scholarly journals Minimal detection bias in the inverse association between statin drug use and advanced prostate cancer risk: A simulation study

2011 ◽  
Vol 35 (4) ◽  
pp. e6-e11 ◽  
Author(s):  
Alison M. Mondul ◽  
Brian Caffo ◽  
Elizabeth A. Platz
2014 ◽  
Vol 192 (2) ◽  
pp. 379-384 ◽  
Author(s):  
Elizabeth A. Platz ◽  
Catherine M. Tangen ◽  
Phyllis J. Goodman ◽  
Cathee Till ◽  
Howard L. Parnes ◽  
...  

2015 ◽  
Vol 193 ◽  
pp. 1-7 ◽  
Author(s):  
Pei-Ying Pai ◽  
Vivian Chia-Rong Hsieh ◽  
Chang-Bi Wang ◽  
Hsi-Chin Wu ◽  
Wen-Miin Liang ◽  
...  

2018 ◽  
Author(s):  
James Yarmolinsky ◽  
Katie Berryman ◽  
Ryan Langdon ◽  
Carolina Bonilla ◽  
George Davey Smith ◽  
...  

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.


2020 ◽  
Author(s):  
Xiaonan Chen ◽  
Yiqiao Zhao ◽  
Zijia Tao ◽  
Kefeng Wang

Abstract Background Although in vitro and in vivo experiments have suggested that coffee may exert inhibitory effects on prostate carcinogenesis, epidemiological studies have reported inconsistent results on the association between coffee consumption and prostate cancer. Methods We conducted a meta-analysis of cohort studies to assess the association between coffee consumption and prostate cancer risk. PubMed and Embase were searched for eligible studies up to Jan 2020. Study-specific risk estimates were combined using fixed or random effects models depending on whether significant heterogeneity was detected. Results Fifteen prospective cohort studies, with 50,200 cases of prostate cancer and 949,752 total cohort members, were included in the meta-analysis. A statistically significant inverse association was detected between coffee consumption and prostate cancer risk. The pooled relative risk (RR) was 0.91 (95% CI: 0.84, 0.98; I 2= 53.2%) for the highest coffee consumption compared with lowest consumption. The association exhibited a linear trend ( P =0.006 for linear trend), and the pooled RR was 0.989 (95% CI: 0.982, 0.997) for an increase of 1 cup of coffee per day. The pooled RRs were 0.93 (95% CI: 0.87, 0.99), 0.88 (95% CI: 0.71, 1.09) and 0.84 (95% CI: 0.66, 1.08) for localized, advanced and fatal prostate cancer, respectively. No publication bias was detected. Conclusions Our findings provide more evidence that increased coffee consumption is associated with lower prostate cancer risk. It implies that men might be encouraged to increase the coffee intake to lower their risk of prostate cancer.


2007 ◽  
Vol 97 (4) ◽  
pp. 557-561 ◽  
Author(s):  
I Cheng ◽  
X Liu ◽  
S J Plummer ◽  
L M Krumroy ◽  
G Casey ◽  
...  

The Prostate ◽  
2017 ◽  
Vol 77 (9) ◽  
pp. 949-954 ◽  
Author(s):  
Andrew Rundle ◽  
Yun Wang ◽  
Sudha Sadasivan ◽  
Dhananjay A. Chitale ◽  
Nilesh S. Gupta ◽  
...  

2019 ◽  
Vol 104 (12) ◽  
pp. 6017-6024
Author(s):  
Yi X Chan ◽  
Helman Alfonso ◽  
P Gerry Fegan ◽  
Leon Flicker ◽  
Bu B Yeap

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.


Author(s):  
Sean Randall ◽  
James Boyd ◽  
Emma Fuller ◽  
Caroline Brooks ◽  
Carole Morris ◽  
...  

IntroductionEvidence on the effect of vasectomy and vasectomy reversal on risk of prostate cancer is conflicting, with the issue of detection bias a key criticism. In this study we examined the effect of vasectomy reversal on prostate cancer risk in a cohort of vasectomised men. Objectives and ApproachA proof of concept study involving the International Population Data Linkage Network which pooled aggregated result data from participating centres in Australia, Canada and the United Kingdom. De-identified linked data extractions took place at each centre. Each participating centre locally conducted Cox proportional hazards regression analysis compared the risk of prostate cancer in those with/without vasectomy reversal in a cohort of vasectomised men. These results were then combined in a meta-analysis. Evidence of a protective effect of vasectomy reversal would suggest the harmful effect of vasectomy on prostate cancer risk, while nullifying detection bias. ResultsData were received from Australia (the states of Western Australia and New South Wales), Canada (the province of Ontario), Wales and Scotland. In total, there were 9,754 men with vasectomy reversals, and 684,660 men with a vasectomy. The combined analysis showed no protective effect of vasectomy reversal on incidence of prostate cancer when compared to those who had vasectomy alone (HR, 95%CI: 0.92, 0.70-1.21). As such, the results align with previous studies which found little or no evidence of a link between vasectomy and prostate cancer. Conclusion/ImplicationsThe study, originally conceived at the first IPDLN meeting in London, found no obvious protective effect of vasectomy reversal on prostate cancer in vasectomised men. The project demonstrated the utility and feasibility of collaborative studies fostered through the IPDLN, despite methodological challenges faced when aggregating international data.


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