Subsequent Risk Of Prostate Cancer Research Articles

Editorial Comment from Dr Mori to Association between antibiotic use and subsequent risk of prostate cancer: A retrospective cohort study in South Korea.

Editorial Comment from Dr Mori to Association between antibiotic use and subsequent risk of prostate cancer: A retrospective cohort study in South Korea.

Editorial Comment on "Association between antibiotic use and subsequent risk of prostate cancer: A retrospective cohort study in South Korea".

Editorial Comment on "Association between antibiotic use and subsequent risk of prostate cancer: A retrospective cohort study in South Korea".

Untreated hypogonadism and testosterone replacement therapy in hypogonadal men are associated with a decreased risk of subsequent prostate cancer: a population-based study.

We sought to understand the relationship between hypogonadism and testosterone replacement therapy (TRT) in hypogonadal men on the risk of developing localized and metastatic prostate cancer. We used the Merative MarketScan database of commercial claims encounters to identify men diagnosed with hypogonadism. These men were matched to eugonadal men who served as controls. Multivariate negative binomial regression analysis of prostate cancer diagnoses, hypogonadism, and TRT in hypogonadal men adjusting for various known confounding factors was used to understand the impact of hypogonadism and TRT on prostate cancer risk. We identified 3,222,904 men who met inclusion criteria, of which 50% were diagnosed with hypogonadism (1,611,452) and each were matched to a control (1,611,452). The incidence of prostate cancer was 2.16%, 1.55%, and 1.99% in eugonadal controls, hypogonadal men on TRT, and hypogonadal men without TRT, respectively (p < 0.001). Untreated hypogonadism was independently associated with a decreased risk of localized prostate cancer (IRR 0.46, 95% CI 0.43-0.50, p < 0.001) compared to eugonadal controls. Hypogonadal men on TRT also had a significantly decreased risk of localized prostate cancer (IRR 0.49, 95% CI 0.45-0.53, p < 0.001). Furthermore, hypogonadal men on TRT (IRR 0.21, 95% CI 0.19-0.24, p < 0.001) or without TRT (IRR 0.20, 95% CI 0.18-0.22, p < 0.001) both had significantly decreased risk of metastatic prostate cancer, respectively. Our population-based analysis suggests that untreated hypogonadism in men is associated with a 50% decreased incidence of localized prostate cancer and an 80% decreased incidence of metastatic prostate cancer. TRT in hypogonadal men was also associated with a decreased risk of subsequent prostate cancer. Further research is needed to better understand the relationship between hypogonadism and TRT in hypogonadal men on the riskof subsequent prostate cancer.

Association between antibiotic use and subsequent risk of prostate cancer: A retrospective cohort study in South Korea.

Several studies suggest that antibiotic use may affect overall cancer incidence, but the association between antibiotics and prostate cancer is still unclear. This retrospective cohort study aimed to assess the association between antibiotics and the risk of prostate cancer. A population-based retrospective cohort study was conducted using the Korean National Health Insurance Service (NHIS) database. 1 032 397 individuals were followed up from January 1, 2007, to December 31, 2019. Multivariable Cox hazards regression was utilized to calculate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for the risk of prostate cancer according to accumulative days of antibiotic use and the number of antibiotic classes used from 2002 to 2006. Individuals who used antibiotics for 180 or more days had a higher risk of prostate cancer (aHR, 1.46; 95% CI, 1.11-1.91) than those who did not use antibiotics. Also, individuals who used four or more kinds of antibiotics had a higher risk of prostate cancer (aHR, 1.18; 95% CI, 1.07-1.30) than antibiotic non-users. An overall trend was observed among participants who underwent health examinations. Our findings suggest that long-term use of antibiotics may affect prostate cancer incidence. Further studies are needed to improve understanding of the association between antibiotic use and prostate cancer incidence.

Causal relationship between prostate cancer and 12 types of cancers: multivariable and bidirectional Mendelian randomization analyses.

