scholarly journals Racial differences in the systemic inflammatory response to prostate cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0252951
Author(s):  
Andrew G. Rundle ◽  
Sudha M. Sadasivan ◽  
Dhananjay A. Chitale ◽  
Nilesh S. Gupta ◽  
Sean R. Williamson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Racial Differences ◽  
Systemic Inflammation ◽  
Prostate Cancer Risk ◽  
White Men ◽  
Case Control ◽  
Lymphocyte Ratio ◽  
Increased Risk ◽  
Over Time

Systemic inflammation may increase risk for prostate cancer progression, but the role it plays in prostate cancer susceptibility is unknown. From a cohort of over 10,000 men who had either a prostate biopsy or transurethral resection that yielded a benign finding, we analyzed 517 incident prostate cancer cases identified during follow-up and 373 controls with one or more white blood cell tests during a follow-up period between one and 18 years. Multilevel, multivariable longitudinal models were fit to two measures of systemic inflammation, neutrophil-to-lymphocyte ratio (NLR) and monocyte-to-lymphocyte ratio (MLR), to determine NLR and MLR trajectories associated with increased risk for prostate cancer. For both measures, we found no significant differences in the trajectories by case/control status, however in modeling NLR trajectories there was a significant interaction between race (white or Black and case-control status. In race specific models, NLR and MLR values were consistently higher over time among white controls than white cases while case-control differences in NLR and MLR trajectories were not apparent among Black men. When cases were classified as aggressive as compared to non-aggressive, the case-control differences in NLR and MLR values over time among white men were most apparent for non-aggressive cases. For NLR among white men, significant case-control differences were observed for the entire duration of observation for men who had inflammation in their initial prostate specimen. It is possible that, among white men, monitoring of NLR and MLR trajectories after an initial negative biopsy may be useful in monitoring prostate cancer risk.

scholarly journals Vasectomy and Risk of Aggressive Prostate Cancer: A 24-Year Follow-Up Study

2014 ◽  
Vol 32 (27) ◽  
pp. 3033-3038 ◽  
Author(s):  
Mohummad Minhaj Siddiqui ◽  
Kathryn M. Wilson ◽  
Mara M. Epstein ◽  
Jennifer R. Rider ◽  
Neil E. Martin ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Treatment ◽  
Specific Antigen ◽  
Prostate Cancer Risk ◽  
The United States ◽  
Low Grade ◽  
High Grade ◽  
Follow Up Study ◽  
Increased Risk

Purpose Conflicting reports remain regarding the association between vasectomy, a common form of male contraception in the United States, and prostate cancer risk. We examined prospectively this association with extended follow-up and an emphasis on advanced and lethal disease. Patients and Methods Among 49,405 US men in the Health Professionals Follow-Up Study, age 40 to 75 years at baseline in 1986, 6,023 patients with prostate cancer were diagnosed during the follow-up to 2010, including 811 lethal cases. In total, 12,321 men (25%) had vasectomies. We used Cox proportional hazards models to estimate the relative risk (RR) and 95% CIs of total, advanced, high-grade, and lethal disease, with adjustment for a variety of possible confounders. Results Vasectomy was associated with a small increased risk of prostate cancer overall (RR, 1.10; 95% CI, 1.04 to 1.17). Risk was elevated for high-grade (Gleason score 8 to 10; RR, 1.22; 95% CI, 1.03 to 1.45) and lethal disease (death or distant metastasis; RR, 1.19; 95% CI, 1.00 to 1.43). Among a subcohort of men receiving regular prostate-specific antigen screening, the association with lethal cancer was stronger (RR, 1.56; 95% CI, 1.03 to 2.36). Vasectomy was not associated with the risk of low-grade or localized disease. Additional analyses suggested that the associations were not driven by differences in sex hormone levels, sexually transmitted infections, or cancer treatment. Conclusion Our data support the hypothesis that vasectomy is associated with a modest increased incidence of lethal prostate cancer. The results do not appear to be due to detection bias, and confounding by infections or cancer treatment is unlikely.

Precision prevention of TMPRSS2:ERG prostate cancer.

