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PubMed1994

Ontogeny of immunocytochemically demonstrable androgen- and androgen receptor-containing cells in the hypothalamus and adenohypophysis of the chick embryo.

Brain sections of male chick embryos, 6.5-18.5 days of age, were examined immunocytochemically for the presence of androgen- and androgen receptor-containing cells in the hypothalamus and adenohypophyseal pars distalis. Using antibodies (Ab) against both androgens (T-Ab) and the androgen receptor (AR-Ab), single- and double-immunostained cells were located in a total of five nuclei of the anterior-, mid-, and posterior-hypothalamus, as well as in the rostral and caudal lobes of the adenohypophyseal pars distalis. From Days 9.5-12.5, the mean number of androgen-immunostained cells within the hypothalamus and pars distalis increased significantly (P < 0.01), while from Days 12.5-18.5 there was no further statistically significant increase. The results of the present investigation support previous findings which suggest that in the chick embryo the negative feedback loop of the hypothalamo-adenohypophyseal-testicular (HATest) axis is functional by the 13th day of development (Woods et al., 1989a,b). They also agree with the observations of Wilson and Glick (1970) that in the male chick embryo testosterone organizes masculine mating behavior prior to Day 13.0.

Androgens↗
PubMedDate not supplied

Analysis of promoter and androgen regulatory sequences required for optimal transcription of the rat androgen-binding protein gene.

The androgen-binding protein (ABP) gene P1 promoter directs cell-specific gene regulation of ABP secreted by Sertoli cells. A recent study using the mouse Sertoli cell line (MSC-1) with a luciferase reporter system demonstrated Sertoli cell-specific gene expression with 619 bp of P1 DNA. Furthermore, based on studies of the rat and human genes, several controversies developed over the promoter characteristics, including the promoter type, the transcription start site, and whether the gene is regulated directly by androgens. In this study, the answers to several of these controversies were deciphered using the MSC-1 cell model. The results of mutagenesis experiments were consistent with the presence of the major transcription start site at 36 bp upstream of the initiating Met residue. Modification of the initiator sequence at the start site reduced activity in MSC-1 and NIH3T3 fibroblast cells. Mutation of a putative modified TATA sequence or conversion to the consensus TATA sequence had no effect on activity. Modification of a consensus RNA splice sequence at the start site also had no effect on activity. Furthermore, a minor start site was localized 179 bp upstream of the major site using reverse transcriptase-polymerase chain reaction with various P1 primers (primer walking), primer extension, and cDNA cloning. RNA transcripts from the minor site contain an untranslated 5' exon but apparently encode the same protein as the major transcript. The effect of androgens on P1 expression was also investigated. Cotransfection experiments with pCMVAR, which encodes the androgen receptor, demonstrated that dihydrotestosterone had no effect on the activity in MSC-1 cells. Taken together, these experiments and previous studies indicate that the rat ABP promoter P1 is regulated at the major start site by an initiator element without a TATA sequence, and the gene appears not to be directly regulated by follicle-stimulating hormone or androgens.

3T3 Cells↗
PubMed2026

Prenatal Androgenization Modifies H3K9me3 Binding in the Promoter of the Androgen Receptor Gene in the Arcuate Nucleus of the Adult Female Mouse.

Animal models have shown that prenatal exposure to excess androgens is associated with the development of polycystic ovary syndrome (PCOS) features. We have identified that prenatally androgenized (PNA) mice modelling PCOS show suppressed androgen receptor mRNA (Ar) expression in the arcuate nucleus (ARC) across development. This could contribute to PCOS-related impaired gonadal steroid hormone feedback to GnRH neurons. However, the mechanism of Ar mRNA suppression following PNA is not determined. We performed a chromatin immunoprecipitation (ChIP) assay coupled with quantitative PCR (qPCR) to investigate histone and transcription factor binding within the Ar gene promoter or enhancer regions in the ARC of female mice at postnatal day (P)60 or gestational day (GD)18.5. In comparison to adult vehicle control (VEH) mice, our ChIP-qPCR revealed that H3K9me3, a repressive histone mark, was increased in adult PNA mice at the promoter regions of the Ar gene. H3K27ac, an active histone mark, and SP1, a transcription factor that acts as a positive regulator of gene expression, were unchanged in the same regions. Increased H3K9me3 seen at the promoter region in adult PNA mice, however, was not observed in the GD18.5 mice ARC following PNA. These results suggest that the deposition of H3K9me3 on the Ar promoter is unlikely to be established by PNA at the time of excess androgen exposure, and instead is likely to be established later in postnatal development or in adulthood. These data provide greater understanding of the developmental mechanisms and timeline underpinning PNA-mediated female dysfunction and PCOS-like reproductive physiology.

