI: 31‒43) after 7 years. Incidence of prostate cancer diagnosis was 11% (95CI: 7.1‒15). Men referred were 7.8 (95CI: 5.3‒11, p < 0.001) times more likely to be diagnosed with prostate cancer than the general Danish male population. The cumulative incidence of biochemical failure (PSA > = 0.2 ng/ml) 4 years after RP was 22% (95CI: 2.3‒41). The main limitation is that not all men underwent a pre-biopsy MRI. We found a high incidence of prostate cancer in men with LP/P BRCA1/2 variants, but this may be explained by the low PSA threshold for scheduling biopsies. More studies are needed to compare this patient population to men with other germline features. The high risk of recurrence after curative therapy is worrisome and requires further evaluation as to whether this is a biological phenomenon.

A Haplotype GWAS in Syndromic Familial Colorectal Cancer.

A previous genome-wide association study (GWAS) in colorectal cancer (CRC) patients with gastric and/or prostate cancer in their families suggested genetic loci with a shared risk for these three cancers. A second haplotype GWAS was undertaken in the same colorectal cancer patients and different controls with the aim of confirming the result and finding novel loci. The haplotype GWAS analysis involved 685 patients with colorectal cancer cases and 1642 healthy controls from Sweden. A logistic regression model was used with a sliding window haplotype approach. Whole-genome and exome sequencing datawere used to find candidate SNPs to be tested in a nested case-control study. In the analysis of 685 colorectal cancer cases and 1642 controls, all ten candidate loci from the previous study were confirmed. Fifty candidate loci were suggested with a p-value < 5 × 10-6 and odds ratios between 1.35-6.52. Two of the 50 loci, on 13q33.3 and 16q23.3, were the same as in the previous study. Whole-genome or exome data from 122 colorectal cancer patients was used to search for candidate variants in these 50 loci. A nested case-control study was performed to test genetic variants at 11 loci in a cohort of 827 familial colorectal cancer and a sub-cohort of 293 familial CRC cases with colorectal, gastric, and/or prostate cancer within their families and 1530 healthy controls. One SNP, rs115943733 on 10q11.21, reached statistical significance (OR = 3.26, p = 0.009). Seven SNPs in 4 loci had a higher OR in the smaller cohort compared to the larger study CRC cases. The results in this GWAS gave support for suggested loci with an increased shared risk of CRC, gastric, and/or prostate cancer. Further studies are needed to confirm the shared risk to be able to use this information in cancer prevention.

Understanding the role of metabolic syndrome in prostate cancer risk: A UK Biobank prospective cohort study

Predictive value of metabolic syndrome for prostate cancer risk is not clear. We aimed to assess the association between metabolic syndrome and its components with prostate cancer incidence. The primary outcome was prostate cancer incidence, i.e., incidence rate ratios and adjusted cumulative incidence curves derived from flexible parametric survival models. Adjusted cumulative incidence curves were derived using a flexible survival parametrical modeling framework. We analysed UK Biobank data including 242,349 adult males, recruited during 2006–2010 and followed up until 2021, during which 6,467 (2.7%) participants were diagnosed with prostate cancer. Our findings indicate that metabolic syndrome, as a whole, was not associated with prostate cancer risk (incidence rate ratios, 1.07; 95% confidence interval, 0.94–1.22). However, specific components such as hypertension and obesity increased the risk (incidence rate ratios, 1.22; 95% confidence interval, 1.03–1.44 and incidence rate ratios, 1.24; 95% confidence interval, 1.05–1.46, respectively). Other components, such as prediabetes/diabetes and low cholesterol, were associated with a reduced risk (incidence rate ratios, 0.80; 95% confidence interval, 0.67–0.94 and incidence rate ratios, 0.82; 95% confidence interval, 0.69–0.97, respectively), while hyperlipidaemia showed no significant effect (incidence rate ratios, 1.07; 95% confidence interval, 0.93–1.24). Further research is needed to understand the underlying mechanisms behind these relationships. Prostate cancer prevention strategies might benefit from targeting modifiable risk factors, particularly hypertension and obesity.