Previous observational studies have shown an association between certain cancers and the subsequent risk of prostate cancer (PCa). However, the causal relationship between these cancers and PCa is still unclear. This study aimed to investigate the causal relationship between 12 common cancers and the risk of PCa. We employed genome-wide association studies (GWAS) to perform forward and reverse Mendelian randomization (MR) within two-sample frameworks. Furthermore, we conducted multivariable MR analyses to investigate the relationships between different types of cancer. In addition, multiple sensitivity analysis methods were employed to assess the robustness of our findings. Our univariable MR analysis showed that genetically predicted hematological cancer was associated with a reduced risk of PCa (OR: 0.911, 95% CI 0.89-0.922, P = 0.03). Furthermore, MR analysis demonstrates that genetically predicted occurrence of thyroid gland and endocrine gland cancer also raised the risk of PCa (all P < 0.05). Multivariable analysis showed that thyroid gland cancer exhibited a higher incidence of PCa (OR: 1.12, 95% CI: 1.08-1.16, P = 0.008). In the reverse MR analysis, we found no significant inverse causal associations between PCa and 12 types of cancers. In summary, this study provided insights into the causal relationships between various types of cancer and PCa. Hematological cancer was suggested to associate with a lower risk of PCa, while thyroid gland cancer and endocrine gland cancer might increase the risk. These findings contribute to the understanding of genetic factors related to PCa and its potential associations with other cancers.

Cutaneous melanoma, prostate-specific antigen testing and the subsequent risk of prostate cancer diagnosis: a prospective analysis of the 45 and Up Study

BackgroundThe association between cutaneous melanoma and subsequent risk of prostate cancer (PC) was examined in a large population-based cohort study.MethodsMale participants in the Sax Institute’s 45 and Up Study (Australia) were recruited between 2006 and 2009. Questionnaire data and linked administrative health data from the Centre for Health Record Linkage and Services Australia identified melanomas diagnosed between 1/1/1994 and 12 months before Study recruitment (i.e., between 2005 and 2008), incident PCs, primary healthcare utilisation and prostate-specific antigen (PSA) tests. Men were excluded from the current analyses if they had a recorded PC or other cancer diagnosis other than melanoma and non-melanoma skin cancer prior to recruitment. Multivariable Cox regression was used to estimate hazard ratios (HRs) adjusting for PSA-testing frequency before PC diagnosis.ResultsOf 96,548 eligible men, 1899 were diagnosed with melanoma during the melanoma diagnosis period and 3677 incident PC diagnosed during follow-up (latest date 31/12/2013). Men with melanoma diagnosis had increased risk of a subsequent PC diagnoses (vs. no melanoma; fully adjusted HR = 1.32; 95% CI: 1.09–1.60). There was weak evidence of higher risks of a subsequent PC diagnosis for men diagnosed with more than one melanoma compared to men diagnosed with only one melanoma (p = 0.077), and if first melanoma diagnosis was 10 to 15 years before Study recruitment (fully adjusted HR = 2.05; 95% CI [1.35, 3.12]).ConclusionMelanoma diagnosis was associated with increased risk of subsequent PC diagnosis, after adjusting for PSA testing and primary healthcare utilisation. While our ability to adjust for PC screening reduced risk of detection bias, we acknowledge that residual confounding from increased medical surveillance after melanoma diagnoses cannot be entirely ruled out.

Race Differences in Telomere Length in Benign Prostate Biopsies and Subsequent Risk of Prostate Cancer.

