Cannabis exposure and risk of testicular cancer: a systematic review and meta-analysis

Abstract

BackgroundThe aetiology of testicular cancer remains elusive. In this manuscript, we review the evidence regarding the association between cannabis use and testicular cancer development.MethodsIn this systematic review and meta-analysis, we reviewed literature published between 1st January 1980 and 13th May 2015 and found three case–control studies that investigated the association between cannabis use and development of testicular germ cell tumours (TGCTs).Results/ConclusionsUsing meta-analysis techniques, we observed that a) current, b) chronic, and c) frequent cannabis use is associated with the development of TGCT, when compared to never-use of the drug. The strongest association was found for non-seminoma development – for example, those using cannabis on at least a weekly basis had two and a half times greater odds of developing a non-seminoma TGCT compared those who never used cannabis (OR: 2.59, 95 % CI 1.60–4.19). We found inconclusive evidence regarding the relationship between cannabis use and the development of seminoma tumours. It must be noted that these observations were derived from three studies all conducted in the United States; and the majority of data collection occurred during the 1990’s.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1905-6) contains supplementary material, which is available to authorized users.

Systematic review of the potential role of cannabinoids as antiproliferative agents for urological cancers

“…4 This initial data was further supported by a recent systematic review and meta-analysis conducted by Gurney et al, which included three case-control studies between 198 and 2015, including a total of 719 cases of testicular germ cell tumours along with 1419 controls. 2,21,22 This study further reinforced the findings of the 2009 case-control study suggesting that current cannabis use at least once weekly or for a long duration (>10 weeks) is associated with the development of testicular germ cell tumour (OR 1.62; 95% CI 1.13-2.31), with the strongest association for non-seminoma tumours.…”

“…23 Cannabis has been shown to disrupt the hypothalamic-pituitary-testicular axis and prolonged exposure to cannabis with subsequent stimulation of cannabinoid receptors is thought to disrupt normal hormone regulation and cell proliferation in the testicles, which ultimately may contribute to testicular neoplasms. 2,23 Additional studies of testicular germ cell tumours are needed to test these hypotheses, including molecular analyses of cannabinoid receptors and endocannabinoid signaling that may provide clues to specific biological mechanisms. If there is a role of the ECS in the development or proliferation of testicular germ cell tumours, it can be a potential target for therapeutic options in the future.…”

“…1 The primary psychoactive component of the cannabis plant -Δ 9 tetrahydrocannabinol, or THC -stimulates neural cannabinoid receptors, mimicking the action of endogenous cannabanoids (termed endocannabinoids). 2 Endocannabinoids exert important pharmacological and physiological actions by activating CB1 (brain type receptors) and CB2 (spleen type) receptors in mammals. 3 They mimic many of the effects of THC and activate both CB1 and CB2.…”

Cannabis and Neuropsychiatry, 1: Benefits and Risks

“…11 This may explain why cannabis use is associated with an increased risk of neoplastic diseases such as oropharyngeal cancers, 11 lung cancer, 17 and testicular cancer. 18 The evidence, however, is weak and inconsistent, 17,19,20 but this should not be considered reassuring; rather, it reflects the paucity of research on the subject.…”

Testicular Germ Cell Tumors

“…These include higher economic status, professional workers, technicians, and other occupational categories [6][7][8][9], immunodeficiency [10], history of sexually transmitted disease [11], past mumps orchitis [12], in utero exposure to estrogen [13], cannabis use [14,15], testicular trauma [11], Down syndrome [16], Marfan syndrome [17], and Klinefelter syndrome [18]. Early male patterned baldness and severe acne have a negative association [19].…”