scholarly journals Estimation of Relative and Absolute Risks in a Competing-Risks Setting Using a Nested Case-Control Study Design: Example From the ProMort Study

2019 ◽  
Vol 188 (6) ◽  
pp. 1165-1173 ◽  
Author(s):  
Renata Zelic ◽  
Daniela Zugna ◽  
Matteo Bottai ◽  
Ove Andrén ◽  
Jonna Fridfeldt ◽  
...  

Abstract In this paper, we describe the Prognostic Factors for Mortality in Prostate Cancer (ProMort) study and use it to demonstrate how the weighted likelihood method can be used in nested case-control studies to estimate both relative and absolute risks in the competing-risks setting. ProMort is a case-control study nested within the National Prostate Cancer Register (NPCR) of Sweden, comprising 1,710 men diagnosed with low- or intermediate-risk prostate cancer between 1998 and 2011 who died from prostate cancer (cases) and 1,710 matched controls. Cause-specific hazard ratios and cumulative incidence functions (CIFs) for prostate cancer death were estimated in ProMort using weighted flexible parametric models and compared with the corresponding estimates from the NPCR cohort. We further drew 1,500 random nested case-control subsamples of the NPCR cohort and quantified the bias in the hazard ratio and CIF estimates. Finally, we compared the ProMort estimates with those obtained by augmenting competing-risks cases and by augmenting both competing-risks cases and controls. The hazard ratios for prostate cancer death estimated in ProMort were comparable to those in the NPCR. The hazard ratios for dying from other causes were biased, which introduced bias in the CIFs estimated in the competing-risks setting. When augmenting both competing-risks cases and controls, the bias was reduced.

2013 ◽  
Vol 24 (6) ◽  
pp. 1079-1085 ◽  
Author(s):  
V. Tagalakis ◽  
H. Tamim ◽  
M. Blostein ◽  
J. A. Hanley ◽  
S. R. Kahn

2016 ◽  
Vol 27 (9) ◽  
pp. 1153-1161 ◽  
Author(s):  
Meng Yang ◽  
Azalea Ayuningtyas ◽  
Stacey A. Kenfield ◽  
Howard D. Sesso ◽  
Hannia Campos ◽  
...  

2007 ◽  
Vol 11 (1) ◽  
pp. 53-60 ◽  
Author(s):  
H M Tamim ◽  
S Mahmud ◽  
J A Hanley ◽  
J-F Boivin ◽  
M R Stang ◽  
...  

2009 ◽  
Vol 101 (1) ◽  
pp. 185-191 ◽  
Author(s):  
S-Y Park ◽  
L R Wilkens ◽  
A A Franke ◽  
L Le Marchand ◽  
K K Kakazu ◽  
...  

2008 ◽  
Vol 26 (36) ◽  
pp. 5923-5929 ◽  
Author(s):  
Norie Kurahashi ◽  
Motoki Iwasaki ◽  
Manami Inoue ◽  
Shizuka Sasazuki ◽  
Shoichiro Tsugane

PurposeThe incidence of prostate cancer is much lower in Japanese than Western populations. Given the preventive effects of isoflavones on carcinogenesis in the prostate in many nonhuman studies and the high consumption of isoflavones in Japanese, this low incidence may be partly due to the effects of soy.Patients and MethodsWe conducted a nested case-control study within the Japan Public Health Center–based Prospective Study. A total of 14,203 men aged 40 to 69 years who had returned the baseline questionnaire and provided blood samples were observed from 1990 to 2005. During a mean of 12.8 years of follow-up, 201 newly diagnosed prostate cancers were identified. Two matched controls for each case were selected from the cohort. Conditional logistic regression model was used to estimate the odds ratios (ORs) and 95% CIs for prostate cancer in relation to plasma levels of isoflavone.ResultsPlasma genistein level tended to be inversely associated with the risk of total prostate cancer. Although plasma daidzein showed no association, the highest tertile for plasma equol, a metabolite of daidzein, was significantly associated with a decreased risk of total prostate cancer (OR = 0.60; 95% CI, 0.36 to 0.99; Ptrend= .04). These inverse associations were strengthened after analysis was confined to localized cases, with ORs in the highest group of plasma genistein and equol compared with the lowest of 0.54 (95% CI, 0.29 to 1.01; Ptrend= .03) and 0.43 (95% CI, 0.22 to 0.82; Ptrend= .02), respectively. Plasma isoflavone levels were not statistically significantly associated with the risk of advanced prostate cancer.ConclusionIsoflavones may prevent the development of prostate cancer.


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