Telomere shortening is linked to aging and may be associated with increased risk for cancer. Most cancer studies have used telomere length in leukocytes rather than in the target tissue of cancer origin. A case-control study of 524 case-control pairs with a benign prostate biopsy nested within a historical cohort of 10,478 men was conducted to determine whether premalignant prostate telomere length (assessed using a modified qRT-PCR) is associated with prostate cancer risk. Telomere lengths in benign prostate biopsies of cases versus controls were similar (1.46 ± 0.38 vs. 1.45 ± 0.42; P = 0.49). African American (AA) men had significantly shorter telomeres compared with White men (1.51 ± 0.38 vs. 1.63 ± 0.39; P < 0.0001). In race-stratified analyses, increasing telomere length was more strongly associated with prostate cancer risk in White men, wherein those with telomere length in the highest quartile had 1.9-fold greater adjusted risk of prostate cancer compared with men with prostate telomere lengths in the lowest quartile [OR = 1.90; 95% confidence interval (CI) = 1.08-3.36]. Men in the highest telomere length quartile also had a greater risk of aggressive prostate cancer compared with men with telomere lengths in the lowest quartile (OR = 2.78; 95% CI = 1.25-6.19). White men have longer telomeres in benign prostate tissue compared with AA men, and those with the longest telomeres may be at increased risk for prostate cancer, particularly the more aggressive form of the disease. Race-specific telomere length measures may be an early biomarker of aggressive prostate cancer.

Abstract 750: Race differences in telomere length in benign prostate and subsequent risk of prostate cancer

Abstract Telomere shortening is linked to aging and thought to be associated with increased risk for cancer. Most cancer studies have used leukocyte telomere length as a surrogate measure for telomere length with few focused upon telomeres in the target tissue of cancer origin. To determine whether telomere length in pre-malignant prostate tissue is associated with subsequent prostate cancer risk, we conducted a case-control study of 530 case-control pairs matched on date, age at cohort entry, and race nested within a historical cohort of 10,478 men with a benign prostate biopsy. Overall mean telomere length assessed using modified quantitative real-time PCR was not different in benign prostate biopsies of prostate cancer cases vs. matched controls (1.65 ± 0.35 vs. 1.64 ± 0.39; p=0.41). However, race was significantly associated with telomere length with African American (AA) men having shorter telomeres in benign prostate biopsy compared with white men (1.59 ± 0.37 vs. 1.70 ± 0.37; p&amp;lt;0.0001). In race-stratified analyses, telomere length only showed a suggestive association with prostate cancer risk in white men, wherein those with telomere length in the highest quartile had 1.5-fold greater risk of prostate cancer compared to men with prostate telomere lengths in the lowest quartile (OR=1.56; 95% CI = 0.89 - 2.73 ). In addition, white men in the highest prostate telomere length quartile had almost three-fold greater risk of aggressive prostate cancer, defined as Gleason group 3 and above, tumor stage 3 or above or PSA 20 ng/ml or higher , compared with men with telomere lengths in the lowest quartile (OR=2.73; 95% CI =1.05 - 7.15). In summary, white men have longer telomeres in benign prostate tissue compared with AA men, and those with the longest telomeres may be at increased risk for prostate cancer, particularly the more aggressive form of the disease. Citation Format: Benjamin A. Rybicki, Sudha M. Sadasivan, Yalei Chen, Ian Loveless, Nilesh S. Gupta, Dhananjay A. Chitale, Sean R. Williamson, Andrew G. Rundle, Deliang Tang. Race differences in telomere length in benign prostate and subsequent risk of prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 750.

Adolescent animal product intake in relation to later prostate cancer risk and mortality in the NIH-AARP Diet and Health Study

BackgroundAdolescent intake of animal products has been proposed to contribute to prostate cancer (PCa) development because of its potentially carcinogenic constituents and influence on hormone levels during adolescence.MethodsWe used data from 159,482 participants in the NIH-AARP Diet and Health Study to investigate associations for recalled adolescent intake of red meat (unprocessed beef and processed red meat), poultry, egg, canned tuna, animal fat and animal protein at ages 12–13 years with subsequent PCa risk and mortality over 14 years of follow-up. Cox proportional hazard regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of total (n = 17,349), advanced (n = 2,297) and fatal (n = 804) PCa.ResultsSuggestive inverse trends were observed for adolescent unprocessed beef intake with risks of total, advanced and fatal PCa (multivariable-adjusted P-trends = 0.01, 0.02 and 0.04, respectively). No consistent patterns of association were observed for other animal products by PCa outcome.ConclusionWe found evidence to suggest that adolescent unprocessed beef intake, or possibly a correlate of beef intake, such as early-life socioeconomic status, may be associated with reduced risk and mortality from PCa. Additional studies with further early-life exposure information are warranted to better understand this association.

