Smoking and prostate cancer risk in young men in Appalachian Kentucky.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e12004-e12004
Author(s):  
Indraneel Gowdar ◽  
Priya Mallikarjun ◽  
Indraneel Reddy ◽  
Anjali Shankar ◽  
Mark Dignan
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Smoking Status ◽  
Adult Population ◽  
Prostate Cancer Risk ◽  
Age At Diagnosis ◽  
Large Hospital ◽  
Age Related ◽  
Increased Risk ◽  
Appalachian Kentucky

e12004 Background: Kentucky has the highest smoking rates in the US, with 25.2% of the adult population considered current smokers compared to 18.4% nationwide (CRC, 2011 statistics), as well as high rates of chronic conditions including diabetes, heart disease, and lung cancer. In particular, the Appalachian area of Kentucky appears to have particularly high rates of both smoking and prostate cancer, beyond what is typical for the state as a whole. Recent data on prostate cancer from the Kentucky State Cancer Registry from 2004-2008 showed an incidence rate of 144 vs. 139.8 per 100,000 for "Appalachia" and Kentucky as a state, respectively. The purpose of this study is to investigate the relationship between smoking and risk of prostate cancer in Appalachian Kentucky. Methods: Data were collected on all prostate cancers diagnosed from 1996-2005 in a large hospital serving the Appalachian region. Data were collected without identifiers. Relevant statistics recorded included age at diagnosis, family history, and smoking status (classified as current smoker, non-smoker, or unknown smoking status). Results: A total of 286 patients with diagnosed prostate cancer were collected. The patients ranged from 45 to 94 years of age at diagnosis (Mean = 71, SD = 9.8). Of the 286, 89 (31.1%) had never smoked, and 94 (32.9%) were current or former cigarette smokers (Mean pack years = 25.4). To control for the age-related increase in cancer risk, patients were separated into two age groups: age 65 and younger (n=86, 30.1%), and older than 65 (n=200, 69.9%). The proportion of the younger group who smoked was significantly greater than that of the older group (44.2% vs. 28%, respectively; p= 0.009, Fischer's exact test). Conclusions: These data suggest that smoking in males younger than 65 is positively associated with an increased risk of prostate cancer in Appalachian Kentucky. Further study is needed to elucidate this relationship, as well as to evaluate any association between smoking severity and Gleason score.

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.

scholarly journals O8A.4 Asbestos exposure and prostate cancer, really?

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A71.1-A71
Author(s):  
Marie-Elise Parent ◽  
M Hugues Richard
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Asbestos Exposure ◽  
Large Population ◽  
Prostate Cancer Risk ◽  
Cumulative Exposure ◽  
Population Exposure ◽  
Specific Information ◽  
Chrysotile Asbestos ◽  
Increased Risk

BackgroundGeneral population exposure to asbestos from residential insulation and from environmental sources during childhood have recently been associated with prostate cancer. While asbestos fibers can be found in the prostate of workplace-exposed men at autopsy, few occupational studies have reported on asbestos exposure and prostate cancer incidence. We examined the association between lifetime occupational exposure to chrysotile asbestos and prostate cancer risk in a large population-based case-control study.MethodsCases were 1933 men with histologically-confirmed incident prostate cancer, aged ≤75 years, diagnosed in 2005–2009 in Montreal. Concurrently, 1994 population controls from the same residential area and age distribution were randomly selected from electoral lists. In-person interviews elicited detailed socio-demographics, lifestyle and work histories. Industrial hygienists used job-specific information to provide semi-quantitative evaluations of intensity and frequency of exposure to 345 chemical agents, including asbestos, and a measure of confidence in the evaluation. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer risk associated with exposure to chrysotile asbestos.ResultsAfter restriction to probable and definite exposure, and application of a 5 year lag, 12.5% of cases and 11.8% of controls were ever exposed to asbestos (OR=1.1, 95% CI 0.9–1.3). For duration of exposure, there was no increase in risk of overall prostate cancer in the lower tertiles of exposure but risk was elevated in the upper tertile (OR=1.6, 95% CI 1.2–2.2). Similarly, for cumulative exposure, risk was elevated in the upper tertile only (OR=1.5, 95% CI 1.1–2.1). Analyses considering tumor grades also showed a higher risk in the upper tertile of cumulative exposure for non-aggressive (OR=1.5, 95% CI 1.1–2.2) and especially aggressive (OR=1.9, 95% CI 1.2–3.0) cancers.ConclusionOur findings are consistent with an increased risk of prostate cancer with prolonged and high cumulative exposure to chrysotile asbestos, and particularly for the aggressive form of the disease.

