Compounds that interact with ANDROGEN RECEPTORS in target tissues to bring about the effects similar to those of TESTOSTERONE. Depending on the target tissues, androgenic effects can be on SEX DIFFERENTIATION; male reproductive organs, SPERMATOGENESIS; secondary male SEX CHARACTERISTICS; LIBIDO; development of muscle mass, strength, and power.
Proteins, generally found in the CYTOPLASM, that specifically bind ANDROGENS and mediate their cellular actions. The complex of the androgen and receptor migrates to the CELL NUCLEUS where it induces transcription of specific segments of DNA.
Compounds which inhibit or antagonize the biosynthesis or actions of androgens.
Compounds that bind to and inhibit the activation of ANDROGEN RECEPTORS.
A potent androgenic metabolite of TESTOSTERONE. It is produced by the action of the enzyme 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE.
A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.
Tumors or cancer of the PROSTATE.
Steroidal compounds related to TESTOSTERONE, the major mammalian male sex hormone. Testosterone congeners include important testosterone precursors in the biosynthetic pathways, metabolites, derivatives, and synthetic steroids with androgenic activities.
A synthetic non-aromatizable androgen and anabolic steroid. It binds strongly to the androgen receptor and has therefore also been used as an affinity label for this receptor in the prostate and in prostatic tumors.
An antiandrogen with about the same potency as cyproterone in rodent and canine species.
A disorder of sexual development transmitted as an X-linked recessive trait. These patients have a karyotype of 46,XY with end-organ resistance to androgen due to mutations in the androgen receptor (RECEPTORS, ANDROGEN) gene. Severity of the defect in receptor quantity or quality correlates with their phenotypes. In these genetic males, the phenotypic spectrum ranges from those with normal female external genitalia, through those with genital ambiguity as in Reifenstein Syndrome, to that of a normal male with INFERTILITY.
A gland in males that surrounds the neck of the URINARY BLADDER and the URETHRA. It secretes a substance that liquefies coagulated semen. It is situated in the pelvic cavity behind the lower part of the PUBIC SYMPHYSIS, above the deep layer of the triangular ligament, and rests upon the RECTUM.
A delta-4 C19 steroid that is produced not only in the TESTIS, but also in the OVARY and the ADRENAL CORTEX. Depending on the tissue type, androstenedione can serve as a precursor to TESTOSTERONE as well as ESTRONE and ESTRADIOL.
Certain tumors that 1, arise in organs that are normally dependent on specific hormones and 2, are stimulated or caused to regress by manipulation of the endocrine environment.
C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of ESTRADIOL to resemble TESTOSTERONE but less one carbon at the 19 position.
The unspecified form of the steroid, normally a major metabolite of TESTOSTERONE with androgenic activity. It has been implicated as a regulator of gonadotropin secretion.
A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.
An enzyme that catalyzes the reduction of TESTOSTERONE to 5-ALPHA DIHYDROTESTOSTERONE.
An agent with anti-androgen and progestational properties. It shows competitive binding with dihydrotestosterone at androgen receptor sites.
The male gonad containing two functional parts: the SEMINIFEROUS TUBULES for the production and transport of male germ cells (SPERMATOGENESIS) and the interstitial compartment containing LEYDIG CELLS that produce ANDROGENS.
A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.
The circulating form of a major C19 steroid produced primarily by the ADRENAL CORTEX. DHEA sulfate serves as a precursor for TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE.
A cell line derived from cultured tumor cells.
An oxidoreductase that catalyzes the conversion of 3-oxo-delta4 steroids into their corresponding 5alpha form. It plays an important role in the conversion of TESTOSTERONE into DIHYDROTESTOSTERONE and PROGESTERONE into DIHYDROPROGESTERONE.
An enzyme that catalyzes the desaturation (aromatization) of the ring A of C19 androgens and converts them to C18 estrogens. In this process, the 19-methyl is removed. This enzyme is membrane-bound, located in the endoplasmic reticulum of estrogen-producing cells of ovaries, placenta, testes, adipose, and brain tissues. Aromatase is encoded by the CYP19 gene, and functions in complex with NADPH-FERRIHEMOPROTEIN REDUCTASE in the cytochrome P-450 system.
Organic compounds containing the -CN radical. The concept is distinguished from CYANIDES, which denotes inorganic salts of HYDROGEN CYANIDE.
Development of female secondary SEX CHARACTERISTICS in the MALE. It is due to the effects of estrogenic metabolites of precursors from endogenous or exogenous sources, such as ADRENAL GLANDS or therapeutic drugs.
The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.
A condition caused by the excessive secretion of ANDROGENS from the ADRENAL CORTEX; the OVARIES; or the TESTES. The clinical significance in males is negligible. In women, the common manifestations are HIRSUTISM and VIRILISM as seen in patients with POLYCYSTIC OVARY SYNDROME and ADRENOCORTICAL HYPERFUNCTION.
Steroid hormones produced by the GONADS. They stimulate reproductive organs, germ cell maturation, and the secondary sex characteristics in the males and the females. The major sex steroid hormones include ESTRADIOL; PROGESTERONE; and TESTOSTERONE.
Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.
Carrier proteins produced in the Sertoli cells of the testis, secreted into the seminiferous tubules, and transported via the efferent ducts to the epididymis. They participate in the transport of androgens. Androgen-binding protein has the same amino acid sequence as SEX HORMONE-BINDING GLOBULIN. They differ by their sites of synthesis and post-translational oligosaccharide modifications.
An ester of TESTOSTERONE with a propionate substitution at the 17-beta position.
A saclike, glandular diverticulum on each ductus deferens in male vertebrates. It is united with the excretory duct and serves for temporary storage of semen. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A glycoprotein migrating as a beta-globulin. Its molecular weight, 52,000 or 95,000-115,000, indicates that it exists as a dimer. The protein binds testosterone, dihydrotestosterone, and estradiol in the plasma. Sex hormone-binding protein has the same amino acid sequence as ANDROGEN-BINDING PROTEIN. They differ by their sites of synthesis and post-translational oligosaccharide modifications.
The male reproductive organs. They are divided into the external organs (PENIS; SCROTUM;and URETHRA) and the internal organs (TESTIS; EPIDIDYMIS; VAS DEFERENS; SEMINAL VESICLES; EJACULATORY DUCTS; PROSTATE; and BULBOURETHRAL GLANDS).
A complex disorder characterized by infertility, HIRSUTISM; OBESITY; and various menstrual disturbances such as OLIGOMENORRHEA; AMENORRHEA; ANOVULATION. Polycystic ovary syndrome is usually associated with bilateral enlarged ovaries studded with atretic follicles, not with cysts. The term, polycystic ovary, is misleading.
The process in developing sex- or gender-specific tissue, organ, or function after SEX DETERMINATION PROCESSES have set the sex of the GONADS. Major areas of sex differentiation occur in the reproductive tract (GENITALIA) and the brain.
Those characteristics that distinguish one SEX from the other. The primary sex characteristics are the OVARIES and TESTES and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction.
An anti-androgen that, in the form of its acetate (CYPROTERONE ACETATE), also has progestational properties. It is used in the treatment of hypersexuality in males, as a palliative in prostatic carcinoma, and, in combination with estrogen, for the therapy of severe acne and hirsutism in females.
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
Antineoplastic agents that are used to treat hormone-sensitive tumors. Hormone-sensitive tumors may be hormone-dependent, hormone-responsive, or both. A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. Hormone-responsive tumors may regress when pharmacologic amounts of hormones are administered regardless of whether previous signs of hormone sensitivity were observed. The major hormone-responsive cancers include carcinomas of the breast, prostate, and endometrium; lymphomas; and certain leukemias. (From AMA Drug Evaluations Annual 1994, p2079)
A condition observed in WOMEN and CHILDREN when there is excess coarse body hair of an adult male distribution pattern, such as facial and chest areas. It is the result of elevated ANDROGENS from the OVARIES, the ADRENAL GLANDS, or exogenous sources. The concept does not include HYPERTRICHOSIS, which is an androgen-independent excessive hair growth.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The convoluted cordlike structure attached to the posterior of the TESTIS. Epididymis consists of the head (caput), the body (corpus), and the tail (cauda). A network of ducts leaving the testis joins into a common epididymal tubule proper which provides the transport, storage, and maturation of SPERMATOZOA.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Unsaturated androstanes which are substituted with one or more hydroxyl groups in any position in the ring system.
A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).
Proteins found usually in the cytoplasm or nucleus that specifically bind steroid hormones and trigger changes influencing the behavior of cells. The steroid receptor-steroid hormone complex regulates the transcription of specific genes.
A major gonadotropin secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Luteinizing hormone regulates steroid production by the interstitial cells of the TESTIS and the OVARY. The preovulatory LUTEINIZING HORMONE surge in females induces OVULATION, and subsequent LUTEINIZATION of the follicle. LUTEINIZING HORMONE consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH and FSH), but the beta subunit is unique and confers its biological specificity.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
Drugs that inhibit 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE. They are commonly used to reduce the production of DIHYDROTESTOSTERONE.
Condition resulting from deficient gonadal functions, such as GAMETOGENESIS and the production of GONADAL STEROID HORMONES. It is characterized by delay in GROWTH, germ cell maturation, and development of secondary sex characteristics. Hypogonadism can be due to a deficiency of GONADOTROPINS (hypogonadotropic hypogonadism) or due to primary gonadal failure (hypergonadotropic hypogonadism).
Thiohydantoin benzene derivative.
Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.
The external and internal organs related to reproduction.
Unsaturated derivatives of the ESTRANES with methyl groups at carbon-13, with no carbon at carbon-10, and with no more than one carbon at carbon-17. They must contain one or more double bonds.
An intermediate in TESTOSTERONE biosynthesis, found in the TESTIS or the ADRENAL GLANDS. Androstenediol, derived from DEHYDROEPIANDROSTERONE by the reduction of the 17-keto group (17-HYDROXYSTEROID DEHYDROGENASES), is converted to TESTOSTERONE by the oxidation of the 3-beta hydroxyl group to a 3-keto group (3-HYDROXYSTEROID DEHYDROGENASES).
Supporting cells projecting inward from the basement membrane of SEMINIFEROUS TUBULES. They surround and nourish the developing male germ cells and secrete ANDROGEN-BINDING PROTEIN and hormones such as ANTI-MULLERIAN HORMONE. The tight junctions of Sertoli cells with the SPERMATOGONIA and SPERMATOCYTES provide a BLOOD-TESTIS BARRIER.
A metabolite of PROGESTERONE with a hydroxyl group at the 17-alpha position. It serves as an intermediate in the biosynthesis of HYDROCORTISONE and GONADAL STEROID HORMONES.
An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.
Proteins that enhance gene expression when associated with ligand bound activated NUCLEAR RECEPTORS. The coactivators may act through an enzymatic process that affects the rate of transcription or the structure of chromatin. Alternatively nuclear receptor coactivators can function as adaptor proteins that bring nuclear receptors into close proximity with transcriptional complexes.
A decapeptide that stimulates the synthesis and secretion of both pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE. GnRH is produced by neurons in the septum PREOPTIC AREA of the HYPOTHALAMUS and released into the pituitary portal blood, leading to stimulation of GONADOTROPHS in the ANTERIOR PITUITARY GLAND.
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.
A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE that regulates the synthesis and release of pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
The reproductive organ (GONADS) in female animals. In vertebrates, the ovary contains two functional parts: the OVARIAN FOLLICLE for the production of female germ cells (OOGENESIS); and the endocrine cells (GRANULOSA CELLS; THECA CELLS; and LUTEAL CELLS) for the production of ESTROGENS and PROGESTERONE.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
These compounds stimulate anabolism and inhibit catabolism. They stimulate the development of muscle mass, strength, and power.
Tumors or cancer of the PROSTATE which can grow in the presence of low or residual amount of androgen hormones such as TESTOSTERONE.
Steroid-producing cells in the interstitial tissue of the TESTIS. They are under the regulation of PITUITARY HORMONES; LUTEINIZING HORMONE; or interstitial cell-stimulating hormone. TESTOSTERONE is the major androgen (ANDROGENS) produced.
A birth defect due to malformation of the URETHRA in which the urethral opening is below its normal location. In the male, the malformed urethra generally opens on the ventral surface of the PENIS or on the PERINEUM. In the female, the malformed urethral opening is in the VAGINA.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
A transcription factor that partners with ligand bound GLUCOCORTICOID RECEPTORS and ESTROGEN RECEPTORS to stimulate GENETIC TRANSCRIPTION. It plays an important role in FERTILITY as well as in METABOLISM of LIPIDS.
A synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE. Goserelin is used in treatments of malignant NEOPLASMS of the prostate, uterine fibromas, and metastatic breast cancer.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Cytoplasmic proteins that bind estrogens and migrate to the nucleus where they regulate DNA transcription. Evaluation of the state of estrogen receptors in breast cancer patients has become clinically important.
Steroidal compounds in which one or more carbon atoms in the steroid ring system have been substituted with nitrogen atoms.
A major gonadotropin secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Follicle-stimulating hormone stimulates GAMETOGENESIS and the supporting cells such as the ovarian GRANULOSA CELLS, the testicular SERTOLI CELLS, and LEYDIG CELLS. FSH consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.
The measurement of an organ in volume, mass, or heaviness.
Achievement of full sexual capacity in animals and in humans.
The process of germ cell development in the male from the primordial germ cells, through SPERMATOGONIA; SPERMATOCYTES; SPERMATIDS; to the mature haploid SPERMATOZOA.
The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra.
One of the ESTROGEN RECEPTORS that has greater affinity for ISOFLAVONES than ESTROGEN RECEPTOR ALPHA does. There is great sequence homology with ER alpha in the DNA-binding domain but not in the ligand binding and hinge domains.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Absence of hair from areas where it is normally present.
The flattened stroma cells forming a sheath or theca outside the basal lamina lining the mature OVARIAN FOLLICLE. Thecal interstitial or stromal cells are steroidogenic, and produce primarily ANDROGENS which serve as precusors of ESTROGENS in the GRANULOSA CELLS.
A developmental defect in which a TESTIS or both TESTES failed to descend from high in the ABDOMEN to the bottom of the SCROTUM. Testicular descent is essential to normal SPERMATOGENESIS which requires temperature lower than the BODY TEMPERATURE. Cryptorchidism can be subclassified by the location of the maldescended testis.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
An X-linked recessive form of spinal muscular atrophy. It is due to a mutation of the gene encoding the ANDROGEN RECEPTOR.
In gonochoristic organisms, congenital conditions in which development of chromosomal, gonadal, or anatomical sex is atypical. Effects from exposure to abnormal levels of GONADAL HORMONES in the maternal environment, or disruption of the function of those hormones by ENDOCRINE DISRUPTORS are included.
An anabolic steroid that has been used in the treatment of male HYPOGONADISM, delayed puberty in males, and in the treatment of breast neoplasms in women.
Disorders characterized by an abnormal reduction in muscle volume due to a decrease in the size or number of muscle fibers. Atrophy may result from diseases intrinsic to muscle tissue (e.g., MUSCULAR DYSTROPHY) or secondary to PERIPHERAL NERVOUS SYSTEM DISEASES that impair innervation to muscle tissue (e.g., MUSCULAR ATROPHY, SPINAL).
The major progestational steroid that is secreted primarily by the CORPUS LUTEUM and the PLACENTA. Progesterone acts on the UTERUS, the MAMMARY GLANDS and the BRAIN. It is required in EMBRYO IMPLANTATION; PREGNANCY maintenance, and the development of mammary tissue for MILK production. Progesterone, converted from PREGNENOLONE, also serves as an intermediate in the biosynthesis of GONADAL STEROID HORMONES and adrenal CORTICOSTEROIDS.
An endocrine state in men, characterized by a significant decline in the production of TESTOSTERONE; DEHYDROEPIANDROSTERONE; and other hormones such as HUMAN GROWTH HORMONE. Andropause symptoms are related to the lack of androgens including DEPRESSION, sexual dysfunction, and OSTEOPOROSIS. Andropause may also result from hormonal ablation therapy for malignant diseases.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
Chemical substances having a specific regulatory effect on the activity of a certain organ or organs. The term was originally applied to substances secreted by various ENDOCRINE GLANDS and transported in the bloodstream to the target organs. It is sometimes extended to include those substances that are not produced by the endocrine glands but that have similar effects.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
One of the ESTROGEN RECEPTORS that has marked affinity for ESTRADIOL. Its expression and function differs from, and in some ways opposes, ESTROGEN RECEPTOR BETA.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A stage of development at which the ADRENAL GLANDS undergo maturation leading to the capability of producing increasing amounts of adrenal androgens, DEHYDROEPIANDROSTERONE and ANDROSTENEDIONE. Adrenarche usually begins at about 7 or 8 years of age before the signs of PUBERTY and continues throughout puberty.
Pregnane derivatives containing two double bonds anywhere within the ring structures.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
All the organs involved in reproduction and the formation and release of URINE. It includes the kidneys, ureters, BLADDER; URETHRA, and the organs of reproduction - ovaries, UTERUS; FALLOPIAN TUBES; VAGINA; and CLITORIS in women and the testes; SEMINAL VESICLES; PROSTATE; seminal ducts; and PENIS in men.
Cytoplasmic proteins that specifically bind glucocorticoids and mediate their cellular effects. The glucocorticoid receptor-glucocorticoid complex acts in the nucleus to induce transcription of DNA. Glucocorticoids were named for their actions on blood glucose concentration, but they have equally important effects on protein and fat metabolism. Cortisol is the most important example.
An aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone, a major mammalian estrogen. It is converted from ANDROSTENEDIONE directly, or from TESTOSTERONE via ESTRADIOL. In humans, it is produced primarily by the cyclic ovaries, PLACENTA, and the ADIPOSE TISSUE of men and postmenopausal women.
Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promoter and enhancer regions.
Small containers or pellets of a solid drug implanted in the body to achieve sustained release of the drug.
A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.