374 Skin melanoma and subsequent risk of prostate cancer: A national cancer institute surveillance, epidemiology, and end results study

Introduction: Prostate cancer and melanoma rank as the first and fifth most common cancers, respectively, among men in the United States. Existing studies have reported prostate and melanoma cancer links due to a shared androgen-dependence hypothesis. However, the relationship between prior melanoma history and subsequent prostate cancer is largely unexplored. We aimed to elucidate the relationship between a history of malignant melanoma (MM) and subsequent risk of prostate cancer (PC) in the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) database.

Herpes zoster and the subsequent risk of prostate cancer in an Asian population: A nationwide population-based cohort study.

It has been suggested that herpes zoster may increase the risk of subsequent prostate cancer (PCa). We aimed to assess the risk of PCa following herpes zoster by the population-based follow-up study.This is a retrospective study and data are from the Taiwan National Health Insurance Research Database (NHIRD). The study cohort comprised all patients with a diagnosis of herpes zoster (International Classification of Diseases, 9th Revision, Clinical Modification code 053.0–053.9) and followed for PCa from 1997 to 2013 (n = 11,376). Subjects younger than 20 years of age were excluded. The match-control cohort was identified from the Registry of Beneficiaries of the NHIRD and randomly selected by matching with the study cohort at a 3:1 ratio based on age (every 5-year span), and year of herpes zoster diagnosis (n = 34,128). We used Cox proportional hazards regression models to estimate the hazard ratios (HRs) for subsequent PCa, after controlling for potential cormobidities.Men with and without herpes zoster had similar age and comorbidity distributions. Among the 45,504 sampled patients, 1011 (2.22%) developed PCa during the 10 years of follow-up, 276 (2.43%) from the study cohort and 735 (2.15%) from the match-control cohort and the incidence rate was 3.13 and 2.72 per 1000 person years respectively. Patients with herpes zoster were more likely to develop PCa than patients in the match-control cohort (HR = 1.15; 95% confidence interval (CI) = 1.00–1.32, P value = .045). After adjusting for age and comorbidities, herpes zoster was associated with a 1.15 increased risk of PCa (adjusted HR = 1.15, 95% CI = 0.99–1.32, P value = .054).Our study indicates that preceding herpes zoster infection is a suggestive risk marker for subsequent PCa after controlling for potential confounders. Further prospective studies are needed to determine the relationship between herpes zoster and PCa.

Risk of subsequent prostate cancer in peptic ulcer patients who received helicobacter pylori eradication therapy: an Asian population-based cohort study

BackgroundStudies have shown diverse results regarding the association between H. pylori (HP) infection and the risk of malignancy. There is accumulating evidence relating HP infection to urological diseases. We investigated whether there was an association between HP-infected peptic ulcers and the subsequent risk of prostate cancer.MethodsWe collected HP-infected male patients from 1998 to 2008 from the Longitudinal Health Insurance Database (LHID). HP-infected patients were identified as those who had a diagnosis of peptic ulcers upon admission and received HP eradication therapy within 1 year after diagnosis. The date of HP infection diagnosis upon admission was defined as the index date. Patients aged < 20 years or with a cancer history were excluded. For each HP-infected patient, we selected four males without peptic ulcers or a history of HP eradication in the LHID for the comparison cohort according to propensity score matching by age, index year, and comorbidity. The risk of prostate cancer and associated risk factors was assessed by Cox proportional hazard regression.ResultsA total of 2620 HP infection treatment patients and 10,480 matched comparisons were selected. There were 36 patients in the HP-infected treatment cohort and 117 patients in the comparison cohort with documented prostate cancer development (1.52 and 1.21 per 1000 person-years, respectively). Compared to the comparison cohort, the HP infection cohort had a 1.26-fold increased prostate cancer risk in the Cox models after adjusting for matched-pairs (95% CI = 0.87–1.34). There were no significant differences in subsequent prostate cancer development between HP-infected treatment patients and the comparison cohort.ConclusionOur findings showed no significant association between HP-infected peptic ulcers and the subsequent risk of prostate cancer. Further studies are warranted to investigate whether this observation is attributable to an HP eradication policy.