Vitamin D-related genetic variants and prostate cancer risk in Black men.

The relationship between vitamin D and prostate cancer has primarily been characterized among White men. Black men, however, have higher prostate cancer incidence and mortality rates, chronically low circulating vitamin D levels, and ancestry-specific genetic variants in vitamin D-related genes. Here, we examine critical genes in the vitamin D pathway and prostate cancer risk in Black men. We assessed a total of 73 candidate variants in genes (namely GC, CYP27A1, CYP27B1, CYP24A1, VDR, and RXRA) including functional variants previously associated with prostate cancer and circulating 25(OHD) in White men. Associations with prostate cancer risk were examined using genome-wide association study data for approximately 10,000 prostate cancer cases and 10,000 controls among Black men and over 85,000 cases and 91,000 controls among White men for comparison. A statistical significance threshold of 0.000685 was used to account for the 73 variants tested. None of the variants examined were significantly associated with prostate cancer risk among Black men after multiple comparison adjustment. Suggestive associations (P < 0.05) for four variants were found in Black men, including two in RXRA (rs41400444 OR=1.09, 95 % CI: 1.01-1.17, P = 0.024 and rs10881574 OR = 0.93, 0.87-1.00, P = 0.046) and two in VDR (rs2853563 OR = 1.07, 1.01-1.13, P = 0.017 and rs1156882 OR = 1.06, 1.00-1.12, P = 0.045). Two variants in VDR were also positively associated with risk in White men (rs11568820 OR = 1.04, 1.02-1.06, P = 0.00024 and rs4516035 OR = 1.03, 1.01-1.04, P = 0.00055). We observed suggestive associations between genetic variants in RXRA and VDR and prostate cancer risk in Black men. Future research exploring the relationship of vitamin D with cancer risk in Black men will need larger sample sizes to identify ancestry-specific variants relevant to risk in this population.

Gut microbiota, metabolites, and cytokines in relation to the risk of prostate cancer in the Asian population

PurposeStudies have shown that gut microbiota is involved in the tumorigenesis and development of prostate cancer. We aimed to perform a comprehensive analysis of causal associations of gut microbiota, metabolites, and cytokines with prostate cancer in the Asian population.Patients and methodsGenome-wide association study (GWAS) summary datasets were collected from the public databases. There were 418 bacterial traits, 452 metabolites, 91 cytokines, 5408 cases of prostate cancer from East Asia, and 109,347 controls included. Mendelian randomization (MR) analyses were performed to investigate their causal relationships. Sensitivity analyses were conducted to test the reliability of MR results. Furthermore, the FinnGen database was used to assess the generalizability of our findings based on Asians.ResultsThere were a total of 17 bacterial traits, 28 metabolites (including 2 microbiota-associated metabolites), and 9 cytokines to be significantly associated with prostate cancer in Asians (P &amp;lt; 0.05). Further MR analyses of these positive results indicated that G_Ruminococcaceae UCG014/TNFSF10 axis, G_Anaerofilum/TNFRSF14 axis, G_Erysipelotrichaceae UCG003/TNFSF10 axis, and P_Proteobacteria/cholesterol axis were key signaling pathways involved in the progression of prostate cancer. Notably, G_Ruminococcaceae UCG014/TNFSF10 axis and G_Anaerofilum/TNFRSF14 axis were found to act as protective factors, while the other two signaling axes played a crucial role in promoting the progression of prostate cancer. Sensitivity analyses further confirmed the reliability of our findings. Using the European population as outcome, we further assessed the generalizability of our conclusions and found limited applicability to Europeans.ConclusionsWe found that there were causal associations of gut microbiota, metabolites, and cytokines with prostate cancer in Asians. The causal effects of gut microbiota on prostate cancer were partially mediated by metabolites and cytokines. These findings might contribute to the development of new therapeutic strategies for prostate cancer.