Animals↗
PubMed2005

Androgen receptor activities of p,p'-DDE, fenvalerate and phoxim detected by androgen receptor reporter gene assay.

In this study, we have developed a transient human androgen receptor (hAR) reporter gene assay using African monkey kidney cell line CV-1. The assay displayed appropriate response to the known androgen receptor (AR) agonist 5alpha-dihydrotestosterone (DHT) and AR antagonist nilutamide. DHT induced AR-mediated transcriptional activity in a concentration-dependent manner with median effective concentration (EC(50)) value of 3.90 x 10(-10) M. Nilutamide exhibited potent antiandrogenic activity with median inhibitory concentration (IC(50)) value of 8.90 x 10(-7) M. The transcription could not be activated by glucocorticoid receptor (GR) agonist dexamethasone, which suggested that the assay system be highly specific to androgenic compounds without cross-talk to GR agonist. The assay shows acceptable repeatability to DHT with intra coefficient of variability (CV) of 9.3% and inter CV of 10.9%. We applied this assay to evaluate the androgenic and antiandrogenic activities of some pesticides including organochlorine p,p'-dichlorodiphenyldichloroethylene (DDE), pyrethroid fenvalerate and organophosphorus phoxim. The results showed that p,p'-DDE exhibited potent antiandrogenic activity. Fenvalerate acted as weak AR antagonist and phoxim did not show AR antagonistic activity. We failed to find AR agonistic effects of the three pesticides. The present study provided a promising tool to screen for AR agonists and antagonists.

Androgen Antagonists↗
PubMed1998

Functional activities of the A and B forms of the human androgen receptor in response to androgen receptor agonists and antagonists.

The androgen receptor (AR) is present in many cells in two forms. The B form migrates with an apparent mass of 110 kDa and constitutes more than 80% of the immunoreactive receptor in most cell types. The A form of the AR migrates with an apparent mass of 87 kDa, appears to derive from internal translation initiation at methionine-188 in the AR open-reading frame, and usually constitutes 20% or less of the immunoreactive AR present. Previous experiments designed to examine the functional capacity of the A and B forms of the AR have been hampered by marked differences in the expression levels of the two isoforms, as the nucleotide sequence surrounding the codon encoding methionine-188 causes it to be used inefficiently as a translation initiation site. To circumvent this, we altered the nucleotide sequence surrounding methionine-188 to render it more similar to that surrounding the codon encoding methionine-1. Transfection of a cDNA containing these changes resulted in similar levels of expression of A and B forms of the AR as assessed by immunoblot assays using antibodies directed at an epitope preserved in both. Functional activities of these cDNAs were assessed using cotransfection assays that employed two model androgen-responsive genes (MMTV-luciferase and PRE2-tk-luciferase) in response to mibolerone, a potent androgen agonist, in three different cell lines. These studies demonstrated subtle differences in the activities of the A and B isoforms, which depended on the promoter and cell context. Additional studies failed to reveal any major differences in the responses of the AR-A and AR-B isoforms to a variety of androgen agonists and antagonists, suggesting that the previously reported functional defect of the AR-A is due principally to its level of expression. When assays of AR function are performed under conditions in which levels of expression of the two isoforms are equivalent, the AR-A and AR-B possess similar functional activities.

Androgen Antagonists↗
PubMed1996

Bone extracellular matrix induces homeobox proteins independent of androgens: possible mechanism for androgen-independent growth in human prostate cancer cells.

