Maternal body mass index and risk of testicular cancer in male offspring: A systematic review and meta-analysis

Alam, Shama S.; Cantwell, Marie; Cardwell, Christopher; Cook, Michael B.; Murray, Liam

doi:10.1016/j.canep.2010.07.006

Cited by 11 publications

(9 citation statements)

References 37 publications

(46 reference statements)

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“…In pre-menopausal women, increased BMI is associated with anovulation, reducing lifetime exposure of circulating oestrogen and progesterone [44], thus lowering breast cancer risk [45] and increasing uterine cancer risk [46]. Higher maternal BMI is also associated with reduced oestrogen exposure in utero [47], which is protective against testicular cancer [48] and in males, elevated BMI reduces serum testosterone [49], reducing prostate cancer risk. Our findings of causal roles of BMI in regulating risk of certain reproductive and hormone-responsive cancers are therefore biologically plausible although the mechanistic links need to be assessed further.…”

Section: Discussionmentioning

confidence: 99%

Body size and composition and site-specific cancers in UK Biobank: a Mendelian randomisation study

Vithayathil

Carter

Kar

et al. 2020

Preprint

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word count: 299 Main text word count: 2,320 Number of Tables: 5 (supplementary) Number of Figures: 4 ABSTRACT Objectives To investigate the casual role of body mass index, body fat composition and height in cancer. DesignTwo stage mendelian randomisation study SettingPrevious genome wide association studies and the UK Biobank ParticipantsGenetic instrumental variables for body mass index (BMI), fat mass index (FMI), fat free mass index (FFMI) and height from previous genome wide association studies and UK Biobank .Cancer outcomes from 367 586 participants of European descent from the UK Biobank. Main outcome measuresOverall cancer risk and 22 site-specific cancers risk for genetic instrumental variables for BMI, FMI, FFMI and height. ResultsGenetically predicted BMI (per 1 kg/m 2 ) was not associated with overall cancer risk (OR 0.99; 95% confidence interval (CI) 0-98-1.00, p=0.105). Elevated BMI was associated with increased risk of stomach cancer (OR 1.15, 95% (CI) 1.05-1.26; p=0.003) and melanoma (OR 0.96, 95% CI 0.92-1.00; p=0.044). For sex-specific cancers, BMI was positively associated with uterine cancer (OR 1.08, 95% CI 1.01-1.14; p=0.015) but inversely associated with breast (OR 0.95, 95% CI 0.92-0.98; p=0.001), prostate (OR 0.95, 95% CI 0.92-0.99; p=0.007) and testicular cancer (OR 0.89, 95% CI 0.81-0.98; p=0.017). Elevated FMI (per 1 kg/m 2 ) was associated with gastrointestinal cancer (stomach cancer OR 4.23, 95% CI 1.18-15.13, p=0.027; colorectal cancer OR 1.94, 95% CI 1.23-3.07; p=0.004). Increased height (per 1 standard deviation, approximately 6.5cm) was associated with increased risk of overall cancer (OR 1.06; 95% 1.04-1.09; p = 2.9710 -8 ) and most site-specific cancers with the strongest estimates for kidney, non-Hodgkin lymphoma, colorectal, lung, melanoma and breast cancer. ConclusionsThere is little evidence for BMI as a casual risk factor for cancer. BMI may have a causal role for sexspecific cancers, although with inconsistent directions of effect, and FMI for gastrointestinal malignancies. Elevated height is a risk factor for overall cancer and multiple site cancers.

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Section: Discussionmentioning

confidence: 99%

Body size and composition and site-specific cancers in UK Biobank: a Mendelian randomisation study

Vithayathil

Carter

Kar

et al. 2020

Preprint

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“…In the absence of such a gold standard, it has been recommended that any tools used to measure study quality should be as specific as possible to the given topic, and involve a simple checklist as opposed to a scale or score [ 14 ]. Given these factors, we assessed study quality and potential for bias using the criteria outlined in the Newcastle-Ottawa Quality Assessment Scale [ 15 , 16 ], but did not determine a quality score [ 17 ]. Two reviewers (JG and JS) independently assessed study quality against these criteria, with disagreements resolved by referral to a third reviewer (DS).…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2015

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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.

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“…Perinatal factors will not be included herein as these factors have been discussed in detail elsewhere. 10, 17, 20-21 …”

Section: Introductionmentioning

confidence: 99%

Adolescent and adult risk factors for testicular cancer

2012

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The incidence of testicular cancer has been increasing over the past several decades in many developed countries. The reasons for the increases are unknown because risk factors for the disease are poorly understood. Some research suggests that exposures in utero or in early childhood are likely to be important in determining an individual's level of risk. However, other research suggests that exposure to various factors in adolecence and adulthood are also linked to the development of testicular cancer. Of these, two occupational exposures—firefighting and aircraft maintenance—and one environmental exposure (to organochloride pesticides) are likely to be associated with increased risk of developing testicular cancer. By contrast, six of the identified factors—diet, types of physical activity, military service as well as exposure to ionizing radiation, electricity and acrylamide—are unlikely to increase the risk of developing testicular cancer. Finally, seven further exposures—to heat, polyvinylchloride, nonionizing radiation, heavy metals, agricultural work, pesticides and polychlorinated biphenyls as well as marijuana use—require further study to determine their association with testicular cancer.

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Maternal body mass index and risk of testicular cancer in male offspring: A systematic review and meta-analysis

Cited by 11 publications

References 37 publications

Body size and composition and site-specific cancers in UK Biobank: a Mendelian randomisation study

Body size and composition and site-specific cancers in UK Biobank: a Mendelian randomisation study

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

Adolescent and adult risk factors for testicular cancer

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