Plasma concentration changes in LH and FSH following electrochemical stimulation of the medial preoptic are or dorsal anterior hypothalamic area of estrogen- or androgen-sterilized rats.(1/3406)


The effects of androgens and antiandrogens on hormone-responsive human breast cancer in long-term tissue culture. (2/3406)

We have examined five human breast cancer cell lines in continuous tissue culture for androgen responsiveness. One of these cell lines shows a 2- to 4-fold stimulation of thymidine incorporation into DNA, apparent as early as 10 hr following androgen addition to cells incubated in serum-free medium. This stimulation is accompanied by an acceleration in cell replication. Antiandrogens [cyproterone acetate (6-chloro-17alpha-acetate-1,2alpha-methylene-4,6-pregnadiene-3,20-dione) and R2956 (17beta-hydroxy-2,2,17alpha-trimethoxyestra-4,9,11-triene-1-one)] inhibit both protein and DNA synthesis below control levels and block androgen-mediated stimulation. Prolonged incubation (greater than 72 hr) in antiandrogen is lethal. The MCF- cell line contains high-affinity receptors for androgenic steroids demonstrable by sucrose density gradients and competitive protein binding analysis. By cross-competition studies, androgen receptors are distinguishable from estrogen receptors also found in this cell line. Concentrations of steroid that saturate androgen receptor sites in vitro are about 1000 times lower than concentrations that maximally stimulate the cells. Changes in quantity and affinity of androgen binding to intact cells at 37 degrees as compared with usual binding techniques using cytosol preparation at 0 degrees do not explain this difference between dissociation of binding and effect. However, this difference can be explained by conversion of [3H]-5alpha-dihydrotestosterone to 5alpha-androstanediol and more polar metabolites at 37 degrees. An examination of incubation media, cytoplasmic extracts and crude nuclear pellets reveals probable conversion of [3H]testosterone to [3H]-5alpha-dihydrotestosterone. Our data provide compelling evidence that some human breast cancer, at least in vitro, may be androgen dependent.  (+info)

Kinetics of neuroendocrine differentiation in an androgen-dependent human prostate xenograft model. (3/3406)

It was previously shown in the PC-295 xenograft that the number of chromogranin A (CgA)-positive neuroendocrine (NE) cells increased after androgen withdrawal. NE cells did not proliferate and differentiated from G0-phase-arrested cells. Here we further characterized NE differentiation, androgen receptor status, and apoptosis-associated Bcl-2 expression in the PC-295 model after androgen withdrawal to assess the origin of NE cells. PC-295 tumor volumes decreased by 50% in 4 days. Intraperitoneal bromodeoxyuridine (BrdU) incorporation and MIB-1 labeling decreased to 0%, and the apoptosis was maximal at day 4. Androgen receptor expression and prostate-specific antigen (PSA) serum levels decreased rapidly within 2 days. The number of NE cells increased 6-fold at day 4 and 30-fold at day 7. Five and ten percent of the CgA-positive cells were BrdU positive after continuous BrdU labeling for 2 and 4 days, respectively. However, no MIB-1 expression was observed in CgA-positive cells. NE cells expressed the regulated secretory pathway marker secretogranin III but were negative for androgen receptor and Bcl-2. Bcl-2 expression did increase in the non-NE tumor cells. In conclusion, androgen withdrawal leads to a rapid PC-295 tumor regression and a proliferation-independent induction of NE differentiation. The strictly androgen-independent NE cells that were still present after 21 days differentiated mainly from G0-phase-arrested cells.  (+info)

Sodefrin: a novel sex pheromone in a newt. (4/3406)

The abdominal gland in the male red-bellied newt, Cynops pyrrhogaster, is the source of a female-attracting pheromone. An attempt was made to isolate and characterize the female-attracting pheromone in the abdominal glands of male newts. The active substance, named sodefrin (from the Japanese 'sodefuri' which means 'soliciting') has been isolated and shown to be a novel decapeptide with the sequence, Ser-Ile-Pro-Ser-Lys-Asp-Ala-Leu-Leu-Lys. Its minimum effective concentration in water is 0.1-1.0 pmol 1-1. Synthetic sodefrin shows a female-attracting activity similar to that of the native peptide, and acts through the olfactory organ of female newts. Electrophysiological studies reveal that sodefrin evokes a marked electroolfactogram response in the vomeronasal epithelium in sexually mature females and in ovariectomized females treated with prolactin and oestrogen. The pheromonal activity of sodefrin appears to be species-specific since it does not attract females of a congeneric species, the sword-tailed newt C. ensicauda. However, C. ensicauda has a variant of sodefrin differing from that in C. pyrrhogaster by substitutions of Leu for Pro at position 3 and Gln for Leu at position 8. The C. ensicauda variant sodefrin does not attract C. pyrrhogaster females. Genes encoding the sodefrin precursor protein have been cloned in both C. pyrrhogaster and C. ensicauda. Immunostaining of the abdominal gland using the antiserum against sodefrin shows that sodefrin occurs in the epithelial cells, predominantly within the secretory granules. Sodefrin content, detected by immunoassay, in C. pyrrhogaster males decreases after castration and hypophysectomy and increases markedly in the castrated and hypophysectomized newts after treatment with androgen and prolactin. This combination of hormones also enhances sodefrin mRNA content in the abdominal gland as assessed by northern blot analysis using sodefrin cDNA.  (+info)