BACKGROUND: Differences in gene expression in prostate cells are believed to be secondary to epithelial-stromal interactions. We theorized that bone matrix may provide a fertile "soil" for prostate cancer by inducing androgen-dependent genes and allowing for androgen-independent growth. METHODS: Human prostate cancer cells (LNCaP) were grown under different conditions and analyzed for differential expression of mRNA. LNCaP cells were grown in the presence of 10 nM dihydrotestosterone (DHT), on extracellular matrix (ECM) derived from bone cells (without exogenous DHT), and on plastic culture dishes without exogenous DHT. A differential display of mRNA produced by LNCaP cells grown in the above conditions was then analyzed. RESULTS: Multiple unique transcripts were present in cells that were grown in the presence of DHT and on bone ECM (without exogenous DHT), but not on plastic culture dishes without exogenous DHT. Nine of these transcripts were then cloned and analyzed. Many (5/9) of these transcripts were found to contain multiple ATTA motifs in their corresponding 3'-untranslated regions. ATTA motifs have been shown to be homeobox protein-binding sites. Homeobox proteins and their target genes are thought to regulate cellular differentiation. Consistent with this, we demonstrated by reverse transcription polymerase chain reaction (PCR) that homeobox genes were differentially expressed in LNCaP cells when the cells were grown in the presence of DHT and on bone ECM (without exogenous DHT), but not on plastic culture dishes without exogenous DHT. Furthermore, we assayed LNCaP/fetal fibroblast chimeric tumors (n = 8) that were grown in male nude mice. Some of these tumors continued to grow in these mice despite treatment with surgical castration. In blinded studies, we were able to determine which tumor samples were androgen independent by their expression of homeobox genes. All samples that were androgen independent (n = 4) expressed the homeobox genes. Finally, gel retardation assay demonstrated that the homeobox proteins were able to bind to our cloned DNA sequences. Furthermore, footprinting analysis showed that the homeobox proteins bound to the ATTA motif in the 3'-region of our target DNA. CONCLUSIONS: Bone ECM, in the absence of DHT, has the ability to regulate androgen-responsive genes. Furthermore, many of these genes contain homeobox binding sites and the expression of homeobox genes may itself be regulated by bone ECM. If so, this may partially explain the clinical observation that bone provides a fertile "soil" for prostate cancer growth and metastasis.

Adenine↗
PubMed2004

Constitutive activation of the androgen receptor by a point mutation in the hinge region: a new mechanism for androgen-independent growth in prostate cancer.

Androgen receptor (AR) mutations that modify both the ligand binding and the transactivation capacities of the AR represent one of the mechanisms involved in the transition of prostate cancer (PCa) from androgen-dependent to androgen-independent growth. We use a yeast-based functional assay to detect and analyze mutant ARs in PCa. We report the detection of 2 different mutant ARs within the same metastatic tumour sample harvested in a patient with advanced PCa who had escaped androgen deprivation. Concomitantly to the widely described T877A mutant AR, we identified an additional double mutant AR harboring the nonsense mutation Q640Stop just downstream the DNA binding domain together with the T877A point mutation. This type of mutation, which leads to a c-terminal truncated AR, has not been described yet in PCa. Using luciferase reporter assays we demonstrated that this truncated AR exhibited constitutive transactivation properties. In conclusion, our data suggest that mutation-induced constitutive activation of the AR could be a mechanism used by PCa cells to escape androgen deprivation.

Adenocarcinoma↗
PubMed1982

Responses to androgens of rat ventral prostate nuclear androgen-binding sites sensitive and resistant to micrococcal nuclease.

Rat ventral prostate nuclei were separated into three major fractions by mild digestion with micrococcal nuclease and two fractions by extensive digestion. All fractions contained androgen-binding sites. Almost 50% of nuclear binding sites were resistant to enzymic digestion when only 5-15% of total DNA was resistant. Under milder digestion conditions, 21% of nuclear binding sites were associated with an intermediate fraction, representing 16% of total nuclear DNA, which was enriched in specific androgen-regulated gene sequences. This fraction was rapidly degraded by more extensive digestion. The nuclease sensitivity of these particular genes was markedly influenced by castration and the administration of dihydrotestosterone to castrated animals. The nuclear content of both nuclease-resistant and -sensitive androgen-binding sites was decreased by castration. Whereas the administration of androgen to animals castrated 1 day previously preferentially replenished nuclease-resistant sites, nuclease-sensitive sites, including those associated with transcriptionally active regions, had apparent priority when androgen was supplied to animals castrated 7 days previously. The significance of these observations to the regulation of nuclear processes and the possible interrelationships of nuclease-sensitive and -insensitive sites are discussed.

Animals↗
PubMed1994

Inhibition of growth and increase of acid phosphatase by testosterone on androgen-independent murine prostatic cancer cells transfected with androgen receptor cDNA.