scholarly journals Association between dietary inflammatory index and prostate cancer among Italian men

2014 ◽  
Vol 113 (2) ◽  
pp. 278-283 ◽  
Author(s):  
Nitin Shivappa ◽  
Cristina Bosetti ◽  
Antonella Zucchetto ◽  
Maurizio Montella ◽  
Diego Serraino ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Smoking Status ◽  
Wide Spectrum ◽  
Prostate Cancer Risk ◽  
Dietary Inflammatory Index ◽  
Logistic Regression Models ◽  
Inflammatory Index ◽  
History Of ◽  
Relationship Of

Previous studies have shown that various dietary components may be implicated in the aetiology of prostate cancer, although the results remain equivocal. The possible relationship of inflammation derived from dietary exposures with prostate cancer risk has not been investigated. We examined the ability of a newly developed dietary inflammatory index (DII) to predict prostate cancer risk in a case–control study conducted in Italy between 1991 and 2002. A total of 1294 patients aged < 75 years with incident, histologically confirmed carcinoma of the prostate served as cases. A total of 1451 subjects aged < 75 years who were admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions served as controls. The DII was computed based on dietary intake assessed using a previously validated seventy-eight-item FFQ. Logistic regression models were used to estimate multivariable OR adjusted for age, study centre, years of education, social class, BMI, smoking status, family history of prostate cancer and total energy intake. Men with higher DII scores had a higher risk of prostate cancer when analysed using the DII as both continuous (OR 1·06, 95 % CI 1·00, 1·13) and categorical, i.e. compared with men in the lowest quartile of the DII, men in the third and fourth quartiles were at elevated risk (ORQuartile 3 v. 1 1·32, 95 % CI 1·03, 1·69 and ORQuartile 4 v. 1 1·33, 95 % CI 1·01, 1·76; Ptrend= 0·04). These data suggest that a pro-inflammatory diet, as indicated by the increasing DII score, is a risk factor of prostate cancer in Italian men.

Smoking and increased breast cancer risk in younger women in Appalachian Kentucky.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e11097-e11097
Author(s):  
Indraneel Reddy ◽  
Anjali Shankar ◽  
Priya Mallikarjun ◽  
Nicola Jabbour ◽  
Mark Dignan
Keyword(s):  
Breast Cancer ◽  
Smoking Status ◽  
Adult Population ◽  
Current Smoker ◽  
The State ◽  
Age At Diagnosis ◽  
Breast Cancers ◽  
Exact Test ◽  
Cancer Data ◽  
Appalachian Kentucky

e11097 Background: Smoking rates in Kentucky are among the highest in the US. Data from the Centers for Disease Control and Prevention for 2011 showed that in Kentucky 25.2% of the adult population are current smokers compared to 18.4% nationwide. In addition, smoking rates in the Appalachian region are substantially higher than the state rate. Breast cancer rates are also elevated in Appalachian Kentucky, with data from the Kentucky State Cancer Registry for 2004-2008 showing an incidence rate of 67.3 per 100,000 in Appalachia compared to 65.6 per 100,000 for the state. Our objective was to evaluate the association of smoking and breast cancer among women in Appalachian Kentucky. Methods: We reviewed all the breast cancer data from a large community hospital serving the Appalachian areas of Kentucky. Data were collected from the hospital tumor registry for the period 1996-2005 and included demographic characteristics and smoking status, in addition to information about the breast cancer. No personal identifiers were collected. Breast cancers were coded as invasive or non-invasive and smoking status was coded as current smoker, non-smoker or unknown. Results: Data from records of 392 patients were included in the analyses. Over 90% of the breast cancers in the 392 were invasive. Age at diagnosis ranged from 24 to 92 and the mean was 59.9 years (standard deviation= 13.5. 21.2% of the records indicated a family history of breast cancer. Of the 392 patients, 162 (41.3%) were smokers. Analysis of the data by age at diagnosis showed that of the 120 women diagnosed with breast cancer at age less than 65, 46.5% were smokers, compared to 31.3% of those age 65 or older (p=.005, Fisher’s Exact Test). Conclusions: The risk of breast cancer in women under age 65 appears to be associated with smoking in this population. Additional research is needed to more fully explore this association.