Relationship between metabolism of androstenone and skatole in intact male pigs. (5/3406)

The relationship between the metabolism of androsterone and skatole, the major compounds responsible for boar taint, was investigated in F4 Swedish Yorkshire x European Wild Pig intact males. The metabolism of androstenone and skatole were studied in liver microsomes, and the testicular steroid production was measured in testes microsomes. Including androstenone in the assays of skatole metabolism reduced the formation of 6-hydroxyskatole (pro-MII), and three other skatole metabolites (P<.05). The formation of three additional metabolites was not affected. Liver microsomal incubations of androstenone produced two metabolites, I and II. The rate of the formation of metabolite I and the rate of androstenone metabolism were correlated with the rate of skatole metabolism. Liver metabolism of androstenone was not related to levels of androstenone in fat. Testicular synthesis of 16-androstene steroids was correlated with combined synthesis of estrogens and androgens, plasma levels of androstenone, levels of skatole in fat, and skatole metabolism in the liver (P<.05). Plasma levels of estrone sulfate were correlated with levels of skatole in fat and with androstenone levels in fat and plasma and were negatively correlated with synthesis of skatole metabolite F-1 and pro-MII sulfation. These results indicate that the liver metabolism of androstenone and skatole are related. However, it is likely that the relationship between levels of androstenone and skatole in fat is due more to a link between the testicular synthesis of androstenone rather than to the metabolism of androstenone and skatole in the liver. Sex steroids may affect this relationship because of their biosynthesis along with androstenone and possible inhibition of skatole metabolism in the liver.  (+info)

The relationship between a polymorphism in CYP17 with plasma hormone levels and breast cancer. (6/3406)

The A2 allele of CYP17 has been associated with polycystic ovarian syndrome, elevated levels of certain steroid hormones in premenopausal women, and increased breast cancer risk. We prospectively assessed the association between the A2 allele of CYP17 and breast cancer risk in a case-control study nested within the Nurses' Health Study cohort. We also evaluated associations between this CYP17 genotype and plasma steroid hormone levels among postmenopausal controls not using hormone replacement to assess the biological significance of this genetic variant. Women with the A2 allele were not at an increased risk of incident breast cancer [OR (odds ratio), 0.85; 95% CI (confidence interval), 0.65-1.12] or advanced breast cancer (OR, 0.84; 95% CI, 0.54-1.32). We did observe evidence that the inverse association of late age at menarche with breast cancer may be modified by the CYP17 A2 allele. The protective effect of later age at menarche was only observed among women without the A2 allele (A1/A1 genotype: for age at menarche > or =13 versus <13; OR, 0.57; 95% CI, 0.36-0.90; A1/A2 and A2/A2 genotypes: OR, 1.05; 95% CI, 0.76-1.45; P for interaction = 0.07). Among controls, we found women with the A2/A2 genotype to have elevated levels of estrone (+14.3%, P = 0.01), estradiol (+13.8%, P = 0.08), testosterone (+8.6%, P = 0.34), androstenedione (+17.1%, P = 0.06), dehydroepiandrosterone (+14.4%, P = 0.02), and dehydroepiandrosterone sulfate (+7.2%, P = 0.26) compared with women with the A1/A1 genotype. These data suggest that the A2 allele of CYP17 modifies endogenous hormone levels, but is not a strong independent risk factor for breast cancer.  (+info)

Prognostic significance of extent of disease in bone in patients with androgen-independent prostate cancer. (7/3406)

PURPOSE: To evaluate the prognostic significance of a bone scan index (BSI) based on the weighted proportion of tumor involvement in individual bones, in relation to other factors and to survival in patients with androgen-independent prostate cancer. PATIENTS AND METHODS: Baseline radionuclide bone scans were reviewed in 191 assessable patients with androgen-independent disease who were enrolled onto an open, randomized trial of liarozole versus prednisone. The extent of skeletal involvement was assessed by scoring each scan using the BSI and independently according to the number of metastatic lesions. The relationship of the scored bone involvement to other known prognostic factors was explored in single- and multiple-variable analyses. RESULTS: In single-variable analyses, the pretreatment factors found to be associated with survival were age (P = .0446), performance status (P = .0005), baseline prostate-specific antigen (P = .0001), hemoglobin (P = .0001), alkaline phosphatase (P = .0002), AST (P = .0021), lactate dehydrogenase (P = .0001), and treatment (P = .0098). The extent of osseous disease was significant using both the BSI (P = .0001) and the number of lesions present (P = .0001). In multiple-variable proportional hazards analyses, only BSI, age, hemoglobin, lactate dehydrogenase, and treatment arm were associated with survival. When the patient population was divided into three equal groups, with BSI values of < 1.4%, 1.4% to 5.1%, and > 5.1%, median survivals of 18.3, 15.5, and 8.1 months, respectively, were observed (P = .0079). CONCLUSION: The BSI quantifies the extent of skeletal involvement by tumor. It allows the identification of patients with distinct prognoses for stratification in clinical trials. Further study is needed to assess the utility of serial BSI determinations in monitoring treatment effects. The BSI may be particularly useful in the evaluation of agents for which prostate-specific antigen changes do not reflect clinical outcomes accurately.  (+info)

Phase I trial of docetaxel with estramustine in androgen-independent prostate cancer. (8/3406)

PURPOSE: To evaluate the toxicity, efficacy, and pharmacokinetics of docetaxel when combined with oral estramustine and dexamethasone in a phase I study in patients with progressive metastatic androgen-independent prostate cancer. PATIENTS AND METHODS: Thirty-four men were stratified into minimally pretreated (MPT) and extensively pretreated (EPT) groups. Estramustine 280 mg PO tid was administered 1 hour before or 2 hours after meals on days 1 through 5, with escalated doses of docetaxel from 40 to 80 mg/m2 on day 2. Treatment was repeated every 21 days. RESULTS: Thirty-four patients were assessable for toxicity and 33 for response. In the MPT patients, dose-limiting myelosuppression was reached at 80 mg/m2, with six patients experiencing grade 3/4 granulocytopenia. In EPT patients, escalation above 70 mg/m2 was not attempted. Fourteen MPT (70%) and six EPT (50%) patients had a > or = 50% decline in serum PSA on two consecutive measurements taken at least 2 weeks apart. The overall 50% PSA response rate was 63% (95% confidence interval [CI], 28% to 81%). Of the 18 patients with bidimensionally measurable disease, five (28%; 95% CI, 11% to 54%) achieved a partial response. At the time of entry onto the study, 15 patients required narcotic analgesics for bone pain; after treatment, eight (53%) discontinued their pain medications. The area under the curve for docetaxel increased linearly from 40 to 70 mg/m2. At 80 mg/m2, the measured area under the curve was 8.37 (standard deviation, 0.724), which was significantly higher than the previously reported values. CONCLUSION: The recommended phase II dose of docetaxel combined with estramustine is 70 mg/m2 in MPT patients and 60 mg/m2 in EPT patients. This combination is active in men with androgen-independent prostate cancer.  (+info)

