Causal relationship between prostatic diseases and prostate cancer: a mendelian randomization study.
Benign prostatic hyperplasia
GWAS
Mendelian randomization
Prostate cancer
Prostatitis
Risk factor
Journal
BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800
Informations de publication
Date de publication:
27 Jun 2024
27 Jun 2024
Historique:
received:
29
10
2023
accepted:
23
06
2024
medline:
28
6
2024
pubmed:
28
6
2024
entrez:
27
6
2024
Statut:
epublish
Résumé
Although it is thought that prostatitis or benign prostatic hyperplasia (BPH) is related to prostate cancer (PCa), the underlying causal effects of these diseases are unclear. We assessed the causal relationship between prostatitis or BPH and PCa using a two-sample Mendelian randomization (MR) approach. The data utilized in this study were sourced from genome-wide association study. The association of genetic variants from cohorts of prostatitis or BPH and PCa patients was determined using inverse-variance weighted and MR Egger regression techniques. The direction of chance was determined using independent genetic variants with genome-wide significance (P < 5 × 10 MR analysis showed that BPH had a significant causal effect on PCa (Odds Ratio = 1.209, 95% Confidence Interval: 0.098-0.281, P = 5.079 × 10 This MR study supports that BPH has a positive causal effect on PCa, while genetically predicted prostatitis has no causal effect on PCa. Nonetheless, further studies should explore the underlying biochemical mechanism and potential therapeutic targets for the prevention of these diseases.
Sections du résumé
BACKGROUND
BACKGROUND
Although it is thought that prostatitis or benign prostatic hyperplasia (BPH) is related to prostate cancer (PCa), the underlying causal effects of these diseases are unclear.
METHODS
METHODS
We assessed the causal relationship between prostatitis or BPH and PCa using a two-sample Mendelian randomization (MR) approach. The data utilized in this study were sourced from genome-wide association study. The association of genetic variants from cohorts of prostatitis or BPH and PCa patients was determined using inverse-variance weighted and MR Egger regression techniques. The direction of chance was determined using independent genetic variants with genome-wide significance (P < 5 × 10
RESULTS
RESULTS
MR analysis showed that BPH had a significant causal effect on PCa (Odds Ratio = 1.209, 95% Confidence Interval: 0.098-0.281, P = 5.079 × 10
CONCLUSIONS
CONCLUSIONS
This MR study supports that BPH has a positive causal effect on PCa, while genetically predicted prostatitis has no causal effect on PCa. Nonetheless, further studies should explore the underlying biochemical mechanism and potential therapeutic targets for the prevention of these diseases.
Identifiants
pubmed: 38937672
doi: 10.1186/s12885-024-12551-9
pii: 10.1186/s12885-024-12551-9
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
774Subventions
Organisme : Foundation of Xiaoshan Science and Technology Bureau of Hangzhou, China
ID : 2020210
Organisme : Zhejiang Provincial Natural Science Foundation of China
ID : LQ21H050003
Informations de copyright
© 2024. The Author(s).
Références
Kimura T, Sato S, Takahashi H, Egawa S. Global trends of latent prostate Cancer in autopsy studies. Cancers (Basel). 2021;13(2).
Giri VN, Hegarty SE, Hyatt C, et al. Germline genetic testing for inherited prostate cancer in practice: implications for genetic testing, precision therapy, and cascade testing. Prostate. 2019;79(4):333–9.
pubmed: 30450585
doi: 10.1002/pros.23739
Sung H, Ferlay J, Siegel RL, et al. Global Cancer statistics 2020: GLOBOCAN estimates of incidence and Mortality Worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2021;71(3):209–49.
pubmed: 33538338
doi: 10.3322/caac.21660
Hemminki K. Familial risk and familial survival in prostate cancer. World J Urol. 2012;30(2):143–8.
pubmed: 22116601
doi: 10.1007/s00345-011-0801-1
Jansson KF, Akre O, Garmo H, et al. Concordance of tumor differentiation among brothers with prostate cancer. Eur Urol. 2012;62(4):656–61.
pubmed: 22386193
doi: 10.1016/j.eururo.2012.02.032
Blanc-Lapierre A, Spence A, Karakiewicz PI, Aprikian A, Saad F, Parent MÉ. Metabolic syndrome and prostate cancer risk in a population-based case-control study in Montreal, Canada. BMC Public Health. 2015;15:913.