scholarly journals Meta-Analysis of the Relationship between XRCC1-Arg399Gln and Arg280His Polymorphisms and the Risk of Prostate Cancer

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jie Yan ◽  
Xiantao Wang ◽  
Hui Tao ◽  
Zengfu Deng ◽  
Wang Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Meta Analysis ◽  
Prostate Cancer Risk ◽  
Recessive Model ◽  
Dominant Model ◽  
Xrcc1 Arg399gln ◽  
Increased Risk ◽  
Arg399gln Polymorphism ◽  
The Relationship

Abstract Prostate cancer is one of the most common noncutaneous malignancies in Western countries. Because there has been a debate regarding the relationship between the XRCC1-Arg399Gln and Arg280His polymorphisms and prostate cancer risk, we therefore performed this meta-analysis. The electronic databases PubMed, EMBASE and Medline were searched prior to October 1, 2014. An odds ratio and 95% confidence interval were used to calculate association. Heterogeneity was tested by both a chi-square test and I2statistic. Funnel plots and Egger’s test were used to assess publication bias. All statistical analyses were performed using STATA 12.0 software. A significant association between the XRCC1-Arg399Gln polymorphism and prostate cancer risk was found under a homozygote model and a recessive model. A significant association between XRCC1-Arg280His and prostate cancer risk was found under a heterozygote model and a dominant model. Overall, the results of this meta-analysis show that the XRCC1-Arg399Gln polymorphism may be associated with an increased risk for prostate cancer under the homozygote model and the recessive model. And XRCC1-Arg280His polymorphism is likely to be related with prostate cancer risk under the heterozygote model and the dominant model. Additional larger well-designed studies are needed to validate our results.

scholarly journals Mendelian randomization does not support serum calcium in prostate cancer risk

2018 ◽  
Author(s):  
James Yarmolinsky ◽  
Katie Berryman ◽  
Ryan Langdon ◽  
Carolina Bonilla ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Causal Inference ◽  
Serum Calcium ◽  
Observational Studies ◽  
Advanced Prostate Cancer ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
A Genome ◽  
Increased Risk

AbstractBackground: Observational studies suggest that dietary and serum calcium are risk factors for prostate cancer. However, such studies suffer from residual confounding (due to unmeasured or imprecisely measured confounders), undermining causal inference. Mendelian randomization uses randomly assigned (hence unconfounded and pre-disease onset) germline genetic variation to proxy for phenotypes and strengthen causal inference in observational studies.Objective: We tested the hypothesis that serum calcium is associated with an increased risk of overall and advanced prostate cancer.Design: A genetic instrument was constructed using 5 single nucleotide polymorphisms robustly associated with serum calcium in a genome-wide association study (N ≤ 61,079). This instrument was then used to test the effect of a 0.5 mg/dL increase (1 standard deviation, SD) in serum calcium on risk of prostate cancer in 72,729 men in the PRACTICAL (Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome) Consortium (44,825 cases, 27,904 controls) and risk of advanced prostate cancer in 33,498 men (6,263 cases, 27,235 controls).Results: We found weak evidence for a protective effect of serum calcium on prostate cancer risk (odds ratio [OR] per 0.5 mg/dL increase in calcium: 0.83, 95% CI: 0.63-1.08; P=0.12). We did not find strong evidence for an effect of serum calcium on advanced prostate cancer (OR per 0.5 mg/dL increase in calcium: 0.98, 95% CI: 0.57-1.70; P=0.93).Conclusions: Our Mendelian randomization analysis does not support the hypothesis that serum calcium increases risk of overall or advanced prostate cancer.