Rethinking prostate cancer screening in transgender women

Introduction: Over the years, the number of people openly identifying as transgender has steadily increased, leading to a greater need for transgender-specific healthcare information. Among transgender women (TW), there remains a risk of prostate cancer since the prostate is not removed during gender-affirming hormone therapy (GAHT) or surgery; however, there is limited knowledge about prostate cancer screening in the transgender population. Although there are few reported cases of prostate cancer screening or prostate-specific antigen (PSA) testing in TW, the impact of hormone therapies on PSA levels is well-documented. Notably, GAHT for TW and hormone therapy for treating prostate cancer share similarities. Drawing on these similarities, we aimed to develop guidelines for baseline PSA levels and prostate cancer screening in TW. Methods: Through a systematic review, we examined the existing PubMed publications on PSA levels and prostate cancer screening in TW, as well as expected PSA levels in patients with prostate cancer undergoing hormone therapies. We also investigated other aspects considered for the diagnosis of prostate cancer. Given the limited research on TW, we also included relevant case studies. These publications and case reports were reviewed and analyzed to create a comprehensive overview of expected baseline PSA levels and prostate cancer screening guidelines for TW. Results: Currently, there are no established guidelines for PSA or prostate cancer screening in TW; however, these case studies indicated a range of PSA values from 3.3 to &lt;100 ng/ml. Existing literature on expected PSA levels in prostate cancer patients undergoing hormone therapy shows a reduction in PSA of over 50% post-therapy. This evidence suggests that PSA values in TW presenting with prostate cancer may be lower than those observed in cisgender males with the disease. Conclusions: While TW exhibit lower prostate cancer incidence compared to cisgender men, the impact of hormone therapy on PSA levels presents significant challenges for screening and diagnosis. The parallels between PSA level reductions in TG women and cisgender men undergoing estrogen therapy highlight the need for revised screening protocols. Addressing these challenges through targeted research and personalized care approaches will be vital for improving prostate cancer management in transgender individuals.

Prostate Cancer and Suicide Risk: A Systematic Review and Meta-Analysis.

Suicide is a substantial public health concern, and there are a variety of contributing factors. Prostate cancer is known to be a disease at high risk of suicide regardless of country and age. Nonetheless, comprehensive information about associated risk levels and underlying determinants remains limited. To systematically evaluate the suicide risk in prostate cancer patients compared to control by systematic review and meta-analysis. PubMed, Embase, and the Cochrane Library were searched from the earliest available indexing date through May 2024. The criteria for selecting the subjects were as follows: (1) studies including patients who had prostate cancer, (2) intervention was not specified, (3) comparison was made with people without prostate cancer selected as the control group, and (4) outcomes were measured as standardized mortality ratio (SMR) or relative risk (RR), or hazard ratio (HR) of suicide in prostate cancer. Random-effects model were used to estimate pooled effect sizes. Meta-regression analyses were conducted to identify the potential moderator effects between prostate cancer and the risk of suicide. A systematic review and meta-analysis of these 25 studies that included a total of 4,987,941 participants were performed. The pooled SMR for overall suicide risk in prostate cancer compared with control groups was 1.251 (95% confidence interval [95% CI]: 1.120-1.383). The pooled RR or HR was 1.712 (95% CI: 1.306-2.243). The suicide risk of prostate cancer patients showed statistically significant in all cases of SMR and RR or HR. The suicide risk was also significantly higher in most subgroup analyses according to age and research follow-up period. The findings of this systematic review and meta-analysis support the association between prostate cancer and increased risk of suicidal tendencies. Follow-up for prostate cancer patients should be highly integrated with psychiatric and psychological care to improve the psychosocial function of patients.

Causal relationship between rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and risk of prostate cancer: Multivariable and bidirectional Mendelian-randomization analyses.