pubmed: 26385727
pmcid: 4574395
doi: 10.1186/s12889-015-2260-x
Esposito K, Chiodini P, Capuano A, et al. Effect of metabolic syndrome and its components on prostate cancer risk: meta-analysis. J Endocrinol Invest. 2013;36(2):132–9.
pubmed: 23481613
doi: 10.1007/BF03346748
Rivera-Izquierdo M, Pérez de Rojas J, Martínez-Ruiz V et al. Obesity as a risk factor for prostate Cancer mortality: a systematic review and dose-response Meta-analysis of 280,199 patients. Cancers (Basel). 2021;13(16).
Vidal AC, Howard LE, Moreira DM, Castro-Santamaria R, Andriole GL Jr, Freedland SJ. Obesity increases the risk for high-grade prostate cancer: results from the REDUCE study. Cancer Epidemiol Biomarkers Prev. 2014;23(12):2936–42.
pubmed: 25261967
pmcid: 4257871
doi: 10.1158/1055-9965.EPI-14-0795
Dickerman BA, Markt SC, Koskenvuo M, Pukkala E, Mucci LA, Kaprio J. Alcohol intake, drinking patterns, and prostate cancer risk and mortality: a 30-year prospective cohort study of Finnish twins. Cancer Causes Control. 2016;27(9):1049–58.
pubmed: 27351919
pmcid: 5278639
doi: 10.1007/s10552-016-0778-6
Zhao J, Stockwell T, Roemer A, Chikritzhs T. Is alcohol consumption a risk factor for prostate cancer? A systematic review and meta-analysis. BMC Cancer. 2016;16(1):845.
pubmed: 27842506
pmcid: 5109713
doi: 10.1186/s12885-016-2891-z
Chen X, Zhao Y, Tao Z, Wang K. Coffee consumption and risk of prostate cancer: a systematic review and meta-analysis. BMJ Open. 2021;11(2):e038902.
pubmed: 33431520
pmcid: 7805365
doi: 10.1136/bmjopen-2020-038902
Key TJ. Nutrition, hormones and prostate cancer risk: results from the European prospective investigation into cancer and nutrition. Recent Results Cancer Res. 2014;202:39–46.
pubmed: 24531775
doi: 10.1007/978-3-642-45195-9_4
Alexander DD, Bassett JK, Weed DL, Barrett EC, Watson H, Harris W. Meta-analysis of long-chain Omega-3 polyunsaturated fatty acids (LCω-3PUFA) and prostate Cancer. Nutr Cancer. 2015;67(4):543–54.
pubmed: 25826711
pmcid: 4440629
doi: 10.1080/01635581.2015.1015745
Lippi G, Mattiuzzi C. Fried food and prostate cancer risk: systematic review and meta-analysis. Int J Food Sci Nutr. 2015;66(5):587–9.
pubmed: 26114920
doi: 10.3109/09637486.2015.1056111
Bylsma LC, Alexander DD. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutr J. 2015;14:125.
pubmed: 26689289
pmcid: 4687294
doi: 10.1186/s12937-015-0111-3
Nouri-Majd S, Salari-Moghaddam A, Aminianfar A, Larijani B, Esmaillzadeh A. Association between Red and processed meat consumption and risk of prostate Cancer: a systematic review and Meta-analysis. Front Nutr. 2022;9:801722.
pubmed: 35198587
pmcid: 8859108
doi: 10.3389/fnut.2022.801722
Kristal AR, Till C, Song X, et al. Plasma vitamin D and prostate cancer risk: results from the selenium and vitamin E Cancer Prevention Trial. Cancer Epidemiol Biomarkers Prev. 2014;23(8):1494–504.
pubmed: 24732629
pmcid: 4119495
doi: 10.1158/1055-9965.EPI-14-0115
Nyame YA, Murphy AB, Bowen DK, et al. Associations between serum vitamin D and adverse Pathology in men undergoing radical prostatectomy. J Clin Oncol. 2016;34(12):1345–9.
pubmed: 26903577
pmcid: 4872348
doi: 10.1200/JCO.2015.65.1463
Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010;140(6):883–99.
