Longitudinal Reproductive Hormone Profiles in Infants: Peak of Inhibin B Levels in Infant Boys Exceeds Levels in Adult Men

Andersson, Anna‐Maria

doi:10.1210/jc.83.2.675

Cited by 228 publications

(349 citation statements)

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“…The expression rapidly declined from ϳ22 weeks of gestation and was gradually lost, whereas gonocytes differentiated into infantile spermatogonia up to ϳ4 months of postnatal age, when the final stage of this differentiation takes place, probably stimulated by the hormonal surge at the "minipuberty" (40,41). Interestingly, in a few prepubertal intersex cases, AP-2␥ was observed in a subset of gonocytes outside the normal window of expression.…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor AP-2γ Is a Developmentally Regulated Marker of Testicular Carcinoma In situ and Germ Cell Tumors

Hoei‐Hansen

Nielsen²,

Almstrup³

et al. 2004

Clinical Cancer Research

159

140

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Purpose: Transcription factor activator protein-2␥ (TFAP2C, AP-2␥) was reported previously in extraembryonic ectoderm and breast carcinomas but not in the testis. In our recent gene expression study we detected AP-2␥ in carcinoma in situ testis (CIS, or intratubular germ cell neoplasia), precursor of testicular germ cell tumors. In this study we aimed to investigate the expression pattern of AP-2␥ and to shed light on this factor in germ cell differentiation and the pathogenesis of germ cell neoplasia.Experimental Design: We analyzed expression pattern of AP-2␥ at the RNA and protein level in normal human tissues and a panel of tumors and tumor-derived cell lines. In the gonads, we established the ontogeny of expression of AP-2␥ in normal and dysgenetic samples. We also investigated the regulation of AP-2␥ by steroids and retinoic acid.Results: We detected abundant AP-2␥ in testicular CIS and in testicular germ cell tumors of young adults and confirmed differential expression of AP-2␥ in somatic tumors. We found that AP-2␥ expression was regulated by retinoic acid in an embryonal carcinoma cell line (NT2). The investigation of ontogeny of AP-2␥ protein expression in fetal gonads revealed that it was confined to oogonia/gonocytes and was down-regulated with germ cell differentiation. In some prepubertal intersex cases, AP-2␥ was detected outside of the normal window of expression, probably marking neoplastic transformation of germ cells.Conclusions: AP-2␥ is developmentally regulated and associated with the undifferentiated phenotype in germ cells. This transcription factor may be involved in self-renewal and survival of immature germ cells and tissue-specific stem cells. AP-2␥ is a novel marker of testicular CIS and CISderived tumors.

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Section: Discussionmentioning

confidence: 99%

Transcription Factor AP-2γ Is a Developmentally Regulated Marker of Testicular Carcinoma In situ and Germ Cell Tumors

Hoei‐Hansen

Nielsen²,

Almstrup³

et al. 2004

Clinical Cancer Research

159

140

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“…Ninety-five percent of testicular tumors derive from germ cells that do not have gonadotropin receptors 81 but depend on testicular growth factors that are produced under gonadotropin stimulation. Gonadotropin levels are high during infancy, decline rapidly after 3 months of age, 82 and remain very low until puberty, when they rise to adult levels. The age-adjusted incidence of testicular cancer follows closely the changes in gonadotropin levels, which suggests that tumorigenesis depends on permissive action of gonadotropins in the testis (Fig 1).…”

Section: Testicular and Prostate Cancermentioning

confidence: 99%

Public Health Implications of Altered Puberty Timing

et al. 2008

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Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrinedisrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.