TY - JOUR. T1 - FKBP51 and Cyp40 are positive regulators of androgen-dependent prostate cancer cell growth and the targets of FK506 and cyclosporin A. AU - Periyasamy, S.. AU - Hinds, T.. AU - Shemshedini, L.. AU - Shou, Weinian. AU - Sanchez, E. R.. PY - 2010/3. Y1 - 2010/3. N2 - Prostate cancer (PCa) growth is dependent on androgens and on the androgen receptor (AR), which acts by modulating gene transcription. Tetratricopeptide repeat (TPR) proteins (FKBP52, FKBP51 and Cyp40) interact with AR in PCa cells, suggesting roles in AR-mediated gene transcription and cell growth. We report here that FKBP51 and Cyp40, but not FKBP52, are significantly elevated in PCa tissues and in androgen-dependent (AD) and androgen-independent (AI) cell lines. Overexpression of FKBP51 in AD LNCaP cells increased AR transcriptional activity in the presence and absence of androgen, whereas siRNA knockdown of FKBP51 dramatically decreased AD gene transcription and proliferation. Knockdown of Cyp40 also inhibited ...
Prostate cancer is one of the leading causes of cancer death in men. Androgen ablation, the most commonly-used therapy for progressive prostate cancer, is ineffective once the cancer cells become androgen-independent. The regulatory mechanisms that cause this transition (from androgen-dependent to androgen-independent) remain unknown. In this study, based on the microarray data comparing global gene expression patterns in the prostate tissue between androgen-dependent and -independent prostate cancer patients, we indentify a set of transcription factors and microRNAs that potentially cause such difference, using a model-based computational approach. From 335 position weight matrices in the TRANSFAC database and 564 microRNAs in the microRNA registry, our model identify 5 transcription factors and 7 microRNAs to be potentially responsible for the level of androgen dependency. Of these transcription factors and microRNAs, the estimated function of all the 5 transcription factors are predicted to be
The goal of this study was to address the controversy over evidence of prenatal androgen exposure reflected in the digit ratios of women with PCOS. Recently our group showed that when 2D:4D were measured with Vernier calipers, women with PCOS did not demonstrate finger length patterns consistent with increased levels of in utero androgen exposure [12]. This was in contrast to a previous report that had also used Vernier calipers to measure 2D:4D in women with PCOS [9]. Since observed differences in 2D:4D are generally small, there is growing support that studies investigating potential effects of prenatal androgens use the most consistent and reliable technique available to measure finger lengths [13-15, 18-20]. In this study, we imaged the hands of women with four clinical phenotypes of PCOS, healthy female controls and men, and used computer-based calipers to measure their finger lengths since this method was recently validated to be the most reliable [14, 15]. Consistent with this being the ...
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This trial assessed efficacy and tolerability of satraplatin together with bevacizumab works in treating patients with metastatic prostate cancer previously
Androgens are required for the male reproductive tissues. In addition, androgens regulate gene ex-pression in several non-reproductive tissues. Defects in androgen signaling are linked to diseases, such as prostate cancer. Androgens act through androgen receptor, AR, a hormone-inducible nuclear receptor. Upon ligand binding, AR is shuttled to the nucleus where it binds to the androgen response elements to regulate gene transcription. Specificity of spatiotemporal androgen regulation in different tissues is achieved by differential usage of coregulators. However, in many target tissues the regulation of cell type specific responses to androgen action remain poorly understood. Given the importance of androgen action, it is necessary to understand how androgen actions are normally regulated. We are especially interested in how tissue-specific androgen responses are mediated via pioneer factors, collaborating transcription factors and small RNAs, namely microRNAs in the male reproductive ...
To determine the time to progression produced by the combination of Novantrone (mitoxantrone) and Erbitux (cetuximab) versus Novantrone alone in metastatic
Changes in cognitive function related to altered serum sex hormone levels are well-recognised but poorly understood. Mild cognitive impairment (MCI) with aging is thought in part to be related to reduction in serum androgen level and international studies are on-going to prevent age-related MCI using androgen replacement therapy. Reduction in cognitive function often leads to morbidity and reduction in quality of life. The commonest therapeutically induced reduction in sex hormone level in men is in the treatment of prostate cancer. As prostate cancer is androgen dependent for growth, androgen-deprivation therapy (ADT) to suppress serum testosterone level to castration levels (, 1.7mM) is the key therapeutic intervention for advanced disease. Up to 1 million men worldwide are estimated to have been prescribed ADT for prostate cancer, mostly using luteinising hormone releasing hormone agonists (LHRHa). ADT is now also used to treat some early prostate cancer and as early asymptomatic prostate ...
Herein, we assessed the efficacy of procyanidins from grape seed against a panel of human prostate cancer (PCa) cell lines which ranged from classical cell lines to the new variants that differed in their androgen responsiveness, castration resistance, and metastatic potential. The classical cell lines chosen were PC3, DU145 and LNCaP. Of these cell lines: PC3 and DU145 do not need androgens for growth, i.e, these are androgen independent (AI); they also lack androgen receptors (AR). The LNCaP cell line on the other hand, demonstrates androgen sensitivity (AS) and also requires androgens for its growth; while it harbors a mutated AR. Of the new variants of PCa cell lines available, we further chose a castration resistant variant of LNCaP, C4-2B, derived from the xenografts of castration resistant LNCaP subline-C4 in castrated mice. C4-2B thus represents castration resistant PCa (CRPC) cell line; while it does not require androgen for growth it demonstrates androgen sensitivity due to the ...
The primary objective of this research is to demonstrate that serum androgen (SA) levels in patients with castration resistant prostate cancer (CRPC) are prognostic of overall survival (OS). A relationship of higher SA to improved survival has been observed in two phase III randomized studies, regardless of treatment arm, but never in a study in which an androgen synthesis inhibitor (ASI) such as abiraterone or ketoconazole was NOT part of the therapy. Patient serum is banked from CALGB 90401 - an NCI sponsored cooperative group randomized phase III that compared docetaxel plus prednisone (DP) to docetaxel/prednisone plus bevacizumab (DPB) in CRPC. Banked serum from this completed study will be used to measure androgen levels via CLIA certified ultrasensitive (liquid chromatography tandem mass spectroscopy) technique and these results will be associated with mature patient survival and outcome data. The underlying hypothesis of this work is that higher serum androgens are associated with ...
Development of resistance to androgen deprivation therapy (ADT) is a major obstacle for the management of advanced prostate cancer. Therapies with androgen receptor (AR) antagonists and androgen withdrawal initially result in tumor regression but development of compensatory mechanisms including AR bypass signaling leads to tumor re-growth, independent of circulating androgens. The result is the emergence of castration resistant prostate cancer (CRPC), a highly morbid disease exhibiting aberrant expression of many protein-coding and non-coding genes. Under the umbrella of non-coding RNAs is a class of small regulatory RNAs referred to as microRNAs (miRNAs). MicroRNAs are believed to function in the maintenance of cell homeostasis but are often differentially expressed in many different types of cancer including CRPC. In this study, the association of genome wide miRNA expression (1113 unique miRNAs) with development of resistance to ADT was determined. Androgen sensitive prostate cancer cells that
Androgens have important physiological effects in women while at the same time they may be implicated in breast cancer pathologies. However, data on the effects of androgens on mammary epithelial proliferation and/or breast cancer incidence are not in full agreement. We performed a literature review evaluating current clinical, genetic and epidemiological data regarding the role of androgens in mammary growth and neoplasia. Epidemiological studies appear to have significant methodological limitations and thus provide inconclusive results. The study of molecular defects involving androgenic pathways in breast cancer is still in its infancy. Clinical and nonhuman primate studies suggest that androgens inhibit mammary epithelial proliferation and breast growth while conventional estrogen treatment suppresses endogenous androgens. Abundant clinical evidence suggests that androgens normally inhibit mammary epithelial proliferation and breast growth. Suppression of androgens using conventional estrogen
The effect of androgens on different aspects of atherogenesis has received little attention despite the marked male predisposition to occlusive vascular disease.1 2 In the present study, we have demonstrated that androgen exposure leads to a dose-related and receptor-mediated increase in human monocyte adhesion to endothelial cells, a key early event in atherosclerosis. This effect is mediated at least in part by an androgen receptor-dependent increase in endothelial cell expression of the important adhesion molecule VCAM-1.. A proatherogenic effect of androgens is supported by recent work in experimental animals. For example, Adams et al8 documented an approximate doubling of coronary artery plaque size in female postmenopausal cynomolgus monkeys treated with testosterone and a cholesterol-enriched diet, and Hutchison et al16 documented arterial endothelial dysfunction in hypercholesterolemic rabbits that were administered androgens. Similar data are not available in humans.. The incidence of ...
TY - JOUR. T1 - Correlates of circulating androgens in mid-life women. T2 - The Study of Womens Health Across the Nation. AU - Santoro, Nanette. AU - Torrens, Javier. AU - Crawford, Sybil. AU - Allsworth, Jenifer E.. AU - Finkelstein, Joel S.. AU - Gold, Ellen B. AU - Korenman, Stan. AU - Lasley, William L.. AU - Luborsky, Judith L.. AU - McConnell, Dan. AU - Sowers, Mary Fran. AU - Weiss, Gerson. PY - 2005/8. Y1 - 2005/8. N2 - Context: Androgens influence sexual differentiation and behavior, body composition, and physical functioning in men, but their role in women is less well understood. Because circulating androgens decline with age, the use of androgen supplementation for women to improve health and well-being has been increasing. Objective: The aim of this study was to assess the association between androgens and a variety of end points thought to be affected by androgens. Design: In a community-based baseline cohort of women aged 42-52 yr from the Study of Womens Health Across the ...
Androgens in women either derive from direct ovarian production or from peripheral conversion of the adrenal sex steroid precursor, dehydroepiandrosterone, towards active androgens. Therefore, loss of adrenal or ovarian function, caused by Addisons disease or consequent to bilateral oophorectomy, results in severe androgen deficiency, clinically often associated with a loss of libido and energy. Importantly, physiological menopause does not necessarily lead to androgen deficiency, as androgen synthesis in the ovaries may persist despite the decline in estrogen production. However, the definition of female androgen deficiency, as recently provided by the Princeton consensus statement, is not precise enough and may lead to over-diagnosis due to the high prevalence of its diagnostic criteria: androgen levels below or within the lower quartile of the normal range and concurrent sexual dysfunction. Importantly, physiological menopause is not necessarily associated with androgen deficiency and ...
COPD may be a chronic inflammatory respiratory organ unwellness that causes clogged flow from the lungs. its foretold by the globe Health Organisation to be the third-leading reason behind malady and death internationally by 2030. Low androgenic hormone is common in men with COPD and will worsen their condition. Men with COPD have shortness of breath and sometimes take steroid-based medications for AN extended time, each of that increase their risk of low androgenic hormone ...
Daughters of women with polycystic ovarian syndrome (PCOS) are five times more likely to be diagnosed with PCOS as adults, and the generational transmission is driven by high androgen levels during pregnancy, researchers at Karolinska Institutet in Sweden report. Their results, which are based on register-based and clinical studies as well as transgenerational animal studies, are published in Nature Medicine.. PCOS affects more than ten percent of women of fertile age and is characterised by high levels of androgens (male sex hormones), ovulation disorders and difficulties conceiving. The syndrome is also associated with mental health conditions and a greatly increased risk of type 2 diabetes and obesity, which aggravate the symptoms. While the causes of PCOS are not fully known, the uterine environment plays a key role.. In this study, researchers at Karolinska Institute combined human and mouse studies to ascertain how and to what extent the syndrome is passed down to coming generations. A ...