Most androgen-unresponsive prostatic cancer cells are found to lack androgen receptor (AR). To clarify the role of AR in the process of the progression from androgen-dependent to androgen-unresponsive tumor, the AR gene was transfected into an AR-negative rat prostatic cancer cell line CUB-II. AR-transfectant cells expressed AR mRNA and showed binding to R1881. AR was found in nuclei of AR-transfectant cells by histochemical examination. Therefore, AR-transfectant cells were considered to contain functional AR. The growth of AR-transfectant cells was markedly inhibited in culture in the presence of testosterone, and the effect of testosterone was reduced by simultaneous addition of flutamide. Moreover, tumors inoculated with AR-transfectant cells in male mice showed much slower growth than those in females. The tumors of AR-transfectant cells in mice consisted of slightly larger spindle-shaped cells when compared to those of CUB-II cells. Moreover, AR-transfectant cells contained a few polynuclear giant cells. Since CUB-II cells contained acid phosphatase (AcP) activity, the addition of testosterone in culture increased AcP activity of AR-transfectant cells. It is concluded that resumption of androgen-dependent processes reduces the growth rate accompanying changes of phenotype.

Acid Phosphatase↗
PubMed1990

Down-regulation of androgen receptor by progestins and interference with estrogenic or androgenic stimulation of mammary carcinoma cell growth.

The regulatory influence of medroxyprogesterone acetate (MPA) on estrogen and androgen receptors of the human breast cancer cell lines MCF-7 and EFM-19 was explored in conjunction with the growth-promoting properties of these steroids. In the absence of steroidal stimulation, up to 1 microM MPA had no effect on the proliferation of the MCF-7 cell strain used and of EFM-19 cells. Under stimulation with 10 nM 17 beta-estradiol or 1 microM dihydrotestosterone, dose-dependent inhibition of the cell proliferation rates by 0.1-1 microM MPA was observed. Binding of MPA to the androgen receptor (Kd = 2.1 nM) but not to the estrogen receptor was demonstrable. During incubation of MCF-7 or EFM-19 cells with 1 microM MPA for 7 days, the estrogen and androgen receptor contents were down-regulated by approximately 50% and 60%, respectively. Likewise, the number of androgen-binding sites was reduced to 35% of the untreated controls after incubation of MCF-7 cells with 1 microM synthetic progestin R5020 for 7 days. The results indicate down-regulation of estrogen and androgen receptors by progestins in the absence of stimulatory effects on the proliferation of mammary carcinoma cells.

Breast Neoplasms↗
PubMed2000

Metabolism of androgens in rat pituitary gland and hypothalamus: catabolism of dihydrotestosterone or transformation of androgen signal?

The role of androgen metabolism and individual androgen metabolites in rat pituitary gland and hypothalamus is discussed on the basis of published data and results of our experiments. It is proposed that metabolism of androgens in these structures is aimed at the formation of not only true sex steroids estradiol-17 beta and 5 alpha-dihydrotestosterone, but also of androgens contributing to the regulation of cell processes, i.e. represents modification (transformation) of androgen signal (testosterone) in target pituitary and hypothalamic cells.

Androgens↗
PubMed1977

Stimulation by androgens of the production of androgen binding protein by cultured Sertoli cells.

The formation of androgen-binding protein (ABP) by cultured Sertoli cells, prepared from testes of immature rats, is increased when androgens or follicle-stimulating hormone (FSH) are present in the medium. Testosterone and 5alpha-dihydrotestosterone are equally effective in stimulating the synthesis and secretion of ABP, but non-androgenic steroids examined (progesterone, 17beta-estradiol and corticosterone) are without influence. Maximal increases are observed when androgens are added at the time of cell plating. Cells maintained in culture medium devoid of hormones become progressively less sensitive to subsequent addition of testosterone or FSH. Data are discussed in relation to the sites of androgen requirements for spermatogenesis.

Androstane-3,17-diol↗
PubMed1979

Androgen-uterine interactions: an assessment of androgen interaction with the testosterone- and estrogen-receptor systems and stimulation of uterine growth and progesterone-receptor synthesis.