Previous studies have suggested an association between autoimmune diseases (AIDs) and the risk of prostate cancer (PCa). However, the causal relationship between AID and PCa remained unclear. The purpose of this study was to investigate the causal association between 3 common AIDs, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS), and the risk of PCa. We used genome-wide association studies summary statistics to conduct forward and reverse Mendelian randomization (MR) in a two-sample framework. We also incorporated risk factors, including smoking and obesity, in the multivariable MR analysis. Multiple sensitivity analysis methods have been adopted to test the robustness of our results. Our univariable MR analysis showed that genetically predicted RA was associated with an increased risk of PCa (odds ratio: 1.036, 95% CI: 1.022-1.049, P < .001). However, there was no significant association between SLE or AS and PCa. The multivariable MR analysis adjusted for smoking and obesity confirmed the positive association between RA and PCa, but not for the other 2 autoimmune diseases. In the reverse MR analysis, we did not find any significant inverse causal associations between PCa and the 3 autoimmune diseases. Our study suggested that genetically predicted RA was likely causally associated with an increased risk of PCa, while there is no significant causal relationship between SLE or AS and PCa. These findings provided new insights into the relationship between autoimmune diseases and PCa and might inform future research and clinical practice.

Exploring the link between sex hormone-binding globulin levels and prostate cancer risk: a comprehensive systematic review and meta-analysis.

Sex hormone-binding globulin (SHBG) plays a critical role in regulating androgen bioavailability and has been hypothesized to influence prostate cancer risk, though existing evidence is inconsistent. This systematic review and meta-analysis aimed to evaluate the association between SHBG levels and prostate cancer risk. A comprehensive search was conducted across PubMed, Embase, and Web of Science for studies published up to December 1, 2024. Observational studies assessing SHBG levels and prostate cancer risk were included. Effect sizes were pooled using random-effects meta-analysis. Heterogeneity was evaluated using the I2 statistic, and quality assessment was performed using the Newcastle-Ottawa Scale. Statistical analysis was performed using R software version 4.4. Sixteen studies, including 720,298 participants and 90,799 prostate cancer cases, were analyzed. The pooled odds ratio (OR) for prostate cancer risk per unit increase in SHBG was 0.907 (95% CI 0.799-1.030), indicating no statistically significant association. Substantial heterogeneity was observed among the included studies (I2 = 79%; P < 0.0001). Subgroup analyses showed no significant variation in effect sizes by study design. However, a Mendelian randomization analysis conducted in 140,254 European-descent males, including 79,148 prostate cancer cases, suggested a modest protective effect of higher SHBG levels, with an OR of 0.944 (95% CI 0.897-0.993). Sensitivity analyses confirmed the robustness of the pooled findings. This meta-analysis showed a complex relationship between SHBG levels and prostate cancer risk. While overall findings do not support a statistically significant association, higher SHBG levels may confer a protective role in specific contexts. Further research is needed to elucidate mechanisms, reduce heterogeneity, and validate SHBG as a biomarker for risk stratification.

Exploring the causal role of plasma metabolites and metabolite ratios in prostate cancer: a two-sample Mendelian randomization study.

