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

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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Cholesterol and prostate cancer risk: a long-term prospective cohort study

BMC Cancer ◽

10.1186/s12885-016-2691-5 ◽

2016 ◽

Vol 16 (1) ◽

Cited By ~ 13

Author(s):

Trond Heir ◽

Ragnhild Sørum Falk ◽

Trude Eid Robsahm ◽

Leiv Sandvik ◽

Jan Erikssen ◽

...

Keyword(s):

Prostate Cancer ◽

Cohort Study ◽

Cancer Risk ◽

Prospective Cohort Study ◽

Prospective Cohort ◽

Prostate Cancer Risk

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O8A.4 Asbestos exposure and prostate cancer, really?

Occupational and Environmental Medicine ◽

10.1136/oem-2019-epi.190 ◽

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.

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Sleep disruption, chronotype, shift work, and prostate cancer risk and mortality: a 30-year prospective cohort study of Finnish twins

Cancer Causes & Control ◽

10.1007/s10552-016-0815-5 ◽

2016 ◽

Vol 27 (11) ◽

pp. 1361-1370 ◽

Cited By ~ 33

Author(s):

Barbra A. Dickerman ◽

Sarah C. Markt ◽

Markku Koskenvuo ◽

Christer Hublin ◽

Eero Pukkala ◽

...

Keyword(s):

Prostate Cancer ◽

Cohort Study ◽

Cancer Risk ◽

Shift Work ◽

Prospective Cohort Study ◽

Prospective Cohort ◽

Prostate Cancer Risk ◽

Sleep Disruption

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P2-275 Cholesterol and the risk of grade-specific prostate cancer incidence: evidence from a large prospective cohort with 37 years follow-up

Journal of Epidemiology & Community Health ◽

10.1136/jech.2011.142976k.8 ◽

2011 ◽

Vol 65 (Suppl 1) ◽

pp. A297-A297

Author(s):

K. Shafique ◽

P. McLoone ◽

K. Qureshi ◽

H. Leung ◽

C. Hart ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Incidence ◽

Prospective Cohort ◽

Prostate Cancer Incidence ◽

Large Prospective Cohort

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

Scientific Reports ◽

10.1038/srep09905 ◽

2015 ◽

Vol 5 (1) ◽

Cited By ~ 10

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.

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Mendelian randomization does not support serum calcium in prostate cancer risk

10.1101/297721 ◽

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.

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

Tumor Biology ◽

10.1177/1010428319830837 ◽

2019 ◽

Vol 41 (3) ◽

pp. 101042831983083 ◽

Cited By ~ 2

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.

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Germline heterozygous BLM mutations and prostate cancer risk.

Journal of Clinical Oncology ◽

10.1200/jco.2019.37.7_suppl.321 ◽

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.

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