This study investigates growth and the induction of progesterone-receptor synthesis in the immature (day 20--23) rat uterus after injection of different doses of 5 alpha-dihydrotestosterone (DHT) and testosterone (T) in long- and short acting injection vehicles. Moderate doses of T (300 microgram/day in saline for 3 days) elicit uterine growth (ca. 250% of control) that is abolished by concomitant injections of antiandrogen (1 mg flutamide/day or 8 mg DIMP/day) but is unaffected by injections of antiestrogens (60 microgram CI-628 or U11,100A/day). Uterine growth evoked by 17 beta-estradiol (3 microgram/day for 3 days) is, however, only antagonized with the antiestrogens but not antiandrogens. Experiments employing whole uteri in vitro indicate that the specific nuclear uptake of 10(-8) M [3H]T is markedly inhibited by the antiandrogens DIMP, flutamide, and the hydroxylated flutamide metabolite (LACT) [LACT greater than DIMP greater than FLUT] while the antiestrogens CI-628 and U11,100A are ineffective. In contrast, the specific nuclear uptake of 10(-8) M [3H]-estradiol is inhibited by only the antiestrogens and not antiandrogens. When very high (5 or 10 mg) doses of DHT Are administered in an oil-containing injection vehicle, nuclear translocation and cytoplasmic depletion of the estrogen receptor does occur and a uterotrophic response is elicited which is resistant to antagonism by antiandrogen. Likewise, the DHT-stimulated increase in progesterone-receptor content is not decreased by concomitant antiandrogen. Similar 5 or 10 mg doses of DHT, administered in a water-soluble dimethylsulfoxide vehicle, show little estrogen-receptor movement and the DHT-induced uterine growth and induction of progesterone-receptor synthesis is almost completely eliminated with antiandrogen. Regardless of the degree of uterine growth stimulation, however, the androgens are poor stimulators of uterine progesterone-receptor synthesis compared with estradiol. These results indicate that androgens may interact with both the androgen- and estrogen-receptor systems in the uterus in inducing uterine growth and that the nature of the cellular mechanism, i.e., whether the androgen- and/or estrogen-receptor system is involved, is dependent critically upon the in vivo dose of androgen and the mode of hormone administration.

Androgen Antagonists↗
PubMed1995

Growth of the androgen-dependent tumor of the prostate: role of androgens and of locally expressed growth modulatory factors.

The crucial role played by androgens in the growth of prostatic carcinoma is now well established. However, the mechanisms of this proliferative action are still poorly understood. Experiments have been performed to clarify: (1) the metabolism of androgens in prostatic tumor cells; and (2) the role played by locally produced growth factors in the autocrine regulation of prostatic tumor cell proliferation and the possible regulation exerted by testosterone (T) on the activity of these factors. These studies have been performed by utilizing the human androgen-responsive prostatic cancer LNCaP cell line. (1) By incubating LNCaP cells with different 14C-labeled androgenic precursors, it has been shown that all the major key enzymes involved in the metabolism of androgens (5 alpha-reductase, 17 beta-hydroxysteroid-oxidoreductase, 3 alpha- and 3 beta-hydroxysteroid-oxidoreductases) are present and active in these cells. In particular, the 5 alpha-reductase, which converts T and delta 4 to DHT and 5 alpha-A respectively, seems to be more active when delta 4 is the substrate, suggesting a preference for this precursor. (2) The hypothesis that LNCaP cells might produce LHRH (or a LHRH-like peptide) has been verified by RT-PCR, performed in the presence of a pair of specific oligonucleotide primers. A cDNA band of the expected size (228 bp), which specifically hybridized with a 32P-labeled LHRH oligonucleotide probe, has been obtained in LNCaP cells. To clarify the possible role played by this factor in the regulation of tumor growth, LNCaP cells, cultured in steroid-free conditions, have been treated with a LHRH antagonist; the treatment resulted in a significant increase of cell proliferation. Taken together, these data indicate that a LHRH (or LHRH-like) growth modulatory system is expressed in LNCaP cells and plays an inhibitory role in the regulation of tumor cell proliferation. This system seems to be regulated in a negative way by steroids. Growth factors endowed with stimulatory activity, such as EGF and TGF alpha, have also been shown to be produced by LNCaP cells. The present studies show that the immunoprecipitation of the EGF receptor with a specific monoclonal antibody (Ab225) reveals a protein band of the expected size (170 kDa) which is phosphorylated even in basal conditions. Moreover, the treatment of LNCaP cells, cultured in serum-free conditions, either with a monoclonal antibody against the EGF receptor, or with immunoneutralizing antibodies against EGF and TGF alpha, results in a significant decrease of cell proliferation.(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗
PubMed2006

Persistent prostate-specific antigen expression after neoadjuvant androgen depletion: an early predictor of relapse or incomplete androgen suppression.

