Androgen receptor gene polymorphisms and risk for androgenetic alopecia: a meta-analysis

Zhuo, Fenglin; Xu, Wei; Wang, L.; Wu, Yan; Xu, Zhou; Zhao, Jian

doi:10.1111/j.1365-2230.2011.04186.x

Cited by 48 publications

(55 citation statements)

References 27 publications

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“…Following the same line of thought that led to the investigation of a potential link between CAGn and 2D:4D (17), numerous studies looked into the link between CAGn and these conditions. Recent meta-analyses of these studies show that evidence for such a link is at best tentative for prostate cancer and absent for the other three (41–43). …”

Section: Discussionmentioning

confidence: 99%

No Evidence that 2D:4D is Related to the Number of CAG Repeats in the Androgen Receptor Gene

Hönekopp

2013

Front. Endocrinol.

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The length ratio of the second to the fourth digit (2D:4D) is a putative marker of prenatal testosterone (T) effects. The number of CAG repeats (CAGn) in the AR gene is negatively correlated with T sensitivity in vitro. Results regarding the relationship between 2D:4D and CAGn are mixed but have featured prominently in arguments for and against the validity of 2D:4D. Here, I present random-effects meta-analyses on 14 relevant samples with altogether 1904 subjects. Results were homogeneous across studies. Even liberal estimates (upper limit of the 95% CI) were close to zero and therefore suggested no substantial relationship of CAGn with either right-hand 2D:4D, left-hand 2D:4D, or the difference between the two. However, closer analysis of the effects of CAGn on T dependent gene activation in vitro and of relationships between CAGn and T dependent phenotypic characteristics suggest that normal variability of CAGn has mostly no, very small, or inconsistent effects. Therefore, the lack of a clear association between CAGn and 2D:4D has no negative implications for the latter’s validity as a marker of prenatal T effects.

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Section: Discussionmentioning

confidence: 99%

No Evidence that 2D:4D is Related to the Number of CAG Repeats in the Androgen Receptor Gene

Hönekopp

2013

Front. Endocrinol.

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“…All four components could play a role and, more broadly, baldness may represent a proxy of the overall androgen status considered as the result of all these components. For example, a meta-analysis (Zhuo et al, 2012) found an association between androgenic alopecia and a polymorphism of the androgen receptor gene (locus Xq11-q12), suggesting that baldness is also related to individual sensitivity to androgens. Indeed there are important ethnic differences both in the androgen status and in the incidence of testicular cancer further suggesting that there is a complex interplay between the different components.…”

Section: Discussionmentioning

confidence: 99%

Baldness and testicular cancer: the EPSAM case–control study

et al. 2016

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SUMMARYThe etiology of testicular cancer is largely unexplained. Research has mainly focused on prenatal exposures, especially to sex hormones, while less attention has been paid to exposures that may act also postnatally. As baldness has been previously associated with testicular cancer risk we focused on baldness and body hairiness, which are both associated with androgen activity. We used data of the Postnatal Exposures and Male Health (EPSAM) study, a case-control study on testicular cancer conducted in the Province of Turin, Italy, involving cases diagnosed between 1997 and 2008. Information was collected using mailed questionnaires. Analyses included 255 cases and 459 controls. We calculated ORs and 95% CIs to estimate testicular cancer risk among those who developed baldness and among those with body hairiness. We found an inverse association between testicular cancer and baldness (OR: 0.67, 95% CI: 0.46-0.98) and body hairiness (OR: 0.78, 95% CI: 0.53-1.16), although the latter had wider CIs. The inverse association between baldness and testicular cancer is consistent with the results from previous studies. These results suggest that androgens activity may influence testicular cancer risk.

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“…One synonymous variant, E213 (rs6152G>A), is located between the two polymorphic CAG and GGN tracts. This variant has been linked to androgenetic alopecia in Caucasian populations, where the minor allele (rs6152A) in these populations was associated with a decreased risk (18)(19)(20). In a previous EMAS analysis, carriers of the rs6152A variant were also found to have significantly lower estradiol levels than those with rs6152G (21).…”

Section: Introductionmentioning

confidence: 94%

Androgen Receptor Polymorphism-Dependent Variation in Prostate-Specific Antigen Concentrations of European Men

Holgersson

Giwercman

Bjartell

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Androgens acting via the androgen receptor (AR) stimulate production of PSA, which is a clinical marker of prostate cancer. Because genetic variants in the AR may have a significant impact on the risk of being diagnosed with prostate cancer, the aim was to investigate whether AR variants were associated with the risk of having PSA above clinically used cutoff thresholds of 3 or 4 ng/mL in men without prostate cancer.Methods: Men without prostate cancer history (n ¼ 1,744) were selected from the European Male Ageing Study cohort of 40 to 79-year-old men from eight different European centers. Using linear and logistic regression models, with age and center as covariates, we investigated whether AR variants (CAG repeatlength and/or SNP genotype) were associated with having serum PSA concentrations above 3 or 4 ng/mL, which often are set as cutoff concentrations for further investigation of prostate cancer.Results: Carriers of the SNP rs1204038 A-allele (16% of the men) were more likely to have PSA>3 and 4 ng/mL (OR; 95% confidence intervals, 1.65; 1.13-2.40 and 1.87; 1.18-2.96, respectively) than G-allele carriers. They also had shorter CAG repeats (median 20 vs. 23, P < 0.0005), but CAG repeat length per se did not affect the PSA concentrations.Conclusion: The A-allele of the SNP rs1204038 gives a 65% higher risk of having PSA above 3 ng/mL than the G-allele in men without prostate cancer, and thereby an increased risk of being referred for further examination on suspicion of prostate cancer.Impact: Serum PSA as a clinical marker could be improved by adjustment for AR-genotype. Cancer Epidemiol Biomarkers Prev; 23(10); 2048-56. Ó2014 AACR.

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Androgen receptor gene polymorphisms and risk for androgenetic alopecia: a meta-analysis

Abstract: Our meta-analysis suggests that the G allele of AR StuI polymorphism might be a potential risk factor for AGA, especially in white populations. However, we did not find any obvious association of the CAG and GGC triplet-repeat polymorphisms of the AR gene with risk for AGA.

Cited by 48 publications

References 27 publications

No Evidence that 2D:4D is Related to the Number of CAG Repeats in the Androgen Receptor Gene

No Evidence that 2D:4D is Related to the Number of CAG Repeats in the Androgen Receptor Gene

Baldness and testicular cancer: the EPSAM case–control study

Androgen Receptor Polymorphism-Dependent Variation in Prostate-Specific Antigen Concentrations of European Men

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