Digoxin lowers the incidence of prostate cancer: A nationwide population-based study.

In vitro studies have confirmed that cardiac glycosides can induce apoptosis in both hormone-dependent and -independent prostate cancer (PCa) cell lines. The aim of this study was to investigate the incidence of PCa among patients treated with and without digoxin using a nationwide population-based database in Taiwan. We retrieved data of men aged 30 years or older who were newly diagnosed with heart failure between January 1998 and December 2003 from the National Health Insurance program database in Taiwan. We divided the patients into digoxin users and non-digoxin users. Kaplan-Meier curves and Cox proportional hazard analysis were used to examine the risk of subsequent PCa between the digoxin and non-digoxin groups. The mean ± SD follow-up (years) periods in the digoxin and non-digoxin groups were 8.6 ± 1.78 and 8.3 ± 1.75, respectively. The cumulative incidence of PCa during the follow-up period was 3.5% (147/4233) in the non-digoxin group compared with 3.0% (65/2154) in the digoxin group. The log-rank test revealed that the digoxin group had a similar incidence of PCa to the non-digoxin group (p = 0.18). After adjusting for age, benign prostatic hyperplasia, and comorbidities, Cox proportional hazard regression analysis showed that digoxin was associated with a significantly decreased risk of developing PCa (hazard ratio, 0.74; 95% CI, 0.548-0.993; p = 0.045). Moreover, logistic regression analysis showed that the risk of PCa decreased with a longer duration of digoxin use during the study period compared to those who had never used digoxin (p = 0.043). The cardiac glycoside digoxin had significant effects on reducing the incidence of PCa in a time-dependent manner. Our findings may imply the potential application of cardiac glycosides in the prevention and management of PCa.

AGE-RELATED ELEVATED CD4+ T HELPER 17 CELL RESPONSE PROMOTES PROSTATE CANCER CELL GROWTH, MIGRATION, AND INVASION

Age is the most important risk factor for prostate cancer (PCa). But, how age contributes to PCa remains unknown. Interleukin-17 (IL-17) -producing CD4+ T helper 17 (Th17) cells play a critical role in inflammatory diseases. It is often elevated in aging humans and mice, however, whether aging affects Th17 cell function and subsequent PCa risk increase is unclear. In this study, we investigated the role of CD4+ T cells in PCa cell growth during the aging process. Splenic T cells were isolated and purified into CD4+CD25- T cells from young and old mice, then cultured in the presence of plate-bound anti-CD3/anti-CD28. Four days later, the cells were re-stimulated with PMA and ionomycin in the presence of brefeldin A for 4 hours and then were collected and used for flow cytometry and/or qPCR. The supernatant (conditioned media) from young and old cultures was collected and used in subsequent experiments. Flow and qPCR results showed that 17-producing T cells and associated cytokines were significantly increased in old mice compared to young mice. When PCa cell lines (LNCaP, DU-145, and PC3) were treated by the conditioned media for 48 and 72 hours. The cell proliferation, migration, and invasion, as well as the activation of NF-B signaling in PCa cells, were significantly increased after exposure to the conditioned media from aged mice, compared to that from young mice. These results indicated that age-related CD4+ Th17 cell responses are elevated in mice in the aging process and play an important role in PCa growth.

Skin Melanoma and Subsequent Risk of Prostate Cancer: A Lithuanian Cancer Registry Study.

