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Published on: August 14, 2019
Prostatitis, benign prostatic hyperplasia, and prostate cancer: a bidirectional Mendelian randomization study and
Yi Wang1,2, Guihua Chen2, Deng Li2
1Department of Urology, Affiliated Hospital of Nantong University, No.20 West Temple Road, Nantong, Jiangsu Province, 226001, China.
Insights
Genetic susceptibility to prostatitis or benign prostatic hyperplasia (BPH) increases prostate cancer (PCa) risk. Mendelian randomization revealed causal links and three vicious circles driving disease progression, offering insights for drug development.
Area of Science:
- Urology
- Genetics
- Epidemiology
Background:
- Lack of authoritative guidelines on interrelationships between prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa).
- No consensus exists among published epidemiological studies or meta-analyses regarding these prostate conditions.
Purpose of the Study:
- To clarify the causal relationships among prostatitis, BPH, and PCa using Mendelian randomization.
- To provide clinical implications for patient populations affected by these prostate conditions.
Main Methods:
- Employed bidirectional two-sample and mediator Mendelian randomization to investigate causal links.
- Conducted comprehensive sensitivity analyses (phenotype scanning, heterogeneity, pleiotropy, leave-one-out, Steiger test) for result validation.
Main Results:
- Confirmed genetic susceptibility to prostatitis or BPH causally increases PCa risk (P < 0.05).
- Identified four mediator pathways (e.g., prostatitis-BPH-PCa) and three vicious circles (prostatitis-BPH, BPH-PCa, prostatitis-BPH-PCa).
- These circles contribute to the progression from benign to malignant prostate diseases.
Conclusions:
- Successfully elucidated the interrelationships among prostatitis, BPH, and PCa.
- Provided significant clinical implications for patient management and decision-making.
- Revealed three vicious circles offering novel avenues for drug development and therapeutic strategies.
Background:
No authoritative books or guidelines are currently available for revealing the interrelationships of prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa). Moreover, no consensus on this issue has been reached among previously published epidemiological studies or meta-analyses.
Purpose:
We first took advantage of Mendelian randomization to clarify this issue and provide clinical implications for these patients' populations.
Methods:
Bidirectional two-sample and mediator Mendelian randomization were applied to explore the causal relationships among prostatitis, BPH, and PCa. Sensitivity analyses, including phenotype scanning, heterogeneity, pleiotropy, leave-one-out analysis, and the Steiger test, were conducted to evaluate the robustness and reliability of our results.
Results:
Our results revealed the interrelationships among prostatitis, BPH, and PCa via Mendelian randomization, confirming that genetic susceptibility to prostatitis or BPH could lead to increased risks of PCa directly or indirectly (P < 0.05). Moreover, mediator Mendelian randomization revealed four potential mediator pathways, including the prostatitis-BPH-PCa, the BPH-PCa-prostatitis, the PCa-prostatitis-BPH, and the PCa-BPH-prostatitis pathways. Based on these, we also provided clinical implications for prostatitis, BPH, and PCa patients' populations, respectively. Interestingly, a total of three vicious circles were revealed by us, including the prostatitis-BPH circle, the BPH-PCa circle, and the prostatitis-BPH-PCa circle. All of these three vicious circles contributed to the progression of benign prostate diseases to malignant diseases.
Conclusion:
We successfully clarified the interrelationships among prostatitis, BPH, and PCa, providing clinical implications for these patients' populations. A total of three vicious circles were also revealed by us to provide novel ideas for future drug development and guide clinical decision-making.
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