Steroid androgen hormones play a key role in the progression and treatment of prostate cancer, with androgen deprivation therapy being the first-line treatment used to control cancer growth. Here we apply a novel search strategy to identify androgen-regulated cellular pathways that may be clinically important in prostate cancer. Using RNASeq data, we searched for genes that showed reciprocal changes in expression in response to acute androgen stimulation in culture, and androgen deprivation in patients with prostate cancer. Amongst 700 genes displaying reciprocal expression patterns we observed a significant enrichment in the cellular process glycosylation. Of 31 reciprocally-regulated glycosylation enzymes, a set of 8 (GALNT7, ST6GalNAc1, GCNT1, UAP1, PGM3, CSGALNACT1, ST6GAL1 and EDEM3) were significantly up-regulated in clinical prostate carcinoma. Androgen exposure stimulated synthesis of glycan structures downstream of this core set of regulated enzymes including sialyl-Tn (sTn), sialyl Lewis(X)
Androgen and androgen receptors (AR) play critical roles in the proliferation of prostate cancer through transcriptional regulation of target genes. Here, we found that androgens upregulated the expression of dynamin-related protein 1 (Drp1), which is involved in the induction of mitochondrial fission, a common event in mitosis and apoptosis. Clinical tissue samples and various prostate cancer cell lines revealed a positive correlation between Drp1 and AR levels. Treatment of androgen-sensitive cells with an AR agonist, R1881, and antagonist, bicalutamide, showed that Drp1 is transcriptionally regulated by androgens, as confirmed by an AR ChIP-seq assay. Live imaging experiments using pAcGFP1-Mito stably transfected LNCaP (mito-green) cells revealed that androgen did not induce significant mitochondrial fission by itself, although Drp1 was upregulated. However, when treated with CGP37157 (CGP), an inhibitor of mitochondrial Ca²⁺ efflux, these cells exhibited mitochondrial fission, which was further
RATIONALE: Androgens can cause the growth of prostate cancer cells. Androgen ablation therapy may lessen the amount of androgens made by the body. Drugs
TY - JOUR. T1 - Age-specific population centiles for androgen status in men. AU - Handelsman, D.J.. AU - Yeap, Bu. AU - Flicker, Leon. AU - Martin, S.. AU - Wittert, G.A.. AU - Ly, L.P.. PY - 2015. Y1 - 2015. N2 - © 2015 European Society of Endocrinology Printed in Great Britain. Aim: The age-specific population profiles in men of circulating testosterone and its two bioactive metabolites dihydrotestosterone (DHT) and estradiol (E2) across the adult lifespan and its determinants are not well described. Objective: Our objective was to deduce smoothed age-specific centiles of circulating testosterone, DHT, and E2 in men using pooled data from population-based studies in three Australian cities from liquid chromatography-mass spectrometry steroid measurements in a single laboratory. Design, setting, and participants: We pooled data of 10 904 serum samples (serum testosterone, DHT, E2, age, height, and weight) from observational population-based studies in three major cities across Australia. Main ...
The Dunning R-3327-H rat prostatic adenocarcinoma is a well-differentiated, slow-growing, serially transplantable tumor of spontaneous origin. When intact male rats bearing such an exponentially growing H-tumor s.c. are castrated, tumor growth abruptly stops, demonstrating the initial androgen sensitivity of this tumor. Eventually, however, after an extended period, the tumor invariably relapses and once again appears to grow exponentially. At the time of relapse, the tumor is no longer androgen sensitive but has irreversibly progressed to a completely insensitive state. The mechanism responsible for this irreversible progression has been demonstrated by fluctuation analysis not to be due to environmentally induced adaptation of initially androgen-dependent H-tumor cells to a new androgen-independent state. Instead, the progression is due to the basic heterogeneity of the original H-tumor (i.e., it is composed of a mixture of preexisting clones of both androgen-dependent and androgen-independent ...
Anose, B.M.; LaGoo, L. and Schwendinger, J. (2008). Characterization of Androgen Regulation of ZEB-1 and PSA in 22Rv1 Prostate Cancer Cells. Adv Exp Med Biol. 2008; 617:541-6 ...
Antiandrogens are a group of medications which bind to intracellular androgen receptors (AR) to prevent androgen effects on organs such as the testes, the hair follicles, the hypothalamus, pituitary, ovaries and the prostate gland, which are targets of endogenous androgens. They are used to treat a variety of clinical conditions which are characterized by hyperandrogenism, such as acne, hirsutism, and prostate cancer.
Dr Lal PathLabs ANDROGEN INDEX in Kolkata is health checkup package includes 4 Tests. ₹200 Cashback and Free Doctor Consultation, Home sample collection and Online reports available. ANDROGEN INDEX in Kolkata covers 4 parameters- ITEM FOR METHOD, SEX HORMONE BINDING GLOBU, TESTO. TOTAL, ANDROGEN INDEX in Kolkata
Biologic effects of androgen on target cells are mediated in part by transcriptional regulation of androgen-regulated genes (ARGs) by androgen receptor. Using serial analysis of gene expression (SAGE), we have identified a comprehensive repertoire of ARGs in LNCaP cells. One of the SAGE-derived tags …
Taxotere (docetaxel) is used to treat adjuvant breast cancer, metastatic androgen independent prostate cancer, advanced non-small cell lung cancer, advanced gastric adenocarcinoma and locally advanced squamous cell carcinoma of the head and neck. Includes Taxotere side effects, interactions and indications.
PRIMARY OBJECTIVES:. I. To evaluate the effect of neoadjuvant degarelix (degarelix acetate) on prostate dihydrotestosterone (DHT) and testosterone levels.. SECONDARY OBJECTIVES:. I. To determine the effect of degarelix acetate on androgen-regulated gene expression and apoptosis as assessed by immunohistochemistry, complementary deoxyribonucleic acid (cDNA) microarray analysis and reverse transcriptase (RT)-polymerase chain reaction (PCR).. II. To determine the effect of degarelix acetate on follicle stimulating hormone (FSH) and FSH receptor expression in prostate cancer and surrounding microenvironment.. OUTLINE:. Patients receive degarelix acetate subcutaneously (SC) on day 1. Treatment repeats every 4 weeks for up to 6 courses. Beginning at week 15, patients also undergo standard external beam radiation therapy (EBRT) for 8.5 weeks. ...
Androgen receptor (AR) targeting remains the gold standard treatment for advanced prostate cancer (PCa); however, treatment resistance remains a major clinical problem. To study the therapeutic effects of clinically used anti-androgens we characterized herein a tissue-mimetic three-dimensional (3D) in vitro model whereby PCa cells were cultured alone or with PCa-associated fibroblasts (CAFs). Notably, the ratio of PCa cells to CAFs significantly increased in time in favor of the tumor cells within the spheroids strongly mimicking PCa in vivo. Despite this loss of CAFs, the stromal cells, which were not sensitive to androgen and even stimulated by the anti-androgens, significantly influenced the sensitivity of PCa cells to androgen and to the anti-androgens bicalutamide and enzalutamide. In particular, DuCaP cells lost sensitivity to enzalutamide when co-cultured with CAFs. In LAPC4/CAF and LNCaP/CAF co-culture spheroids the impact of the CAFs was less pronounced. In addition, 3D spheroids exhibited a
Androgens are involved in prostate cancer (PCa) cell growth. Genes involved in androgen metabolism mediate key steps in sex steroid metabolism.
The first step in answering a question like this is to kick the tires in the lab, before ever road-testing it with humans. And so Dawn Cochrane, PhD, instructor in the Richer Lab, treated breast cancer cells lines with both casodex and a new anti-androgen drug MDV-3100,developed by Dr. Charles Sawyers at Memorial-Sloan Kettering and is currently in phase III clinical trials for treatment of prostate cancer.. Interestingly not only did MDV-3100 completely abolish androgen-mediated breast cancer, but it stopped estrogen-mediated breast cancer proliferation, as well, Richer says.. This was true despite the fact that MDV-3100 only binds to androgen receptors and not estrogen receptors. And casodex? Well, while it brought its prostate cancer bag of tricks to bear on androgen-driven breast cancer, on the other hand it augmented the growth of estrogen-driven breast cancer cells. So while casodex may someday prove useful for patients with androgen - but not estrogen! - driven cancers, MDV-3100 is a ...
In this study, we present data to support the use of cabozantinib with abiraterone for treatment of prostate cancer. This paper also describes abiraterones compensatory upregulation of p-IGFIR and activation of the downstream survival pathway (p-MEK and p-ERK) and cabozantinibs ability to inhibit phosphorylation of IGFIR as well as abiraterone-induced phosphorylation of MEK and ERK. In short, the work suggests the cabozantinib blocked one of the abiraterones short term compensatory adaptive resistance mechanisms.. The in vivo LAPC4-CR is a CRPC model that develops rapid resistance to abiraterone. As can be seen, cabozantinib has single-agent activity and more activity is seen when cabozantinib is combined with abiraterone. It is notable that the LAPC4-CR in vivo is a completely androgen-independent prostate cancer cell line and had undergone two passages in mice in our experiments. Therefore, it is probable that the cellular processes may have already been changed to produce an ...
As an adult woman, you probably know hormones have a lot to do with your acne! Learn how to treat breakouts casued by high androgen levels
TY - JOUR. T1 - Peroxynitrite mediates testosterone-induced vasodilation of microvascular resistance vessels. AU - Puttabyatappa, Yashoda. AU - Stallone, John N.. AU - Ergul, Adviye. AU - El-Remessy, Azza B.. AU - Kumar, Sanjiv. AU - Black, Stephen Matthew. AU - Johnson, Maribeth H. AU - Owen, Mary P.. AU - White, Richard E.. PY - 2013/4/1. Y1 - 2013/4/1. N2 - Our knowledge of how androgens influence the cardiovascular system is far from complete, and this lack of understanding is especially true of how androgens affect resistance vessels. Our aim was to identify the signaling mechanisms stimulated by testosterone (TES) in microvascular arteries and to understand how these mechanisms mediate TES-induced vasodilation. Mesenteric microvessels were isolated from male Sprague-Dawley rats. Tension studies demonstrated a rapid, concentration-dependent, vasodilatory response to TES that did not involve protein synthesis or aromatization to 17β-estradiol. Dichlorofluorescein fluorescence and ...
BACKGROUND. Prostasin is downregulated in hormone-refractory prostate cancers (HRPC). The mechanisms by which androgens regulate prostasin expression are unclear. METHODS. LNCaP cells were treated with dihydrotestosterone (DHT), and mRNA expression of prostasin, SREBPs, SNAIL, and SLUG was examined by real-time PCR following reverse transcription. A human prostasin promoter was evaluated in HEK-293 cells cotransfected with transcription factor cDNAs. Regulation of endogenous prostasin expression by transfected SREBP-2 or SLUG was evaluated. Expression of SNAIL and SLUG mRNA in DU-145 cells treated with epidermal growth factor (EGF) was examined. RESULTS. Prostasin mRNA expression in LNCaP cells was not responsive to DHT treatment. DHT marginally upregulated mRNA expression of SREBP-1c, SREBP-2, and SNAIL, but not SREBP-la, while dramatically increased SLUG mRNA expression, in a dose-dependent manner. Co-transfection of prostasin promoter and SREBP cDNA in HEK-293 cells resulted in stimulation of Ken-ichi Takayama, Takashi Suzuki, Shuichi Tsutsumi, Tetsuya Fujimura, Tomohiko Urano, Satoru Takahashi, Yukio Homma, Hiroyuki Aburatani, Satoshi Inoue
BMB Rep. 2010 Oct;43(10):688-92. Preventable effect of L-threonate, an ascorbate metabolite, on androgen-driven balding via repression of dihydrotestosterone-in
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Androgen, also named androgenic hormones or testoids, could be the generic phrase for just about any organically grown or artificial compound, normally a steroid hormone, that stimulates or controls the enlargement and upkeep of male qualities in vertebrates by binding to androgen receptors. This consists of the actions belonging toward accessory male sex organs and [...]
6.4.1 Hair growth in androgen insufficiency syndromes As described in Chapters 1 and 2 of this book, androgens from the blood stream enter the cell and bind to