scholarly journals Genetic polymorphisms in CDH1 and Exo1 genes elevate the prostate cancer risk in Bangladeshi population

Tumor Biology ◽  
2019 ◽  
Vol 41 (3) ◽  
pp. 101042831983083 ◽  
Author(s):  
Hasnain Imtiaz ◽  
Sharmin Afroz ◽  
Md Amir Hossain ◽  
Sm Faysal Bellah ◽  
Md Mostafizur Rahman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Confidence Interval ◽  
Genetic Polymorphisms ◽  
Odds Ratio ◽  
Prostate Cancer Risk ◽  
Polymorphism Analysis ◽  
Increased Risk ◽  
Bangladeshi Population ◽  
Increased Susceptibility

The polymorphisms of invasion suppressor gene CDH1 and DNA mismatch repair gene Exo1 have been reported to play critical role in the development, tumorigenesis, and progression of several kinds of cancers including prostate cancer. This study was designed to analyze the contribution of single-nucleotide polymorphisms of the CDH1 (-160C/A) and Exo1 (K589E) to prostate cancer susceptibility in Bangladeshi population. The study included 100 prostate cancer cases and age-matched 100 healthy controls. Polymerase chain reaction-restriction fragment length polymorphism analysis was used to determine the genetic polymorphisms. A significant association was found between CDH1 -160C/A (rs16260) and Exo1 (rs1047840, K589E) polymorphisms and prostate cancer risk. In case of CDH1 -160C/A polymorphism, the frequencies of the three genotypes C/C,C/A, and A/A were 45%, 48%, and 7% in cases and 63%, 32%, and 5% in controls, respectively. The heterozygote C/A genotype and combined C/A + A/A genotypes showed 2.10-fold (odds ratio = 2.1000, 95% confidence interval = 1.2956–4.0905, p = 0.013) and 2.08-fold (odds ratio = 2.0811, 95% confidence interval = 1.1820–3.6641, p = 0.011) increased risk of prostate cancer, respectively, when compared with homozygous C/C genotypes. The variant A allele also was associated with increased risk of prostate cancer (odds ratio = 1.6901, 95% confidence interval = 1.0740–2.6597, p = 0.0233). In case of Exo1 (K589E) polymorphism, G/A heterozygote, A/A homozygote, and combined G/A + A/A genotypes were found to be associated with 2.30-, 4.85-, and 3.04-fold higher risk of prostate cancer, respectively (odds ratio = 2.3021, 95% confidence interval = 2.956–4.0905, p = 0.0031; odds ratio = 4.8462, 95% confidence interval = 1.0198–23.0284, p = 0.0291; OR = 3.0362, 95% confidence interval = 1.7054–5.4053, p = 0.0001, respectively). The “A” allele showed significant association with increased susceptibility (2.29-fold) to prostate cancer (odds ratio = 2.2955, 95% confidence interval = 1.4529–3.6270, p = 0.0004). Our results suggest that CDH1 -160C/A and Exo1 K589E polymorphisms are associated with increased susceptibility to prostate cancer in Bangladeshi population.

Germline heterozygous BLM mutations and prostate cancer risk.

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 321-321
Author(s):  
Elisa Ledet ◽  
Emmanuel S. Antonarakis ◽  
Colin Pritchard ◽  
William B. Isaacs ◽  
A. Oliver Sartor
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Dna Sequencing ◽  
Cancer Patients ◽  
Genetic Disorder ◽  
Prostate Cancer Risk ◽  
Dna Helicase ◽  
Cancer Center ◽  
Increased Risk