Prostate cancer (PCa), the most prevalent malignant neoplasm in males, involves complex biological mechanisms and risk factors, many of which remain unidentified. By employing a novel two-sample Mendelian randomization (MR) approach, this study aims to elucidate the causal relationships between the circulating metabolome and PCa risk, utilizing comprehensive data on genetically determined plasma metabolites and metabolite ratios. For the MR analysis, we utilized data from the GWAS Catalog database to analyze 1,091 plasma metabolites and 309 ratios in relation to PCa outcomes within two independent GWAS datasets. The inverse variance weighted (IVW) method was the primary approach for determining the existence of the causal relationship, supplemented by additional MR methods for heterogeneity, pleiotropy, and cross-validation. The false discovery rate (FDR) and Bonferroni correction were applied to identify the most significant causative associations. Additionally, reverse MR and Steiger filtering were conducted to ascertain whether PCa influenced the observed metabolite levels. Furthermore, metabolic pathway analysis was conducted with MetaboAnalyst 6.0 software. In the MR analysis, our findings reveal three overlapped metabolite ratios (arginine to glutamate, phosphate to uridine, and glycerol to mannitol/sorbitol) inversely associated with PCa risk. Following FDR correction (FDR < 0.05), cysteinylglycine disulfide was identified as a potential reducer of PCa risk, whereas Uridine and N-acetyl-L-glutamine (NAG) were pinpointed as potential risk factors. Notably, NAG (OR 1.044; 95% CI 1.025-1.063) emerged as a metabolite with significant causal influence, as confirmed by stringent Bonferroni correction (P < 0.05/1400). Steiger's directionality test (P < 0.001) and reverse MR confirmed the proposed causal direction. Furthermore, metabolic pathway analysis revealed a significant association between the "Glutathione Metabolism" pathway and PCa development. This study provides novel insights into the potential causal effects of plasma metabolites and metabolite ratios on PCa. The identified metabolites and ratios could serve as candidate biomarkers, contributing to the elucidation of PCa's biological mechanisms.

Insights of prostate diseases risk among patients with male pattern baldness: a mendelian randomized study.

Male pattern baldness (MPB) is commonly associated with prostate diseases, both of which can significantly impact men's quality of life. However, the relationship and causality between them remain unclear. In this study, we investigated the causal relationship between the two. Inverse variance weighting (IVW) was the primary Mendelian randomization method, with MR Egger, weighted median, and MRPRESSO as complements. Sensitivity analyses included Cochran's Q, MR Egger intercept, and MRPRESSO. MPB was found to be negatively correlated with prostate cancer (IVW: OR = 0.986, 95% CI = 0.974-0.999, P = 0.033). This causal relationship was further supported by the weighted median (OR = 0.981, 95% CI = 0.969-0.993, P = 0.002), MR-Egger (OR = 0.977, 95% CI = 0.960-0.994, P = 0.010), and MRPRESSO (OR = 0.986, 95% CI = 0.974-0.999, P = 0.037) methods. Additionally, the weighted median analysis indicated that MPB was positively correlated with benign prostatic hyperplasia (BPH) (OR = 1.027, 95% CI = 1.003-1.052, P = 0.024). Our findings suggest that genetically predicted MPB may reduce prostate cancer risk but increase the risk of benign prostatic hyperplasia. Timely prostate screening in patients with MPB could help prevent and manage prostate diseases.

Kidney and gallbladder stones and the risk of prostate cancer: Results from the EPICAP study.

Prostate cancer remains the most frequent cancer among men, representing a significant health burden. Despite its high morbidity and mortality rates, the etiology of prostate cancer remains relatively unknown, with only non-modifiable established risk factors. Chronic inflammation has emerged as a potential factor in prostate carcinogenesis. We investigated the role of kidney and gallbladder stones and the risk of prostate cancer. We used data from EPICAP, a population-based case-control study. A total of 819 diagnosed prostate cancer cases and 879 controls were face-to-face interviewed using a standardized questionnaire that collected information on personal medical history, including history of kidney and gallbladder stones. Odds Ratios (OR) and their 95% confidence interval (CI) were estimated using multivariate unconditional logistic regression. Our study revealed intriguing patterns regarding kidney and gallbladder stones in relation to prostate cancer risk. The analysis indicated significant potential associations between kidney stones and the risk of prostate cancer (OR: 1.46 95% CI: 1.13-1.90), particularly in men with a history of kidney infection. Additionally, our data suggested a possible relationship between gallbladder stones and prostate cancer when considering triglyceride (OR: 2.27, 95% CI: 0.99-5.28), although further research is needed for a conclusive understanding. Our results suggest an association between calculi and the risk of prostate cancer. Findings from this study underscore the need for a more comprehensive investigation to understand the role of chronic inflammation or metabolism and delineate the mechanisms underlying these potential associations in order to guide the development of targeted preventive strategies for aggressive prostate cancer.