TY - JOUR. T1 - Evaluation of genetic variations in the androgen and estrogen metabolic pathways as risk factors for sporadic and familial prostate cancer. AU - Cunningham, Julie M.. AU - Hebbring, Scott J.. AU - McDonnell, Shannon K.. AU - Cicek, Mine S.. AU - Christensen, G. Bryce. AU - Wang, Liang. AU - Jacobsen, Steven J.. AU - Cerhan, James R.. AU - Blute, Michael L.. AU - Schaid, Daniel J.. AU - Thibodeau, Stephen N.. PY - 2007/5. Y1 - 2007/5. N2 - Previous studies suggest that enzymes involved in the androgen metabolic pathway are susceptibility factors for prostate cancer. Estrogen metabolites functioning as genotoxins have also been proposed as risk factors. In this study, we systematically tested the hypothesis that common genetic variations for those enzymes involved in the androgen and estrogen metabolic pathways increase risk for sporadic and familial prostate cancer. From these two pathways, 46 polymorphisms (34 single nucleotide polymorphisms, 10 short tandem repeat polymorphisms, ...
Ligandrol and also LGD-4033 is an important human being androgenic hormone receptors modulator (SARM) get from Ligand Medications plus owing to of at present acquiring done anything about by Viking Thérapeutics. AOD9604 is actually a peptide break up (hGH Sherd 177-191) on the C-terminus about People Building Hormonal agent to which your tyrosiné is normally applied in thé N-terminal keep going part. Its moreover known by the numerical period LGD-4033 not to mention quite a few men as well as young girls think about it to start an individual of the finest SARM improvements recent in the industry at present. Ligandrol changes the particular develop associated with narrow muscles cells weight with grasping individuals together with the Androgenic hormone Réceptors show found in the over-all body. Both products and steroids and SARMs succeeds found in a related approach by way of keeping typically the androgenic hormone receptors within your body, with regard to helping the growth ánd ...
Consider an XY fetus. For the androgens (testosterone and dihydrotestosterone) to do their work in its brain, they must bind to special receptors tailored specially for androgens. The androgens fit into the receptors like a key into a lock. The receptors are actually proteins, made by genes. Even small variations in the gene (SRY) involved in making androgen receptors can lead to a hitch. And small variations in that gene are not uncommon. In some genetic variants, the receptor lacks the right shape to allow the androgens to bind to it. This prevents the process of masculinizing the gonads and the brain. In other genetic variants, no receptor proteins are produced at all, so the androgen has nothing to bind to. In these conditions, the androgens cannot masculinize the brain or the body, despite the XY genetic makeup. In consequence, the baby, though a genetic male, will probably have a small vagina and will be believed to be female when born. This baby will grow breasts at puberty, though she/he ...
Introduction : The focus of this study was to assess cognitive functions in relation to androgens and specifically testosterone and dehydroepiandrosterone in postmenopausal women as well as the correlation between cognitive functions and these two androgens according to polymorphism of the...
Treatment with a potent anabolic androgen may produce significant increases in muscle mass and strength after only 6 weeks in healthy older men. However, such treatment did not improve leg muscle power or walking speed.
To assess prescribing practices for androgens at Wilford Hall USAF Medical Center, the authors analyzed prescriptions for all patients receiving therapy during a 12-month period n=201 and reviewed the available outpatient records not maintained elsewhere n=105. The most commonly prescribed androgens were testosterone enanthate 144/201; 56.7%,...
I am currently working with an androgen independent prostate ,cancer cell line. Using the Oncor ApopTag kit, I have gotten beautiful ,pictures of cells undergoing apoptosis, however, there are a few ,phenomenas that I notice that I cant explain- namely: , 1. Apoptosis is supposed to be marked by cell shrinkage whereas ,my cells (which underwent ionizing irradiation) are markedly larger than ,the control cells. Cells undergoing apoptosis do tend to shrink during the loss of cytoplasm as apoptotic bodies are formed and released. Cells undergoing radiation induced cell death will swell if they are undergoing necrosis. What you may be observing are necrotic cells, which also contain degraded DNA, stained positive by the ApopTag Kit. Also, what dose range are you using? David W. Voehringer Department of Experimental Radiotherapy Univ. of Texas M.D. Anderson Cancer Center 1515 Holcombe Bvld. Houston, Tx. 77030 (713) 792-3797 ...
SAHA is a promising agent currently in clinical trials for treatment of hematologic malignancies and solid tumors. Although previous studies suggest that SAHA can effectively inhibit the growth of prostate cancer cells (16), the mechanism of growth inhibition is not well understood. Moreover, it was evident from our previous studies that SAHA is more efficacious in terms of growth inhibition and induction of cell death in androgen-responsive cells (e.g., LNCaP and CWR22) than in cells that lack AR (PC-3; ref. 16), suggesting that a component of the activity of SAHA in prostate cancer cells relates to the presence of a functional androgen signaling axis. Our current data, showing the modulation of the AR and genes involved in AR signaling, including its direct target genes PSA and kallikrein 2, as well as genes reported to be androgen regulated, such as transmembrane serine protease and NEDD4L, provide direct evidence of an effect of SAHA on AR signaling. In addition, our demonstration that both ...
Cancer cell invasion is one of the crucial events in local spreading, growth, and metastasis of tumors. First evidence suggesting an anti-invasive action was published by Nithipatikom et al. (2004) who showed that 2-AG inhibits invasion of androgen-independent prostate cancer cells by a mechanism involving CB1 receptor activation. However, the precise mechanism leading to decreased invasiveness by cannabinoids remained elusive. Recently, several investigations have provided new insight into how cannabinoids could achieve their anti-invasive action.. In this context, several studies suggest a modulation of the MMP system by cannabinoids as part of their anti-invasive action. MMPs belong to a group of enzymes exerting an important function during tumor invasion, metastasis, and angiogenesis through degradation of ECM components (Curran and Murray, 2000; Stamenkovic, 2000). Of all MMPs, particularly MMP-2 and -9, are known to facilitate tumor invasion by proteolytic degradation of major basement ...
Gonadal androgens account for up to 80% of serum androgenic steroids (10). Castration, therefore, does not suppress adrenal androgens and achieves a hormone-reduced rather than a hormone-free state, hence, the recent renaming of this stage of the disease as castration-resistant in preference to hormone-refractory. CRPC cells undergo a number of genomic and expression changes involving the AR and its associated coactivators and corepressors that could allow continued activation of the AR signaling axis by castrate levels of androgens (11). Moreover, intratumoral hormone synthesis associated with overexpression of key enzymes, including CYP17, could cause resistance to castration (12-14). Although the latter remains a very challenging phenomenon to unequivocally prove, the body of circumstantial evidence for suggesting tumors synthesize their own androgens is compelling and introduces the interesting possibility of therapeutically directly targeting tumor hormone synthesis. In 2005, we ...
Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen ... Higher androgen levels lead to increased expression of androgen receptor. Circulating levels of androgens can influence human ... Andrology Endocrine system Exercise and androgen levels Androgen insensitivity syndrome Androgen insufficiency syndrome ... see the androgen replacement therapy and anabolic steroid articles. The main subset of androgens, known as adrenal androgens, ...
An androgen or anabolic steroid ester is an ester of an androgen/anabolic steroid (AAS) such as the natural testosterone or ... List of androgen esters List of androgens/anabolic steroids Steroid ester Estrogen ester Progestogen ester Richard Lawrence ... They are used in androgen replacement therapy (ART), among other indications. Examples of androgen esters include testosterone ... Androgen esters, Androgens and anabolic steroids, Androstanes, Prodrugs). ...
... is a medical treatment to suppress or block the production or action of male sex hormones, typically in ...
In contrast to androgens, conjugates of androgens do not bind to the androgen receptor and are hormonally inactive. However, ... androgen conjugates can be converted back into active androgens through enzymes like steroid sulfatase. Examples of androgen ... An androgen conjugate is a conjugate of an androgen, such as testosterone. They occur naturally in the body as metabolites of ... Androgen conjugates are conjugated at the C3 and/or C17β positions, where hydroxyl groups are available. Androgen ester ...
Heinlein CA, Chang C (October 2002). "The roles of androgen receptors and androgen-binding proteins in nongenomic androgen ... Via the androgen receptor, androgens play a key role in the maintenance of male skeletal integrity. The regulation of this ... The androgen receptor dimer binds to a specific sequence of DNA known as a hormone response element. Androgen receptors ... Androgen binding to cytoplasmic androgen receptors can cause rapid changes in cell function independent of changes in gene ...
Androgenic activity is mediated by androgens (a class of steroid hormones with varying affinities for the androgen receptor), ... Androgen deficiency is not usually checked for diagnosis in healthy women. Treatment may consist of hormone replacement therapy ... Wierman ME, Arlt W, Basson R, Davis SR, Miller KK, Murad MH, Rosner W, Santoro N (October 2014). "Androgen therapy in women: a ... It may also be the result of conditions such as androgen insensitivity syndrome or hyperestrogenism. Old age may also be a ...
... may refer to: Testosterone (medication) Androgen replacement therapy Anabolic steroid Androgen This ... disambiguation page lists medication articles associated with the title Androgen. If an internal link led you here, you may ...
An androgen prohormone, or proandrogen, is a prohormone (or prodrug) of an anabolic-androgenic steroid (AAS). They can be ... This legislation places both AAS and some androgen prohormones on a list of controlled substances (a new type of "regulatory ... Androgens and anabolic steroids, Androstanes, Estranes, Prodrugs, World Anti-Doping Agency prohibited substances). ...
This article pertains to steroidal androgens; nonsteroidal androgens like the selective androgen receptor modulators (SARMs) ... List of steroids List of designer drugs § Androgens List of androgens/anabolic steroids available in the United States ? = ... This is a list of androgens/anabolic steroids (AAS) or testosterone derivatives. Esters are mostly not included in this list; ... "Structure-activity relationships of synthetic progestins in a yeast-based in vitro androgen bioassay". J. Steroid Biochem. Mol ...
... (ADT), also called androgen suppression therapy, is an antihormone therapy whose main use is in ... Prostate cancer cells usually require androgen hormones, such as testosterone, to grow. ADT reduces the levels of androgen ... The therapy can also eliminate cancer cells by inducing androgen deprivation-induced senescence. Lowering androgen levels or ... Prostate cells contain an Androgen Receptor (AR), that when stimulated by androgens like testosterone, promotes growth and ...
... which bind and are activated by testosterone and/or other androgens. Unlike the androgen receptor (AR), a nuclear receptor ... 3α-Androstanediol, an active metabolite of dihydrotestosterone (DHT) and a weak androgen as well as a neurosteroid via acting ... Membrane steroid receptor Bennett NC, Gardiner RA, Hooper JD, Johnson DW, Gobe GC (2010). "Molecular cell biology of androgen ... Membrane androgen receptors (mARs) are a group of G protein-coupled receptors (GPCRs) ...
... among other androgen-dependent conditions. Because androgens are the endogenous precursors of estrogens, androgen synthesis ... An androgen synthesis inhibitor is a type of drug which inhibits the enzymatic synthesis of androgens, such as testosterone and ... inactive androgen sulfates into active androgens like testosterone Inhibitors of cholesterol synthesis can also reduce androgen ... including androgens 17β-Hydroxysteroid dehydrogenase inhibitors (17β-HSD inhibitors): inhibit the interconversion of androgens ...
If there is an excess of androgens in a male fetus it will give rise to infant hercules syndrome. J Money Sin, Sickness, or ... Androgen-induced hermaphroditism is a syndrome resulting from a hermaphroditic birth defect of the genital organs. They are ...
... (FAI) is a ratio used to determine abnormal androgen status in humans. The ratio is the total testosterone ... The free androgen index is intended to give a guide to the free testosterone level, but it is not very accurate (especially in ... The Free Androgen Index is not valid for adult males [dead link] Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN (March ... "Free Androgen Index". Online Medical Encyclopedia. University of Rochester Medical Center. Retrieved 11 July 2014. Morris PD, ...