321 Background: The BLM gene encodes a RecQ DNA helicase that is involved in homologous recombination. Biallelic BLM inactivation leads to Bloom syndrome, an inherited genetic disorder marked by chromosomal instability and multiple cancer susceptibilities. Conflicting studies have suggested that heterozygous BLM mutation carriers may have an increased risk of various cancers. Here we explored the role of germline pathogenic BLM mutations in prostate cancer. Methods: Prostate cancer patients with heterozygous BLM mutations were assembled from Tulane Cancer Center (TCC), Johns Hopkins Hospital (JHH) and University of Washington (UW). BLM germline mutations were identified either through commercial germline testing (Invitae), the UW-BROCA panel, or whole-exome sequencing. Corresponding tumor tissue was analyzed by DNA sequencing for somatic alterations. Population level control data were obtained from the Genome Aggregation Database (gnomAD). Results: 6 BLM germline carriers were identified among 985 advanced prostate cancer case; 2/295 TCC patients, 2/172 JHH patients, and 2/518 UW patients. Overall, pathogenic BLM mutations were detected in 0.609% (6/985) of prostate cancer cases. All mutations were loss-of-function truncating lesions (splicing or nonsense alterations). No Ashkenazi BLM mutations were observed. The population frequency of pathogenic or likely pathogenic BLM alterations detected in gnomAD was 0.025% (31/124,589). Compared to gnomAD controls, the relative risk of BLM mutations in prostate cancer patients was 24.3 (95% CI 10.2 to 58.2; P < 0.0001). One family had a pathogenic splice variant in BLM that cosegregated with disease in three of three cases with lethal/high risk prostate cancer. Tumor DNA sequencing was possible in 5 of 6 BLM carriers; no case demonstrated LOH or additional somatic BLM mutations. Interestingly, 2/5 cases on tumor sequencing also had bi-allelic BRCA2 inactivation. Conclusions: Germline BLM mutations may play a role in prostate cancer risk. Given the role of BLM in chromosomal stability and evidence of concurrent BRCA2 inactivation in a subset of cases, larger cohorts and functional analyses will be critical for better understanding the role of BLM in prostate cancer.

scholarly journals Neither Hormonal Factors Nor AGEs Explain Lower Prostate Cancer Risk in Older Men With Diabetes Mellitus

2019 ◽  
Vol 104 (12) ◽  
pp. 6017-6024
Author(s):  
Yi X Chan ◽  
Helman Alfonso ◽  
P Gerry Fegan ◽  
Leon Flicker ◽  
Bu B Yeap
Keyword(s):  
Prostate Cancer ◽  
Diabetes Mellitus ◽  
Cancer Risk ◽  
Prostate Cancer Risk ◽  
Sex Hormone ◽  
Inverse Association ◽  
Metabolic Disturbances ◽  
Hormonal Factors ◽  
Increased Risk ◽  
Risk Of Cancer

Abstract Context Diabetes mellitus is conventionally associated with an increased risk of cancer; however, inverse associations of diabetes with prostate cancer are well described. Mechanisms are unclear, although hormonal factors, including alterations in sex hormone and IGF1 concentrations due to metabolic disturbances, have been hypothesized to play a role. Objective To assess sex hormones, IGF1, glucose, and advanced glycation end products (AGEs) as potential mediators of the association between diabetes mellitus and prostate cancer. Design and Participants Longitudinal cohort study. The association of baseline diabetes with prostate cancer incidence was assessed using proportional hazards competing risks analysis in 3149 men followed for 12 years. Baseline hormone, glucose, and carboxymethyllysine (CML) levels were examined as potential mediators of this association. Results Diabetes was associated with a lower prostate cancer risk (fully adjusted subhazard ratio, 0.63; 95% CI, 0.43 to 0.92; P = 0.017). This association was unchanged after accounting for testosterone, DHT, estradiol, or SHBG. Similarly, the addition of IGF1 or its binding proteins 1 and 3, or glucose, did not alter this association. CML was not associated with the risk of prostate cancer, and additional correction for CML in the fully adjusted model did not alter the inverse association of diabetes and prostate cancer risk. Conclusions In this study, alterations in sex hormone, IGF1, glucose, and CML levels did not account for the inverse association of diabetes and prostate cancer risk. Further studies are required to provide more insight into underlying causes of this association.

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.

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