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 78-78
Author(s):  
Lorelei A. Mucci ◽  
Thomas Ahearn ◽  
Kathryn Penney ◽  
Andreas Pettersson ◽  
Rebecca E Graff ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Molecular Subtype ◽  
Prostate Cancer Risk ◽  
Health Study ◽  
Tumor Biomarker ◽  
Common Disease ◽  
Study Cohort ◽  
Increased Risk ◽  
Biomarker Data

78 Background: Increased integration of tumor biomarker data into prostate cancer epidemiology studies is needed to identify molecular subtypes that underlie its etiology and progression. We hypothesize that the TMPRSS2:ERG gene fusion is a unique prostate cancer subtype that is etiologically distinct from cancers lacking TMPRSS2:ERG. Methods: We leveraged the Physicians’ Health Study and Health Professionals Follow-up Study cohort data on pre- and post-diagnostic lifestyle factors, inherited genetic variants, circulating biomarkers, and clinical data and follow-up for 30 years. We have a tumor repository of men with prostate cancer and tumor tissue microarrays. Using immunohistochemistry, we characterized TMPRSS2:ERG status for 1,491 incident prostate cancer cases in these cohorts, and also have biomarker data on a range of additional markers from immunohistochemistry and mRNA expression profiling. Results: Fifty percent of prostate cancer cases were ERG-positive. ERG-positive cancers show much higher expression of insulin/IGF signaling, PTEN loss, higher VDR expression, as well as expression of mismatch repair genes. In contrast, ERG-negative prostate cancer is characterized by increased presence of chronic inflammation and atrophy. We found higher pre-diagnostic free testosterone levels, but not other sex hormones, were associated with increased risk of ERG-positive (OR = 1.4, 95% CI = 1.0-1.8) but not ERG-negative disease (OR = 0.9, 95% CI = 0.7-1.2). Of 39 known genetic risk loci, six were significantly associated (p < 0.05) with ERG+ versus ERG- cancer (2 expected by chance). Prostate cancer risk factors such as taller height (an indicator of growth factors in puberty) are uniquely associated with ERG-positive prostate cancer. Moreover, we observe a complex interaction of components of insulin/IGF and ERG-status on prostate cancer mortality. Conclusions: TMPRSS2:ERG is a highly prevalent somatic event in prostate cancer that likely defines a unique molecular subtype of this common disease. Understanding the differences between these two prostate cancer subtypes may enhance opportunities for prevention.

scholarly journals Do African American Men Have Lower Survival From Prostate Cancer Compared With White Men? A Meta-analysis

2010 ◽  
Vol 4 (3) ◽  
pp. 189-206 ◽  
Author(s):  
Gayathri Sridhar ◽  
Saba W. Masho ◽  
Tilahun Adera ◽  
Viswanathan Ramakrishnan ◽  
John D. Roberts
Keyword(s):  
Prostate Cancer ◽  
African American ◽  
Racial Differences ◽  
African American Men ◽  
Meta Analysis ◽  
White Men ◽  
Cancer Specific Survival ◽  
Increased Risk ◽  
Significant Difference ◽  
The Relationship

Prostate cancer is the second leading cause of cancer-related mortality in men. This meta-analysis was conducted to investigate the relationship between race and survival from prostate cancer. A systematic review of articles published from 1968 to 2007 assessing survival from prostate cancer was conducted. Analysis of unadjusted studies reported that African American men have an increased risk of all-cause mortality (hazard ratio [HR] = 1.47, 95% confidence interval [CI] = 1.31-1.65, p < .001). However, examination of adjusted studies identified no difference (HR = 1.07, 95% CI = 0.94-1.22, p = .308). No statistically significant difference was observed in prostate cancer—specific survival in both analyses using unadjusted (HR = 1.11, 95% CI = 0.94-1.31, p = .209) and adjusted studies (HR = 1.15, 95% CI = 0.95-1.41, p = .157). This meta-analysis concludes that there are no racial differences in the overall and prostate cancer—specific survival between African American and White men.

scholarly journals Androgen Deprivation Therapy and the Risk for Inguinal Hernia: An Observational Nested Case Control Study

2021 ◽  
Vol 15 (6) ◽  
pp. 155798832110586
Author(s):  
Maria Hermann ◽  
Hanna Vikman ◽  
Pär Stattin ◽  
Asmatullah Katawazai ◽  
Ove Gustafsson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Inguinal Hernia ◽  
Androgen Deprivation Therapy ◽  
Case Control Study ◽  
Prostate Cancer Risk ◽  
Case Control ◽  
Androgen Deprivation ◽  
Increased Risk ◽  
Nested Case Control ◽  
Control Study

It has been suggested that hypogonadism increases the risk for inguinal hernia (IH). The aim of this study was to investigate any association between androgen deprivation therapy (ADT) for prostate cancer and increased risk for IH. The study population in this population-based nested case-control study was based on data from the Prostate Cancer Database Sweden. The cohort included all men with prostate cancer who had not received curative treatment. Men who had been diagnosed or had undergone IH repair ( n = 1,324) were cases and controls, where not diagnosed, nor operated on for IH, matched only on birth year ( n = 13,240). Conditional multivariate logistic regression models were used to assess any temporal association between ADT and IH, adjusting for marital status, education level, prostate cancer risk category, Charlson Comorbidity Index, ADT, time since prostate cancer diagnosis, and primary prostate cancer treatment. Odds ratio (OR) for diagnosis/repair of IH 0 to 1 year from start of ADT was 0.5 (95% confidence interval [CI] = [0.38, 0.68]); between 1 and 3 years after, the OR was 0.35 (95% CI = [0.26, 0.47]); between 3 and 5 years after, the OR was 0.39 (95% CI = [0.26, 0.56]); between 5 and 7 years after, the OR was 0.6 (95% CI = [0.41, 0.97]); and >9 years after, the OR was 3.68 (95% CI = [2.45, 5.53]). The marked increase in OR for IH after 9 years of ADT supports the hypothesis that low testosterone levels increase the risk for IH. The low risk for IH during the first 8 years on ADT is likely caused by selection of men with advanced cancer unlikely to be diagnosed or treated for IH.