The androgen backdoor pathway is a collective name for all metabolic pathways where clinically relevant androgens are ... In February 2003, Jean Wilson and colleagues described that DHT, a 5α-reduced androgen, can be synthesized from 17-OHP by two ... The primary feature of the androgen backdoor pathway is that 17α-hydroxyprogesterone (17-OHP) can be 5α-reduced and finally ... Turcu AF, Nanba AT, Auchus RJ (2018). "The Rise, Fall, and Resurrection of 11-Oxygenated Androgens in Human Physiology and ...
Maximum or maximal androgen blockade (MAB) or complete or combined androgen blockade (CAB) is a medical treatment involving the ... antagonism and inhibition or suppression of androgen production to attain maximal effectiveness in androgen deprivation therapy ... Triple androgen blockade (TrAB) is a method of ADT in which a 5α-reductase inhibitor such as finasteride or dutasteride is ... Hellerstedt, Beth A; Pienta, Kenneth J (2003). "The truth is out there: an overall perspective on androgen deprivation". ...
... is a condition most commonly affecting women, and is also called Female androgen insufficiency ... "Serum androgen levels in healthy premenopausal women with and without sexual dysfunction: Part A. Serum androgen levels in ... Rivera-Woll, L. M.; Papalia, M.; Davis, S. R.; Burger, H. G. (October 1, 2004). "Androgen insufficiency in women: diagnostic ... Davison, Sonia L; Davis, Susan R (June 1, 2003). "Androgens in women". The Journal of Steroid Biochemistry and Molecular ...
Other symptoms of androgen deficiency are similar in both sexes, such as muscle loss and physical fatigue. The androgens used ... As with men, symptoms associated with androgen deficiency are most prevalent with age, and androgen replacement therapy has ... Androgen replacement is the classic treatment of hypogonadism., It is also used in men who have lost the ability to produce ... Androgen deficiencies in women have also, as of 2001, been recognized as a medical disorder that can be treated with ART. ...
Both androgens exert their influence through binding with the androgen receptor. Androgen binds with the androgen receptor. The ... but rather are the result of androgens bound to androgen receptors; the androgen receptor mediates the effects of androgens in ... the androgen receptor is bound to heat shock proteins. These heat shock proteins are released upon androgen binding. Androgen ... certain mutant androgen receptors can function without androgens; in vitro studies have demonstrated that a mutant androgen ...
Androgen deprivation therapy Androgen insensitivity syndrome Estrogen-dependent condition Spinal bulbar muscular atrophy Joseph ... An androgen-dependent condition, disease, disorder, or syndrome, is a medical condition that is, in part or full, dependent on ... 1994-. ISBN 978-0-08-058373-0. Shukla, G. C.; Plaga, A. R.; Shankar, E.; Gupta, S. (2016). "Androgen receptor-related diseases ... and androgen-secreting tumors (gonadal or adrenal tumor). Such conditions may be treated with drugs with antiandrogen actions, ...
... s or SARMs are a class of androgen receptor ligands that maintain some of the desirable ... Kearbey JD, Gao W, Narayanan R, Fisher SJ, Wu D, Miller DD, Dalton JT (February 2007). "Selective Androgen Receptor Modulator ( ... Also, there is a relationship between Amyloid β, androgens, and circulating testosterone levels which all can affect the course ... The binding of ligands to the androgen receptor (AR) results in a conformational change, this consequentially alters surface ...
Adrenal androgen stimulating hormone (AASH), also known as cortical androgen stimulating hormone (CASH), is a hypothetical ... Parker LN (June 1991). "Control of adrenal androgen secretion". Endocrinol Metab Clin North Am. 20 (2): 401-21. doi:10.1016/ ... Adrenocorticotrophic hormone (ACTH) Anderson DC (August 1980). "The adrenal androgen-stimulating hormone does not exist". ... hormone which has been proposed to stimulate the adrenal glands to produce adrenal androgens such as dehydroepiandrosterone ( ...
"Discordant measures of androgen-binding kinetics in two mutant androgen receptors causing mild or partial androgen ... MAIS is the mildest and least known form of androgen insensitivity syndrome. The existence of a variant of androgen ... Grino PB, Griffin JE, Cushard WG, Wilson JD (April 1988). "A mutation of the androgen receptor associated with partial androgen ... Tsukada T, Inoue M, Tachibana S, Nakai Y, Takebe H (October 1994). "An androgen receptor mutation causing androgen resistance ...
Skeletal muscle androgen receptor expression increases with acute exercise in correlation to free testosterone. When comparing ... Lupo C, Baldi L, Bonifazi M, Lodi L, Martelli G, Viti A, Carli G (1985). "Androgen levels following a football match". European ... Androgens increased in response to exercise, particularly resistance, while cortisol only increased with resistance. DHEA ... SHBG is protective against DHT as it binds free androgen. In acute assessment of hormone levels in soccer players before, ...
... mild androgen insensitivity syndrome (MAIS) when the external genitalia is that of a typical male, and partial androgen ... "A novel mutation c.118delA in exon 1 of the androgen receptor gene resulting in complete androgen insensitivity syndrome within ... "A frame shift mutation in the DNA-binding domain of the androgen receptor gene associated with complete androgen insensitivity ... and genetic characteristics of androgen insensitivity syndrome in a Brazilian cohort: five novel mutations in the androgen ...
... (or ADIS) refers to the induction of cellular senescence as a result of androgen ... ADIS is observed in prostate cancer cells that are dependent on androgens for cell proliferation. Androgen withdrawal induces ... "Androgen Deprivation-Induced Senescence Promotes Outgrowth of Androgen-Refractory Prostate Cancer Cells". PLOS ONE. 8 (6): ... Ewald, JA; Desotelle, JA; Church, DR; Yang, B; Huang, W; Laurila, TA; Jarrard, DF (March 2013). "Androgen deprivation induces ...
This is a list of androgen esters, including esters (as well as ethers) of natural androgens like testosterone and ... CS1 Russian-language sources (ru), Articles with short description, Short description is different from Wikidata, Androgen ... 17β-tetrahydropyran ether of the 17α-demethylated analogue of stanozolol List of androgens/anabolic steroids List of estrogen ... and Clinical Applications of Androgens: Current Status and Future Prospects. John Wiley & Sons. pp. 471-. ISBN 978-0-471-13320- ...
"Discordant measures of androgen-binding kinetics in two mutant androgen receptors causing mild or partial androgen ... Partial androgen insensitivity syndrome is diagnosed when the degree of androgen insensitivity in an individual with a 46,XY ... "Androgen insensitivity syndrome: somatic mosaicism of the androgen receptor in seven families and consequences for sex ... androgen receptor binding, and mutational analysis in 278 clinical cases reported as androgen insensitivity syndrome". J. Clin ...
A selective androgen receptor degrader or downregulator (SARD) is a type of drug which interacts with the androgen receptor (AR ... Androgen deprivation therapy Lai, AC; Crews, CM (25 November 2016). "Induced protein degradation: an emerging drug discovery ... They are under investigation for the treatment of prostate cancer and other androgen-dependent conditions. As of 2017, ...
... is a protein in humans that is encoded by the ADTRP gene. GRCh38: Ensembl release 89 ... "Entrez Gene: Androgen-dependent TFPI-regulating protein". Retrieved 2013-02-07. v t e (Articles with short description, Short ...
Ovarian overproduction of androgens is a condition in which the ovaries make too much testosterone. This leads to the ... Ovarian overproduction of androgens is a condition in which the ovaries make too much testosterone. This leads to the ... Androgen excess in women. In: Gershenson DM, Lentz GM, Valea FA, Lobo RA, eds. Comprehensive Gynecology. 8th ed. Philadelphia, ... Tumors in the adrenal glands can also cause too much production of androgens and can lead to male body characteristics in women ...
Androgen. Class Summary. Exogenous androgen (testosterone) is the treatment of choice for many aspects of Klinefelter syndrome. ... Androgen replacement therapy is used to correct androgen deficiency, to provide appropriate virilization, and to improve ... Positive effects of early androgen therapy on the behavioral phenotype of boys with 47,XXY. Am J Med Genet C Semin Med Genet. ... Androgen Treatment Effects on Motor Function, Cognition, and Behavior in Boys with Klinefelter Syndrome. J Pediatr. 2017 Mar 10 ...
Partial androgen insensitivity syndrome (PAIS) is a genetic (inherited) condition that occurs when the body cant respond to ... male sex hormones (androgens). Testosterone is a male sex hormone. ... PAIS is a type of androgen insensitivity syndrome. Androgen insensitivity syndrome is one of the conditions that are described ... It also depends on the levels of androgens. In a baby with XY chromosomes, high levels of androgens are made in the testes. ...
... and androgens (57852) is part of a group of 46 such profiles that provide information about chemicals or industrial processes ... This information profile on estrogens (57636) and androgens (57852) is part of a group of 46 such profiles that provide ...
Androgens. Class Summary. Androgens are primarily of benefit in men with low levels of serum testosterone (hypogonadism). Men ... Foresta C, Caretta N, Rossato M, Garolla A, Ferlin A. Role of androgens in erectile function. J Urol. 2004 Jun. 171(6 Pt 1): ... Androgens and penile erection: evidence for a direct relationship between free testosterone and cavernous vasodilation in men ... Morales A, Johnston B, Heaton JW, Clark A. Oral androgens in the treatment of hypogonadal impotent men. J Urol. 1994 Oct. 152(4 ...
Find out about androgen insensitivity syndrome (AIS), a rare condition that affects the development of a persons genitals and ... The 2 types of AIS are called complete androgen insensitivity syndrome (CAIS) and partial androgen insensitivity syndrome (PAIS ... Androgen insensitivity syndrome (AIS) affects the development of a persons genitals and reproductive organs. ... complete androgen insensitivity syndrome (CAIS) - where testosterone has no effect on sex development, so the genitals are ...
Metabolomic analysis identifies androgens as a biomarker in dry eye. ... "The exciting discov-ery that androgen deficiency seems to be associated with DED, along with other work in this area, may lead ... Three other molecules involved in androgen metabolism were also lower in the subjects with DED but did not attain metabolome- ... found an association between DED and decreased serum androgens.2 Although smaller studies by other groups have suggested a ...
Androgen Deprivation Therapy for Advanced Prostate Cancer on the Ground of Androgen Milieu in the Prostate. (Tsutomu Nishiyama ... Clinical Model of Androgen Deficiency - Androgen Deprivation Therapy and its Effect on Bone Metabolism, Metabolism and ... Androgens, Androgen Suppression, and Prostate Cancer: Recent Preclinical and Clinical Findings and Implications. (Jeanny B. ... In this book, the authors present current research in the study of androgens including androgen deprivation therapy for ...
WHO Special Programme of Research, Development and Research Training in Human Reproduction & Workshop Conference on Androgen ... Appendix: Consensus report / Workshop Conference on Androgen Therapy : Biologic and Clinical Consequences, 17 - 20 January 1990 ... 1992)‎. Guidelines for the use of androgens in men. World Health Organization. ...
Pharmacological Actions : Androgen Antagonists, Antiproliferative , Wnt/β-catenin signaling pathway modulation. Additional ... 6 Abstracts with Androgen Antagonists Research. Filter by Study Type. Animal Study. ... A novel dietary flavonoid fisetin inhibits androgen receptor signaling and tumor growth in athymic mice. Oct 15, 2008. ... A compound within Pygeum bark antagonizes human androgen receptor in the prostate gland. Sep 23, 2009. ...
Since the landmark discovery by Huggins and Hodges, gonadal depletion of androgens has remained a mainstay of therapy for ... The androgen-signaling axis plays a pivotal role in the pathogenesis of prostate cancer. ... Androgen Signaling in Prostate Cancer April 11, 2017 The androgen-signaling axis plays a pivotal role in the pathogenesis of ... Since the landmark discovery by Huggins and Hodges, gonadal depletion of androgens has remained a mainstay of therapy for ...
... called androgens). As a result, the person has some of ... Androgen insensitivity syndrome (AIS) is when a person who is ... Androgen insensitivity syndrome (AIS) is when a person who is genetically male (who has one X and one Y chromosome) is ... Other blood tests may be done to help tell the difference between AIS and androgen deficiency. ... resistant to male hormones (called androgens). As a result, the person has some of the physical traits of a woman, but the ...
... notably androgens and oestrogens - promote breast tumour development. In spite of this evidence, postmenopausal androgen ... The results from this study caution against the use of DHEA(S), or other androgens, for postmenopausal androgen replacement ... For the androgens, relative risk estimates (95% confidence intervals) between the top and bottom quintiles of the exposure ... Postmenopausal serum androgens, oestrogens and breast cancer risk: the European prospective investigation into cancer and ...