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“…In prepubertal boys, stimulation of Sertoli cells by follicle-stimulating hormone (FSH) increases circulating inhibin B levels (3). In boys of 3 months of age, early activation of the pituitarygonadal axis results in markedly increased inhibin B levels, which remain elevated up to the age of 15 months, while FSH, luteinizing hormone (LH) and testosterone at the age of 6 -9 months decrease into the normal range observed later in childhood (4). The onset of male puberty is associated with increasing…”

Section: Introductionmentioning

confidence: 99%

Serum inhibin B, FSH, LH and testosterone levels before and after human chorionic gonadotropin stimulation in prepubertal boys with cryptorchidism

Christiansen

Andersson²,

Ne³

et al. 2002

Eur J Endocrinol

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Background: Several studies have indicated that cryptorchidism is associated with degenerative changes in both Sertoli cells and germ cells. The gonadal peptide hormone inhibin B reflects Sertoli cell function. Low inhibin B levels are found in a large portion of formerly cryptorchid men who show compromised seminiferous tubule function. It is not known if inhibin B can be used to demonstrate early damage of seminiferous tubules in prepubertal boys with cryptorchidism. Methods: We investigated the relationship between serum levels of inhibin B, testosterone, FSH and LH in 62 prepubertal boys with uni-and bilateral cryptorchidism. Furthermore, we investigated the changes in serum levels of inhibin B and the corresponding changes in serum levels of FSH, LH and testosterone during a short course (3 weeks) of human chorionic gonadotropin (hCG) injections in 18 of these cryptorchid boys. Results: In the 62 prepubertal boys with uni-or bilateral cryptorchidism there were no significant differences in baseline levels (median and range) of inhibin B (88 (20-195) pg/ml vs 78 (35-182) pg/ml; not significant), LH (0.08 (,0.05 -0.99) IU/l vs 0.06 (,0.05 -1.61) IU/l; not significant) and FSH (0.60 (0.08-3.73) IU/l vs 0.85 (0.25 -2.55); not significant) compared with 156 healthy prepubertal boys, and there were no differences in hormonal levels between boys with unior bilateral cryptorchidism. There was no correlation between baseline levels of inhibin B and FSH. In boys younger than 9 years, we found no correlation between baseline levels of inhibin B and LH whereas, in boys older than 9 years, baseline levels of inhibin B were positively correlated to baseline LH (Spearman rank correlation coefficient ððR s Þ ¼ 0:58; P ¼ 0:03Þ: Treatment with hCG (1500 IU intramuscularly twice weekly for 3 weeks) resulted in descensus of testes in 9 out of 18 patients. In all boys but one, irrespective of age, hCG induced a marked increase in testosterone into the adult range (from undetectable to 21.8 (7.0 -35.4) nmol/l; P , 0:001) and completely suppressed FSH and LH levels. Serum levels of inhibin B increased significantly from 116 (50 -195) pg/ml to 147 (94 -248) pg/ml ðP , 0:05Þ; but not uniformly. The increase in serum levels of inhibin B was inversely correlated to baseline inhibin B ðRs ¼ 20:52; P ¼ 0:03Þ and baseline FSH ðR s ¼ 20:59; P , 0:01Þ: Conclusions: We therefore suggest that, in the prepubertal testes, inhibin B is secreted from the prepubertal Sertoli cells following hCG, whereas early pubertal testes with more differentiated Sertoli cells are not able to secrete inhibin B in response to hCG stimulation, perhaps due to lack of germ cell-derived bB-subunits. We found (a) normal inhibin B levels in prepubertal boys with uni-or bilateral cryptorchidism, (b) that hCG stimulated testosterone markedly and suppressed FSH and LH levels and (c) that hCG treatment stimulated inhibin B levels in the youngest cryptorchid boys. In the oldest prepubertal boys no hCG-induced changes in inhibin B were shown.

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Longitudinal Reproductive Hormone Profiles in Infants: Peak of Inhibin B Levels in Infant Boys Exceeds Levels in Adult Men

Cited by 228 publications

References 0 publications

Transcription Factor AP-2γ Is a Developmentally Regulated Marker of Testicular Carcinoma In situ and Germ Cell Tumors

Transcription Factor AP-2γ Is a Developmentally Regulated Marker of Testicular Carcinoma In situ and Germ Cell Tumors

Public Health Implications of Altered Puberty Timing

Serum inhibin B, FSH, LH and testosterone levels before and after human chorionic gonadotropin stimulation in prepubertal boys with cryptorchidism

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