Emerging data indicates that melanoma may be linked to prostate cancer. We evaluated if the incidence of melanoma was associated with subsequent risk of prostate cancer (PC). We extracted data from the Lithuanian cancer registry from 1993 to 2012. We calculated the standardized incidence ratios (SIRs) for PC as a ratio of observed number of cancer cases in people with previous melanoma diagnosis to the expected number of cancer cases in the underlying general population. Therein, 95% confidence intervals for the SIRs were estimated assuming the number of observed cancer cases follows the Poisson distribution. Overall, 65 PCs were observed versus 52.5 expected (SIR 1.24; 95% CI: 0.97–1.58) within a period of 24 years. A significantly increased risk of PC was found in patients with melanoma diagnosis over 70 years (SIR 1.62; 95% CI: 1.11–2.39) and in two periods of diagnosis (SIRs 1.76 and 1.62 in 1993–1997 and 2009–2012, respectively). A significantly increased risk was also found five to nine years after melanoma diagnosis (SIR 1.58; 95% CI: 1.05–2.38). Further studies are needed to evaluate the relationship between melanoma and subsequent risk of prostate cancer.

Abstract LB-172: Understanding the mechanism underlying vitamin D and prostate cancer: Exploring telomere length

Abstract Background: In an effort to understand the molecular mechanism behind the association between circulating vitamin D and prostate cancer, we measured relative telomere length and 25(OH)D levels in a cohort of older Finnish men. Methods: Using a nested study design, we examined quantitative PCR measured telomere length, season-adjusted serum 25-hydroxyvitamin D [25(OH)D], and subsequent prostate cancer risk in 1000 men (n=500 cases, 500 matched controls) participating in the extension study of the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Trial. Conditional regression models were used to explore mediation and effect modification of telomere length on the relation between serum 25(OH)D and prostate cancer risk. Results: An increased risk of prostate cancer was observed among men with longer (&amp;gt;median) relative telomere length (OR = 1.41, 95% CI: 1.06 to 1.90; continuous: OR = 2.36, 95%CI: 0.96 to 5.83) as well as men with higher 25(OH)D concentrations (OR = 1.67, 95% CI: 1.08 to 2.57 for highest vs. lowest quintile, P-trend = 0.03). No significant association between 25(OH)D levels and telomere length was observed. A suggested joint effect of 25(OH)D and telomere length on prostate cancer risk was observed. Conclusion: Serum 25(OH)D and relative telomere length are independent predictors of prostate cancer risk in this sample of older male Finnish smokers. No evidence of mediation between circulating vitamin D concentrations and telomere length was observed. Future studies are needed to further clarify the underlying biologic mechanisms of the 25(OH)D-prostate cancer association. Citation Format: Jacqueline M. Major, Barry I. Graubard, Stephanie J. Weinstein, Jeeyun Kim, Immaculata De Vivo, Jarmo Virtamo, Sharon A. Savage, Demetrius Albanes. Understanding the mechanism underlying vitamin D and prostate cancer: Exploring telomere length [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr LB-172.

Patterns in metabolite profile are associated with risk of more aggressive prostate cancer: A prospective study of 3,057 matched case-control sets from EPIC.

Metabolomics may reveal novel insights into the etiology of prostate cancer, for which few risk factors are established. We investigated the association between patterns in baseline plasma metabolite profile and subsequent prostate cancer risk, using data from 3,057 matched case–control sets from the European Prospective Investigation into Cancer and Nutrition (EPIC). We measured 119 metabolite concentrations in plasma samples, collected on average 9.4 years before diagnosis, by mass spectrometry (AbsoluteIDQ p180 Kit, Biocrates Life Sciences AG). Metabolite patterns were identified using treelet transform, a statistical method for identification of groups of correlated metabolites. Associations of metabolite patterns with prostate cancer risk (OR1SD) were estimated by conditional logistic regression. Supplementary analyses were conducted for metabolite patterns derived using principal component analysis and for individual metabolites. Men with metabolite profiles characterized by higher concentrations of either phosphatidylcholines or hydroxysphingomyelins (OR1SD = 0.77, 95% confidence interval 0.66–0.89), acylcarnitines C18:1 and C18:2, glutamate, ornithine and taurine (OR1SD = 0.72, 0.57–0.90), or lysophosphatidylcholines (OR1SD = 0.81, 0.69–0.95) had lower risk of advanced stage prostate cancer at diagnosis, with no evidence of heterogeneity by follow‐up time. Similar associations were observed for the two former patterns with aggressive disease risk (the more aggressive subset of advanced stage), while the latter pattern was inversely related to risk of prostate cancer death (OR1SD = 0.77, 0.61–0.96). No associations were observed for prostate cancer overall or less aggressive tumor subtypes. In conclusion, metabolite patterns may be related to lower risk of more aggressive prostate tumors and prostate cancer death, and might be relevant to etiology of advanced stage prostate cancer.