Vasectomy and Prostate Cancer Risk: A 38-Year Nationwide Cohort Study

2019 ◽  
Author(s):  
Anders Husby ◽  
Jan Wohlfahrt ◽  
Mads Melbye
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Socioeconomic Factors ◽  
Sperm Quality ◽  
Prostate Cancer Risk ◽  
Reproductive Factors ◽  
Personal Identification ◽  
Increased Risk ◽  
Log Linear

Abstract Background A man’s risk of prostate cancer has been linked to his prior reproductive history, with low sperm quality, low ejaculation frequency, and a low number of offspring being associated with increased prostate cancer risk. It is, however, highly controversial whether vasectomy, a common sterilization procedure for men, influences prostate cancer risk. Methods We established a cohort of all Danish men (born between 1937 and 1996) and linked information on vasectomy, doctor visits, socioeconomic factors, and cancer from nationwide registries using unique personal identification numbers. Incidence risk ratios for prostate cancer by time since vasectomy and age at vasectomy during the follow-up were estimated using log-linear Poisson regression. Results Overall, 26 238 cases of prostate cancer occurred among 2 150 162 Danish men during 53.4 million person-years of follow-up. Overall, vasectomized men had an increased risk of prostate cancer compared with nonvasectomized men (relative risk = 1.15, 95% confidence interval = 1.10 to 1.20). The increased risk of prostate cancer following vasectomy persisted for at least 30 years after the procedure and was observed regardless of age at vasectomy and cancer stage at diagnosis. Adjustment for the number of visits to the doctor and socioeconomic factors did not explain the association. Conclusions Vasectomy is associated with a statistically significantly increased long-term risk of prostate cancer. The absolute increased risk following vasectomy is nevertheless small, but our finding supports a relationship between reproductive factors and prostate cancer risk.

scholarly journals Social Jetlag and Prostate Cancer Incidence in Alberta’s Tomorrow Project: A Prospective Cohort Study

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3873
Author(s):  
Liang Hu ◽  
Andrew Harper ◽  
Emily Heer ◽  
Jessica McNeil ◽  
Chao Cao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Cancer Incidence ◽  
Repeated Measures ◽  
Prospective Cohort ◽  
Prostate Cancer Risk ◽  
Absolute Difference ◽  
Prostate Cancer Incidence ◽  
Social Jetlag ◽  
Increased Risk

We investigated the association of social jetlag (misalignment between the internal clock and socially required timing of activities) and prostate cancer incidence in a prospective cohort in Alberta, Canada. Data were collected from 7455 cancer-free men aged 35–69 years enrolled in Alberta’s Tomorrow Project (ATP) from 2001–2007. In the 2008 survey, participants reported usual bed- and wake-times on weekdays and weekend days. Social jetlag was defined as the absolute difference in waking time between weekday and weekend days, and was categorized into three groups: 0–<1 h (from 0 to anything smaller than 1), 1–<2 h (from 1 to anything smaller than 2), and 2+ h. ATP facilitated data linkage with the Alberta Cancer Registry in June 2018 to determine incident prostate cancer cases (n = 250). Hazard ratios (HR) were estimated using Cox proportional hazards regressions, adjusting for a range of covariates. Median follow-up was 9.57 years, yielding 68,499 person-years. Baseline presence of social jetlag of 1–<2 h (HR = 1.52, 95% CI: 1.10 to 2.01), and 2+ hours (HR = 1.69, 95% CI: 1.15 to 2.46) were associated with increased prostate cancer risk vs. those reporting no social jetlag (p for trend = 0.004). These associations remained after adjusting for sleep duration (p for trend = 0.006). With respect to chronotype, the association between social jetlag and prostate cancer risk remained significant in men with early chronotypes (p for trend = 0.003) but attenuated to null in men with intermediate (p for trend = 0.150) or late chronotype (p for trend = 0.381). Our findings suggest that greater than one hour of habitual social jetlag is associated with an increased risk of prostate cancer. Longitudinal studies with repeated measures of social jetlag and large samples with sufficient advanced prostate cancer cases are needed to confirm these findings.

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