pubmed: 20303878
pmcid: 2866629
doi: 10.1016/j.cell.2010.01.025
Mantovani A, Allavena P, Sica A, Balkwill F. Cancer-related inflammation. Nature. 2008;454(7203):436–44.
pubmed: 18650914
doi: 10.1038/nature07205
Jung G, Kim JK, Kim H, Lee J, Hong SK. The association between prostatitis and risk of prostate cancer: a National Health Insurance Database study. World J Urol. 2022;40(11):2781–7.
pubmed: 36201020
doi: 10.1007/s00345-022-04165-2
Alcaraz A, Hammerer P, Tubaro A, Schröder FH, Castro R. Is there evidence of a relationship between benign prostatic hyperplasia and prostate cancer? Findings of a literature review. Eur Urol. 2009;55(4):864–73.
pubmed: 19027219
doi: 10.1016/j.eururo.2008.11.011
Chokkalingam AP, Nyrén O, Johansson JE, et al. Prostate carcinoma risk subsequent to diagnosis of benign prostatic hyperplasia: a population-based cohort study in Sweden. Cancer. 2003;98(8):1727–34.
pubmed: 14534890
doi: 10.1002/cncr.11710
Ørsted DD, Bojesen SE, Nielsen SF, Nordestgaard BG. Association of clinical benign prostate hyperplasia with prostate cancer incidence and mortality revisited: a nationwide cohort study of 3,009,258 men. Eur Urol. 2011;60(4):691–8.
pubmed: 21705134
doi: 10.1016/j.eururo.2011.06.016
Freedland SJ, Isaacs WB, Platz EA, et al. Prostate size and risk of high-grade, advanced prostate cancer and biochemical progression after radical prostatectomy: a search database study. J Clin Oncol. 2005;23(30):7546–54.
pubmed: 16234520
doi: 10.1200/JCO.2005.05.525
Schenk JM, Kristal AR, Arnold KB, et al. Association of symptomatic benign prostatic hyperplasia and prostate cancer: results from the prostate cancer prevention trial. Am J Epidemiol. 2011;173(12):1419–28.
pubmed: 21540324
pmcid: 3276227
doi: 10.1093/aje/kwq493
Simons BD, Morrison AS, Young RH, Verhoek-Oftedahl W. The relation of surgery for prostatic hypertrophy to carcinoma of the prostate. Am J Epidemiol. 1993;138(5):294–300.
pubmed: 7689295
doi: 10.1093/oxfordjournals.aje.a116858
Davey Smith G, Hemani G. Mendelian randomization: genetic anchors for causal inference in epidemiological studies. Hum Mol Genet. 2014;23(R1):R89–98.
pubmed: 25064373
pmcid: 4170722
doi: 10.1093/hmg/ddu328
Sekula P, Del Greco MF, Pattaro C, Köttgen A. Mendelian randomization as an Approach to assess causality using Observational Data. J Am Soc Nephrol. 2016;27(11):3253–65.
pubmed: 27486138
pmcid: 5084898
doi: 10.1681/ASN.2016010098
Hemani G, Zheng J, Elsworth B et al. The MR-Base platform supports systematic causal inference across the human phenome. Elife. 2018;7.
Bowden J, Del Greco MF, Minelli C, Davey Smith G, Sheehan NA, Thompson JR. Assessing the suitability of summary data for two-sample mendelian randomization analyses using MR-Egger regression: the role of the I2 statistic. Int J Epidemiol. 2016;45(6):1961–74.
pubmed: 27616674
pmcid: 5446088
Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol. 2015;44(2):512–25.
pubmed: 26050253
pmcid: 4469799
doi: 10.1093/ije/dyv080
Ong JS, MacGregor S. Implementing MR-PRESSO and GCTA-GSMR for pleiotropy assessment in mendelian randomization studies from a practitioner’s perspective. Genet Epidemiol. 2019;43(6):609–16.
pubmed: 31045282
pmcid: 6767464
doi: 10.1002/gepi.22207
Burgess S, Thompson SG. Interpreting findings from mendelian randomization using the MR-Egger method. Eur J Epidemiol. 2017;32(5):377–89.