Placing prostate cancer disparities within a psychosocial context: challenges and opportunities for future research.

Black men are more likely to be diagnosed with prostate cancer compared with White men. Despite advances in prevention and treatment strategies, disparities in prostate cancer among Black men persist. While research on the causes of higher incidence and mortality is ongoing, there is limited evidence in the existing literature that clearly speaks to the potential psychological or social factors that may contribute to disparities in prostate cancer incidence. Given the lack of attention to this issue, we review scientific evidence of the ways in which social factors, including socioeconomic status and racial segregation, as well as psychological factors, like depression and anxiety, are related to subsequent prostate cancer risk, which could occur through behavioral and biological processes. Our objective is to illuminate psychosocial factors and their context, using a racial disparity lens, which suggests opportunities for future research on the determinants of prostate cancer. Ultimately, we aim to contribute to a robust research agenda for the development of new prostate cancer prevention measures to reduce racial disparities.

Higher baseline dietary fat and fatty acid intake is associated with increased risk of incident prostate cancer in the SABOR study.

To study the association of nutrient intake measured by baseline food frequency questionnaire and risk of subsequent prostate cancer (PCa) in the SABOR (San Antonio Biomarkers of Risk) cohort study. After IRB approval, more than 1903 men enrolled in a prospective cohort from 2000 to 2010 as part of the SABOR clinical validation site for the National Cancer Institute Early Detection Research Network. Food and nutrient intakes were calculated using a Food Frequency Questionnaire. Cox proportional hazards modeling and covariate-balanced propensity scores were used to assess the associations between all nutrients and PCa. A total of 229 men were diagnosed with PCa by prostate biopsy. Among all nutrients, increased risk of PCa was associated with intake of dietary fat scaled by the total caloric intake, particularly saturated fatty acid (SFA) [HR 1.19; 95% CI, 1.07-1.32), P value < 0.001, False discovery rate (FDR) 0.047] and trans fatty acid (TFA) [HR per quintile 1.21; (95% CI) (1.08-1.35), P < 0.001, FDR 0.039]. There was an increased risk of PCa with increasing intake of monounsaturated fatty acid (MUFA) (HR per quintile 1.14; 95% CI 1.03-1.27, P = 0.01, FDR 0.15) and cholesterol [HR per quintile 1.13; 95% confidence interval (95% CI) (1.02-1.26), P-value 0.02, FDR 0.19]. After examining a large, population-based cohort for PCa diagnosis, we identified dietary total fat and certain fatty acids as associated with increased risk of PCa. We found no factors that were protective from PCa. Dietary modification of fatty acid intake may reduce risk of PCa.

Protein Palmitoylation Plays an Important Role in Trichomonas vaginalis Adherence

The flagellated protozoan parasite Trichomonas vaginalis is the etiologic agent of trichomoniasis, the most common non-viral sexually transmitted infection worldwide. As an obligate extracellular pathogen, adherence to epithelial cells is critical for parasite survival within the human host and a better understanding of this process is a prerequisite for the development of therapies to combat infection. In this sense, recent work has shown S-acylation as a key modification that regulates pathogenesis in different protozoan parasites. However, there are no reports indicating whether this post-translational modification is a mechanism operating in T. vaginalis In order to study the extent and function of S-acylation in T. vaginalis biology, we undertook a proteomic study to profile the full scope of S-acylated proteins in this parasite and reported the identification of 363 proteins involved in a variety of biological processes such as protein transport, pathogenesis related and signaling, among others. Importantly, treatment of parasites with the palmitoylation inhibitor 2-bromopalmitate causes a significant decrease in parasite: parasite aggregation as well as adherence to host cells suggesting that palmitoylation could be modifying proteins that are key regulators of Trichomonas vaginalis pathogenesis.