Evidence map›Paper›PMID 39695756›Full record

ArticleBiology direct2024

Prostatitis, benign prostatic hyperplasia, and prostate cancer: a bidirectional Mendelian randomization study and clinical implications for these patients' populations.

Yi Wang, Guihua Chen, Deng Li, Dongliang Zhang, Qianwei Xing

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Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yi Wang *Department of Urology, Affiliated Hospital of Nantong University, No.20 West Temple Road, Nantong, Jiangsu Province, 226001, China.
Guihua Chen *Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.85 Wujin Road, Shanghai, 200080, China.
Deng Li *Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.85 Wujin Road, Shanghai, 200080, China.
Dongliang ZhangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.85 Wujin Road, Shanghai, 200080, China. zhangdlmn@163.com.ORCID 0000-0001-5308-6977
Qianwei XingDepartment of Urology, Affiliated Hospital of Nantong University, No.20 West Temple Road, Nantong, Jiangsu Province, 226001, China. xingqianwei@ntu.edu.cn.ORCID 0000-0001-7466-908X

Funding

Jiangsu Provincial Research Hospital YJXYY202204-YSB36
6 · The paper itself

Abstract

backgroundNo 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.

methodsBidirectional 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.

resultsOur 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.

conclusionWe 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.

Indexed as

Mendelian Randomization AnalysisProstatic HyperplasiaProstatic NeoplasmsProstatitisGenetic Predisposition to DiseaseHumansMaleBenign Prostatic HyperplasiaClinical implicationsMendelian randomizationProstate CancerProstatitis

Identifiers

PMID39695756
PMCPMC11658280

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