OBJECTIVES: To analyze post-androgen depletion (AD) primary tumors to identify markers of treatment failure because AD does not reduce the probability of prostate-specific antigen (PSA) failure after prostatectomy. METHODS: Tumors removed by radical prostatectomy after 3 months of AD from 21 patients were analyzed for gene expression using oligonucleotide arrays. Differences between patients with and without relapse were identified using a conservative significance criteria of a threefold change and delta 0.68, ensuring a false discovery rate of less than 11%. RESULTS: At 50 months of follow-up, 7 of the 18 evaluable patients developed a biochemical recurrence. Gleason grade, pretherapy PSA level, T stage, and margin status were similar between the two groups. Patients with recurrence had greater post-AD PSA levels than those without recurrence (0.87 versus 0.19 ng/mL; P = 0.042). Gene expression analysis revealed 35 probe sets overexpressed in tumors from patients who relapsed. Among the highest ranked probe sets were PSA and other androgen-responsive genes. Serum PSA values during AD revealed similar findings. After 40 days of AD, the PSA level in those without recurrence was 1.21 ng/mL versus 4.5 ng/mL in those with recurrence (P = 0.0034). Immunohistochemistry of post-AD tumors also demonstrated a high PSA staining intensity in many tumors that recurred relative to those that didn't. CONCLUSIONS: The results of our study show that early recurrence is associated with expression of androgen-responsive genes. Surprisingly, these could be identified as early as 3 months after the initiation of AD therapy. Whether this represents a failure to abrogate androgen receptor mediated signaling with androgen depletion or early reactivation of signaling is under study.

Androgen Antagonists↗
PubMed1992

Androgen-responsive expression and mitogenic activity of schwannoma-derived growth factor on an androgen-dependent Shionogi mouse mammary carcinoma cell line.

We report here, using the androgen-dependent SC2G cell line derived from Shionogi mouse mammary carcinoma SC115, that cDNA encoding mouse homologue of the rat schwannoma-derived growth factor (SDGF) was isolated and its protein product was identified to be an autocrine growth factor which is expressed in response to androgen in this hormone-dependent cell line. The androgen-independent SC1G cells derived from SC115 were shown to express SDGF even in the absence of androgen, while Northern analysis probed with mouse mammary tumor virus (MMTV) DNA showed that the androgen inducible transcriptional machinery remains functional in this hormone independent cell line.

Amino Acid Sequence↗
PubMed2003

Analysis of G/A polymorphism in the androgen response element I of the PSA gene and its interactions with the androgen receptor polymorphisms.

OBJECTIVES: To compare the in vitro functional activity of the prostate-specific antigen (PSA) androgen response element (ARE) I alleles alone or in combination with androgen receptor (AR) polymorphisms and to determine the association of ARE I alleles with serum PSA in men without clinical prostatic disease. Data are conflicting regarding the association of PSA promoter alleles with serum PSA in men. METHODS: In vitro functional analyses of ARE I and AR polymorphisms were conducted by luciferase reporter assays in LNCaP and PC-3 cells. Associations among serum PSA, ARE I, and AR genotypes were determined by genotyping 109 white and 71 African-American men determined to be free of clinical prostatic disease. RESULTS: We found no significant difference in the androgen responsiveness of the two alleles when cells were transfected with PSA promoter reporter constructs differing only in the ARE I single nucleotide polymorphism and treated with varying doses of androgen. The response to androgens of the ARE I alleles co-transfected with AR expression vectors of 9, 21, and 29 CAG repeat lengths were identical. No individual or combined effects of the ARE I genotype and the AR genotype on serum PSA were noted. CONCLUSIONS: Our data indicate that ARE I polymorphisms, alone or in combination with AR polymorphisms, have no functional effect on the activity of the PSA promoter in vitro and in vivo.

Adult↗
PubMed1984

Becker's nevus: an androgen-mediated hyperplasia with increased androgen receptors.

Becker's nevus is an uncommon, unilateral, hyperpigmented, hairy cutaneous hamartoma which usually begins in adolescence. Its clinical features and its occurrence mainly in male individuals suggest that androgen stimulation may play a role in its pathogenesis. Androgen receptor assays were performed in a 16-year-old patient with a Becker's nevus. The patient coincidentally had acanthosis nigricans. Lesional tissue showed an androgen receptor level of 634.1 fm/mg protein. A specimen from the contralateral left pectoral area showed no dectectable androgen receptor activity (less than 2.0 fm/mg protein). These results suggest that exquisite androgen sensitivity and stimulation may explain the clinical manifestations of Becker's nevus.

Acanthosis Nigricans↗