Androgen receptor CAG repeat length correlates with semen PSA levels in adolescence

Giwercman, Yvonne Lundberg; Richthoff, Jonas; Lilja, Hans; Anderberg, Camilla; Abrahamsson, Per‐Anders; Giwercman, Aleksander

doi:10.1002/pros.10366

Cited by 22 publications

(18 citation statements)

References 27 publications

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“…Lower androgen sensitivity, with higher LH levels, was found in men with long CAG tracts (28). It could be anticipated that the risk of hypogonadism is modified by the length of this repeat.…”

Section: Discussionmentioning

confidence: 95%

Risk factors for post-treatment hypogonadism in testicular cancer patients.

Eberhard

Ståhl

Cwikiel

et al. 2008

European Journal of Endocrinology

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Objectives: Testicular germ-cell cancer (TGCC) patients are at risk of developing hypogonadism but no risk factors have yet been defined. Methods: Blood was collected from 143 TGCC patients (after orchidectomy, prior to further therapy (T0) and 6, 12, 24, 36 and 60 months (T6, T12, T24, T36 and T60) after therapy). Biological hypogonadism (BH) was defined as: serum testosterone below 10 nmol/l and/or LH O10 IU/l; odds ratios (ORs) for BH with BH at T0, age, stage of disease, testicular characteristics, and androgen receptor polymorphism as predictors were calculated as well as the OR for developing BH post-treatment (one to two cycles of adjuvant chemotherapy (ACT) versus three to four cycles of higher dose chemotherapy (HCT) versus adjuvant radiotherapy (RT)). Results: HCT increased the OR for BH at T6 (OR 22, 95% confidence interval (CI) 4.4-118) and T12 (OR 5.8, 95% CI 1.5-22). RT increased the OR at T6 (OR 10, 95% CI 2.1-47) and at T12 (OR 3.9, 95% CI 1.1-14). Microlithiasis predicted BH at T0 (OR 11, 95% CI 1.2-112), T12 (OR 3.9, 95% CI 1.1-13), T24 (OR 3.0, 95% CI 1.0-8.8), T36 (OR 5.4, 95% CI 1.7-17) and T60 (OR 4.4, 95% CI 1.2-16). BH at T0 was a risk for BH at T6 (OR 53,, T12 (OR 125, 95% CI 37-430), T24 (OR 88, 95% CI 26-300) and T36 (OR 121, 95% CI 32-460). Conclusions: It is clinically relevant that BH at T0 and testicular microlithiasis were predictive factors for post-treatment BH. HCT and RT gave temporary BH.

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Section: Discussionmentioning

confidence: 95%

Risk factors for post-treatment hypogonadism in testicular cancer patients.

Eberhard

Ståhl

Cwikiel

et al. 2008

European Journal of Endocrinology

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“…[35]). Decreased repeat length is associated with increased production of prostate specific antigen and increased sperm count in adolescent males [36,37]. Hence, repeat length for the CAG repeat region may evolve under a tradeoff between sexual selection (favoring decreased length and increased activity) and natural selection (favoring increased length and reduced risk of prostate cancer).…”

Section: Introductionmentioning

confidence: 99%

The androgen receptor and prostate cancer: A role for sexual selection and sexual conflict?

Summers

Crespi

2008

Medical Hypotheses

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Summary We propose and evaluate the hypothesis that the CAG repeat region of the androgen receptor represents a locus of antagonistic pleiotropy in the context of sexual selection and sexual conflict. Short repeats are associated with increased transactivation of the androgen receptor at the molecular level, and increased fertility at the phenotypic level. However, short repeats are also associated with increased risk of prostate cancer, and with more aggressive forms of the disease. The somatic evolution of cancer cell lineages also shows a repeated pattern of shortening of the CAG repeat in association with cancer progression, apparently as a result of positive selection among cell lineages. We further postulate that other genes associated with prostate cancer are likely to mediate antagonistic pleiotropy in the context of sexual selection and sexual conflict. A key prediction of this hypothesis is that the genes mediating antagonistic pleiotropy will show historical evidence of positive selection, particularly in the context of sexual conflict. Previous research on the molecular evolution of specific genes associated with prostate cancer supports this prediction, and we suggest further critical tests of the role for genomic conflicts and tradeoffs in the evolution of cancer risk.

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“…The CAG number varies in length between individuals from approximately 10 to 30 repeats and displays population based diversity with African Americans having on average fewer CAG repeats than Caucasians and Far-Eastern Asians [20][21]. In Caucasian populations the median CAG repeat length is 22 amino acids [22][23], which recently was demonstrated to exhibit the highest transcriptional activity as compared to CAG repeat lengths in the outer normal ranges [24] .…”

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confidence: 99%

Persistent organic pollutants have dose and CAG repeat length dependent effects on androgen receptor activity in vitro

Björk

Nenonen

Giwercman

et al. 2011

Reproductive Toxicology

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Androgen receptor CAG repeat length correlates with semen PSA levels in adolescence

Abstract: In adolescence, AR genotype, but not serum testosterone, is associated with the level of seminal PSA.

Cited by 22 publications

References 27 publications

Risk factors for post-treatment hypogonadism in testicular cancer patients.

Risk factors for post-treatment hypogonadism in testicular cancer patients.

The androgen receptor and prostate cancer: A role for sexual selection and sexual conflict?

Persistent organic pollutants have dose and CAG repeat length dependent effects on androgen receptor activity in vitro

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