Diet and the microbiome as mediators of prostate cancer risk, progression, and therapy response.

Complex relationships between the human microbiome and cancer are increasingly recognized for cancer sites that harbor commensal microbial communities such as the gut, genitourinary tract, and skin. For organ sites that likely do not contain commensal microbiota, there is still a substantial capacity for the human-associated microbiota to influence disease etiology across the cancer spectrum. We propose such a relationship for prostate cancer, the most commonly diagnosed cancer in males in the United States. This review explores the current evidence for a role for the urinary and gut microbiota in prostate cancer risk, via both direct interactions (prostate infections) and long-distance interactions such as via the metabolism of procarcinogenic or anticarcinogenic dietary metabolites. We further explore a newly recognized role of the gut microbiota in mediating cancer treatment response or resistance either via production of androgens and/or procarcinogenic metabolites or via direct metabolism of anticancer drugs that are used to treat advanced disease. Overall, we present the current state of knowledge relating to how the human microbiome mediates prostate cancer risk, progression, and therapy response, as well as suggest future research directions for the field.

Development and Validation of a Deep Learning Model Based on MRI and Clinical Characteristics to Predict Risk of Prostate Cancer Progression.

Purpose To validate a deep learning (DL) model for predicting the risk of prostate cancer (PCa) progression based on MRI and clinical parameters and compare it with established models. Materials and Methods This retrospective study included 1607 MRI scans of 1143 male patients (median age, 64 years; IQR, 59-68 years) undergoing MRI for suspicion of clinically significant PCa (csPCa) (International Society of Urological Pathology grade > 1) between January 2012 and May 2022 who were negative for csPCa at baseline MRI. A DL model was developed using baseline MRI and clinical parameters (age, prostate-specific antigen [PSA] level, PSA density, and prostate volume) to predict the time to PCa progression (defined as csPCa diagnosis at follow-up). Internal and external testing was performed. The model's ability to predict progression to csPCa was assessed by Cox regression analyses. Predictive performance of the DL model up to 5 years after baseline MRI in comparison with the European Randomized Study of Screening for Prostate Cancer (ERSPC) future-risk calculator, Prostate Cancer Prevention Trial (PCPT) risk calculator, and Prostate Imaging Reporting and Data System (PI-RADS) was assessed using the Harrell C-index. Optimized follow-up intervals were derived from Kaplan-Meier curves. Results DL scores predicted csPCa progression (internal cohort: hazard ratio [HR], 1.97 [95% CI: 1.61, 2.41; P < .001]; external cohort: HR, 1.32 [95% CI: 1.14, 1.55; P < .001]). The model identified a subgroup of patients (approximately 20%) with risks for csPCa of 3% or less, 8% or less, and 18% or less after 1-, 2-, and 4-year follow-up, respectively. DL scores had a C-index of 0.68 (95% CI: 0.63, 0.74) at internal testing and 0.56 (95% CI: 0.51, 0.61) at external testing, outperforming ERSPC and PCPT (both P < .001) at internal testing. Conclusion The DL model accurately predicted PCa progression and provided improved risk estimations, demonstrating its ability to aid in personalized follow-up for low-risk PCa. Keywords: MRI, Prostate Cancer, Deep Learning Supplemental material is available for this article. ©RSNA, 2025.

Beyond Medical Bills: The Indirect Costs of Prostate Cancer.