pubmed: 28527048
pmcid: 5506233
doi: 10.1007/s10654-017-0255-x
Verbanck M, Chen CY, Neale B, Do R. Detection of widespread horizontal pleiotropy in causal relationships inferred from mendelian randomization between complex traits and diseases. Nat Genet. 2018;50(5):693–8.
pubmed: 29686387
pmcid: 6083837
doi: 10.1038/s41588-018-0099-7
Boehm K, Valdivieso R, Meskawi M, et al. BPH: a tell-tale sign of prostate cancer? Results from the prostate Cancer and Environment Study (PROtEuS). World J Urol. 2015;33(12):2063–9.
pubmed: 25824539
doi: 10.1007/s00345-015-1546-z
Parsons JK. Benign Prostatic Hyperplasia and male lower urinary tract symptoms: epidemiology and risk factors. Curr Bladder Dysfunct Rep. 2010;5(4):212–8.
pubmed: 21475707
pmcid: 3061630
doi: 10.1007/s11884-010-0067-2
Pearson JD, Lei HH, Beaty TH, et al. Familial aggregation of bothersome benign prostatic hyperplasia symptoms. Urology. 2003;61(4):781–5.
pubmed: 12670565
doi: 10.1016/S0090-4295(02)02509-8
Di Silverio F, Gentile V, De Matteis A, et al. Distribution of inflammation, pre-malignant lesions, incidental carcinoma in histologically confirmed benign prostatic hyperplasia: a retrospective analysis. Eur Urol. 2003;43(2):164–75.
pubmed: 12565775
doi: 10.1016/S0302-2838(02)00548-1
Haffner S, Taegtmeyer H. Epidemic obesity and the metabolic syndrome. Circulation. 2003;108(13):1541–5.
pubmed: 14517149
doi: 10.1161/01.CIR.0000088845.17586.EC
Kristal AR, Arnold KB, Schenk JM, et al. Dietary patterns, supplement use, and the risk of symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial. Am J Epidemiol. 2008;167(8):925–34.
pubmed: 18263602
doi: 10.1093/aje/kwm389
Nickel JC, Downey J, Young I, Boag S. Asymptomatic inflammation and/or infection in benign prostatic hyperplasia. BJU Int. 1999;84(9):976–81.
pubmed: 10571623
doi: 10.1046/j.1464-410x.1999.00352.x
Parsons JK, Carter HB, Partin AW, et al. Metabolic factors associated with benign prostatic hyperplasia. J Clin Endocrinol Metab. 2006;91(7):2562–8.
pubmed: 16608892
doi: 10.1210/jc.2005-2799
Parsons JK, Sarma AV, McVary K, Wei JT. Obesity and benign prostatic hyperplasia: clinical connections, emerging etiological paradigms and future directions. J Urol. 2009;182(6 Suppl):S27–31.
pubmed: 19846130
doi: 10.1016/S0022-5347(09)60088-4
Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;420(6917):860–7.
pubmed: 12490959
pmcid: 2803035
doi: 10.1038/nature01322
Dennis LK, Lynch CF, Torner JC. Epidemiologic association between prostatitis and prostate cancer. Urology. 2002;60(1):78–83.
pubmed: 12100928
doi: 10.1016/S0090-4295(02)01637-0
Roberts RO, Bergstralh EJ, Bass SE, Lieber MM, Jacobsen SJ. Prostatitis as a risk factor for prostate cancer. Epidemiology. 2004;15(1):93–9.
pubmed: 14712152
doi: 10.1097/01.ede.0000101022.38330.7c
Delongchamps NB, de la Roza G, Chandan V, et al. Evaluation of prostatitis in autopsied prostates–is chronic inflammation more associated with benign prostatic hyperplasia or cancer. J Urol. 2008;179(5):1736–40.
pubmed: 18343414
pmcid: 2661538
doi: 10.1016/j.juro.2008.01.034
McNeal JE, Redwine EA, Freiha FS, Stamey TA. Zonal distribution of prostatic adenocarcinoma. Correlation with histologic pattern and direction of spread. Am J Surg Pathol. 1988;12(12):897–906.
pubmed: 3202246
doi: 10.1097/00000478-198812000-00001
Pavelić J, Zeljko Z. [Prostate gland-transition zone lesions. Etiology, growth regulation, growth factors, genetic changes]. Lijec Vjesn. 2002;124(6–7):211–9.
pubmed: 19658339