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Pubertal development and prostate cancer risk: Mendelian randomization study in a population-based cohort
Carolina Bonilla1,2, Sarah J Lewis1,2, Richard M Martin3,4,5
1School of Social and Community Medicine, University of Bristol, Bristol, UK.
BMC Medicine
|April 6, 2016
Summary
Later puberty onset in boys is causally linked to reduced prostate cancer risk, particularly aggressive forms. This study used genetic data to confirm the link between pubertal development and cancer outcomes.
Area of Science:
- Genetics and Epidemiology
- Reproductive Health
- Oncology
Background:
- Observational studies suggest a link between early sexual maturation and increased prostate cancer risk.
- Previous estimates were limited by imprecise markers and potential confounding factors.
- Mendelian randomization (MR) offers a method to investigate causal relationships using genetic data.
Purpose of the Study:
- To determine the causal effect of pubertal development timing on prostate cancer risk.
- To utilize genetic polymorphisms associated with Tanner stage for a robust analysis.
- To investigate the association with prostate cancer risk, stage, and grade.
Main Methods:
- Derived a weighted genetic risk score for pubertal development using 13 SNPs linked to male Tanner stage.
- Employed a Mendelian randomization approach to estimate causal effects.
- Validated findings in the UK-based ProtecT study and the PRACTICAL consortium.
Main Results:
- A higher genetic score (indicating later puberty) was inversely associated with prostate cancer grade in ProtecT.
- Later physical development in adolescence causally reduced the odds of high Gleason prostate cancer by 77%.
- In the PRACTICAL consortium, the score was associated with reduced odds of advanced prostate cancer stage and prostate cancer-specific mortality.
Conclusions:
- Older age at sexual maturation is causally associated with a lower risk of developing prostate cancer.
- This protective effect is particularly pronounced for aggressive forms of the disease.
- Genetic analysis strengthens the evidence for a causal link between pubertal timing and prostate cancer outcomes.
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