Both direct and indirect costs contribute to financial toxicity in prostate cancer. Indirect costs are difficult to assess and quantify and therefore remain understudied. We sought to describe the indirect costs of prostate cancer across risk groups as well as identify any associated sociodemographic factors. Patients with localized prostate cancer were surveyed regarding their indirect costs at baseline and at 3-, 6-, 12-, and 24-month follow-up. Out-of-pocket indirect costs were defined as costs paid for medication, parking, transportation, meals outside the home, and caregivers. "Imputed indirect costs" were calculated based on hour estimates for traveling time, missed work, additional time spent on work, and additional time dedicated to their care by caregivers. Generalized linear model regressions were performed to evaluate for potential associations between sociodemographic or clinical features with these indirect costs, stratifying by prostate cancer risk group. Four hundred and ninety-five localized prostate cancer patients were included in the analysis. Indirect costs ranged from $154.00 to $717.40 for out-of-pocket and $352 to $3389 for imputed per month and did tend to be higher for higher-risk disease. In regression models, sociodemographic factors did not appear to play a strong role in variation in indirect costs. Within a 24-month follow-up period, we observed that indirect costs of localized prostate cancer range from $608 to $4107 per month when including lost productivity costs. Further work must be done to identify what factors contribute to increased indirect costs and financial toxicity.

Night shift work and prostate cancer: a large cohort study from UK Biobank and Mendelian randomisation study

ObjectiveThe global concern regarding the health implications of night shift work has escalated. Nevertheless, variations exist in the observed association between night shift work and prostate cancer (PCa). This study...

Unveiling DENND2D as a Novel Prognostic Biomarker for Prostate Cancer Recurrence: From Gene to Prognosis.

Background: Prostate cancer is a major global health burden, with biochemical recurrence (BCR) following radical prostatectomy affecting 20-40% of patients and posing significant challenges to prognosis and treatment. Emerging evidence suggests a critical role for differentially expressed in normal and neoplastic cell (DENN) domain-containing genes in oncogenesis; however, their implications in prostate cancer and BCR risk remain underexplored. Methods: This study systematically evaluated 151 single-nucleotide polymorphisms in DENN domain-containing genes in 458 patients with prostate cancer and BCR, followed by validation in an independent cohort of 185 patients. Results: Multivariate Cox regression analyses identified DENND2D rs610261 G>A as significantly associated with improved BCR-free survival in both cohorts (adjusted hazard ratio = 0.39, 95% confidence interval = 0.23-0.66, p = 0.001). Functional analysis revealed rs610261's regulatory potential, with the protective A allele correlating with increased DENND2D expression in various human tissues. Compared to normal prostate tissues, DENND2D expression was reduced in prostate cancer, with higher expression being linked to favorable patient prognosis (p = 0.03). Gene set enrichment analysis revealed an association between DENND2D expression and the negative regulation of MYC target genes, including MAD2L1, ERH, and CLNS1A, which are overexpressed in prostate cancer and associated with poor survival. Furthermore, the elevated DENND2D expression promotes immune infiltration in prostate cancer, supporting its role in immune modulation. Conclusions:DENND2D is a prognostic biomarker for BCR in prostate cancer and offers new avenues for personalized treatment strategies.

Relationships between blood cadmium concentration and risk of nine cancers: evidence from the NHANES 1999–2018 and Mendelian randomization analyses

BackgroundPrevious observational studies examining the relationship between cadmium exposure and various cancers have yielded conflicting results. This study aims to comprehensively clarify the relationship between blood cadmium concentration (BCC) and nine specific cancers.MethodsA retrospective analysis of National Health and Nutrition Examination Survey (NHANES) 1999–2018 identified 36,991 participants. Multivariable logistic regression was used to assess the association between BCC and the risk of nine specific cancers. Additionally, Mendelian randomization (MR) analyses were conducted to investigate potential causal relationships.ResultsMultivariable logistic regression analysis of the NHANES data indicated a positive association between BCC and the risk of bladder and lung cancers (P < 0.05) and a negative association with the risk of kidney and prostate cancers (P < 0.05). The MR analyses demonstrated a causal relationship between BCC and kidney cancer (P < 0.05). Additionally, it uncovered causal associations with breast, cervical, and colon cancers (P < 0.05).ConclusionElevated BCC was associated with an increased risk of bladder and lung cancers while demonstrating an inverse relationship with kidney and prostate cancers. MR analysis revealed that cadmium exposure may act as a protective factor against breast, cervical, colon, and kidney cancers, that must be confirmed with new studies.