... a repeat disorder caused by polyglutamine-expanded androgen receptor (polyQ-AR). We found that polyQ-AR reduced long-term ... is a neurodegenerative disorder that results from a polyglutamine repeat expansion in the androgen receptor (polyQ-AR). In this ... Loss of endogenous androgen receptor protein accelerates motor neuron degeneration and accentuates androgen insensitivity in a ... Polyglutamine-expanded androgen receptor interferes with TFEB to elicit autophagy defects in SBMA. *Constanza J Cortes1 na1, ...
Androgen Replacement Therapy Market Androgen replacement therapy or low testosterone therapy is commonly called as hormone ... Androgen Replacement Therapy Market: Making New Commitments ..., MENAFN.COM. .navbar-collapse.collapse { display: block ! ... Androgen Replacement Therapy Market. Androgen replacement therapy or low testosterone therapy is commonly called as hormone ... Androgen Replacement Therapy Market: Making New Commitments To The Sustainable Future , Abbvie, Bayer, Simple Pharma,. ...
Learn about the signs and symptoms of androgen insensitivity syndrome, what causes it, and how its diagnosed and treated at ... Androgen insensitivity syndrome is a genetic condition which affects a childs sexual development before birth and during ... In partial androgen insensitivity syndrome, the body responds partially to androgen. Partial androgen insensitivity occurs at ... In complete androgen insensitivity syndrome, the body does not respond to androgen at all. This form of the syndrome occurs in ...
... Does this test have other names?. FAI. What is this test?. A free androgen index (FAI) is a ratio figured ... For example, androgens play a role in making the female hormone estrogen. When a woman makes too many androgen hormones, she ... Its used to see whether you have abnormal androgen levels.. Both men and women make male hormones called androgens, which ... With too little androgen hormones, a woman may become very tired, lose bone mass, or have little interest in sex. ...
What drew you to study androgen-indifferent prostate cancer in particular?. Viscuse: I became interested in androgen- ... Androgen indifference has been classically associated with variant histology, such as small cell or neuroendocrine prostate ... Paul Viscuse, MD, on Androgen-Indifferent Prostate Cancers. - He received JCOs 2021 Conquer Cancer Young Investigator Award ... What are some of the chief variants of androgen indifferent prostate cancer, and how common are they? ...
Female external anatomy is the default pathway of development, while male genital development requires testicular testosterone plus dihydrotestosterone made in genital skin. This Primer explores recent evidence that an additional backdoor pathway to masculinization involves androsterone, derived from placental progesterone.
Extending the duration of androgen suppression in men with intermediate-risk prostate cancer prior to radiotherapy led to more ... 1 to either 8 weeks of androgen suppression then radiotherapy with an additional 8 weeks of concurrent androgen suppression for ... noted that the question of whether the shorter androgen suppression regimen is sufficient or whether any androgen suppression ... Extending the duration of androgen suppression from 8 weeks to 28 weeks prior to radiotherapy led to more sexual and endocrine ...
Androgens flashcards from Nicole Pritchard's St. Georges University class online, or in Brainscape's iPhone or Android ... Gonadal Hormones: Androgens Flashcards Preview Pharm: Final Exam Drugs , Gonadal Hormones: Androgens , Flashcards ... over dosage of androgens can result in feminization as a result of negative feedback inhibition and conversion of exogenous ... Its an androgen derivative, a partial agonist of progestin and glucocorticoid receptors Used in endometriosis and fibrocystic ...
Highly specific and rigorously validated in-house, Androgen Receptor (E3S4N) Rabbit Monoclonal Antibody (Carboxy-terminal ... Monoclonal Antibody for studying Androgen Receptor. Validated for WB, IP, IF. ... Androgen Receptor (E3S4N) Rabbit mAb (Carboxy-terminal Antigen) recognizes endogenous levels of total Androgen Receptor protein ... Androgen Receptor (E3S4N) Rabbit mAb (Carboxy-terminal Antigen) 70317. Toggle Between Dark and Light Modes Filter: *WB ...
Androgens. Class Summary. Certain androgenic preparations have been used historically to treat mild-to-moderate bleeding, ... Competes with androgen and progesterone at receptor level, resulting in amenorrhea within 3 mo. ...
title = "Androgen deprivation therapy complications",. abstract = "Androgen deprivation therapy (ADT) is increasingly used to ... Androgen deprivation therapy complications. Carolyn Anne Allan, Veronica Rose Collins, Mark Frydenberg, Robert I McLachlan, ... Androgen deprivation therapy (ADT) is increasingly used to treat advanced prostate cancer and is also utilised as adjuvant or ... N2 - Androgen deprivation therapy (ADT) is increasingly used to treat advanced prostate cancer and is also utilised as adjuvant ...
2 Studies found for: Recruiting, Not yet recruiting, Available Studies , Androgen Insensitivity Syndrome ...
The primary and most well-known androgen is testosterone.. Types of androgens. A subset of androgens, adrenal androgens, ... Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen ... Androgen. Print this page. Androgen is the generic term for any natural or synthetic compound, usually a steroid hormone, that ... Insensitivity to androgen in humans. Reduced ability of a XY karyotype fetus to respond to androgens can result in one of ...
Androgens, in particular testosterone, produced during pregnancy act on the brain to produce permanent gender differences in ... Few endocrine disrupting chemicals are known to act on androgens; however, triclosans and triclocarbans (TCS/TCC) have been ... Prenatal Antimicrobial Agent Exposure, Fetal Androgens and ASD Risk. *Newschaffer, Craig (PI) ...
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... explains the progress needed to better understand androgen receptors. ... An older study found that patients with elevated circulating levels of adrenal androgens responded better and longer to ... Theoretically, Mohler says, an oncologist could biopsy a patients prostate gland, measure tissue levels of androgens, and ... James Mohler, MD, Roswell Park Cancer Institute, explains the progress needed to better understand androgen receptors. ...
  • Partial androgen insensitivity syndrome (PAIS) is a genetic (inherited) condition that occurs when the body can't respond to male sex hormones (androgens). (
  • PAIS is a type of androgen insensitivity syndrome . (
  • Androgen insensitivity syndrome is one of the conditions that are described as intersex or difference of sex development (DSD). (
  • Androgen insensitivity syndrome (AIS) affects the development of a person's genitals and reproductive organs. (
  • The 2 types of AIS are called complete androgen insensitivity syndrome (CAIS) and partial androgen insensitivity syndrome (PAIS). (
  • Androgen insensitivity syndrome (AIS) is when a person who is genetically male (who has one X and one Y chromosome) is resistant to male hormones (called androgens). (
  • Androgen insensitivity syndrome is a genetic condition which affects a child's sexual development before birth and during puberty. (
  • There are two categories of androgen insensitivity syndrome: complete and partial. (
  • In complete androgen insensitivity syndrome, the body does not respond to androgen at all. (
  • In partial androgen insensitivity syndrome, the body responds partially to androgen. (
  • Partial androgen insensitivity occurs at about the same rate as complete androgen insensitivity syndrome. (
  • Infants with complete androgen insensitivity syndrome appear to be female at birth, but do not have a uterus, fallopian tubes or ovaries. (
  • Babies born with complete androgen insensitivity syndrome are typically raised as girls and have a female gender identity. (
  • Babies born with partial androgen insensitivity syndrome may have sexual characteristics that are typical of a male, a female, or both. (
  • Other symptoms of partial androgen insensitivity syndrome include failure of one or both of the testicles to descend into the scrotum after birth and an abnormal penis in which the urethra opens on the underside, instead of at the tip. (
  • In the least severe cases, the only sign of androgen insensitivity syndrome is male infertility. (
  • Androgen insensitivity syndrome is an inherited condition passed down by the mother. (
  • In androgen insensitivity syndrome, a defect on the X chromosome fully or partially blocks testosterone's effect on the body. (
  • Complete androgen insensitivity syndrome may be discovered in infancy when a testicle is felt as a mass in the groin or abdomen. (
  • Complete androgen insensitivity syndrome is treated with estrogen replacement therapy after puberty. (
  • Treatment for partial androgen insensitivity syndrome may include corrective surgery to match gender identity. (
  • Children with androgen insensitivity syndrome will become infertile as adults. (
  • Androgen insensitivity syndrome (AIS) , also known as the testicular feminization syndrome , results from end-organ resistance to androgens, particularly testosterone. (
  • 4. Yalinkaya A, Yayla M, Erdemoglu M. Prenatal diagnosis of a fetus with androgen insensitivity syndrome (AIS). (
  • Androgen insensitivity syndrome: in utero diagnosis by four-dimensional sonography and amniotic fluid karyotype. (
  • Role of imaging in the diagnosis and management of complete androgen insensitivity syndrome in adults. (
  • 8. Tank J, Knoll A, Gilet A, Kim S. Imaging characteristics of androgen insensitivity syndrome. (
  • 9. Khan S, Mannel L, Koopman CL, Chimpiri R, Hansen KR, Craig LB. The use of MRI in the pre-surgical evaluation of patients with androgen insensitivity syndrome. (
  • 10. Nezzo M, De Visschere P, T'sjoen G, Weyers S, Villeirs G. Role of imaging in the diagnosis and management of complete androgen insensitivity syndrome in adults. (
  • Babies with androgen insensitivity syndrome (AIS) will be genetically male, but will either have female genitals or an appearance between male and female genitalia. (
  • This is a case report of complete androgen insensitivity syndrome and literature review of preoperative diagnostic methods. (
  • We present a 3 years and 6 months old child with female phenotype, born in São Paulo, Brazil which was diagnosed intraoperatively with complete androgen insensitivity syndrome, during inguinal hernia repair and present potential diagnostic alternatives that we consider viable options in order to avoid this kind of surprise during surgery. (
  • The studies described below may be indicated in patients with androgen insensitivity syndrome (AIS). (
  • An elevated ratio of testosterone to DHT indicates a 5-alpha reductase deficiency, a possible differential for patients with partial androgen insensitivity syndrome but usually not for complete androgen insensitivity syndrome. (
  • It detects upwards of 95% of the mutations for complete androgen insensitivity syndrome and partial androgen insensitivity syndrome. (
  • Identification of any müllerian structures, such as uterus or fallopian tubes, is inconsistent with a diagnosis of complete androgen insensitivity syndrome or partial androgen insensitivity syndrome. (
  • Histologic examination of the testes in patients with complete androgen insensitivity syndrome or partial androgen insensitivity syndrome should show fairly normal testicular structure, although the numbers of spermatogonia and/or sperm may be reduced markedly in postpubertal patients. (
  • Oakes MB, Eyvazzadeh AD, Quint E, Smith YR. Complete androgen insensitivity syndrome--a review. (
  • Tordjman KM, Yaron M, Berkovitz A, Botchan A, Sultan C, Lumbroso S. Fertility after high-dose testosterone and intracytoplasmic sperm injection in a patient with androgen insensitivity syndrome with a previously unreported androgen receptor mutation. (
  • Bertelloni S, Dati E, Baroncelli GI, Hiort O. Hormonal management of complete androgen insensitivity syndrome from adolescence onward. (
  • Androgen Insensitivity Syndrome: Management Considerations from Infancy to Adulthood. (
  • Androgen insensitivity syndrome can be inherited as an X linked disorder as evidenced by previousstudies. (
  • Androgen insensitivity syndrome (AIS), also linked to the chromosome Xq11 - 123, known as testicular feminization syndrome1, which is the gene encoding the androgen includes a widely varied group of mutations receptor, of a genetically male individual that is related to androgen receptor (46 XY)3,4. (
  • While awaiting these results, "withholding androgen deprivation therapy in men with favorable intermediate-risk prostate cancer and adding 4 or 6 months of androgen deprivation therapy to radiotherapy in men with unfavorable intermediate-risk prostate cancer are reasonable options based on the available evidence," concludes D'Amico. (
  • Androgen deprivation therapy (ADT) is increasingly used to treat advanced prostate cancer and is also utilised as adjuvant or neo-adjuvant treatment for high-risk disease. (
  • Hormone therapy, also known as androgen deprivation (or suppression) therapy, is designed to block male hormones (particularly testosterone) from stimulating the growth of prostate cancer. (
  • Long-Term Androgen Deprivation Associated with Improved Survival in Prostate Cancer Patients with High PSA Levels. (
  • What Is Androgen Deprivation Therapy (ADT)? (
  • Androgen deprivation therapy (ADT) is a prostate cancer treatment that suppresses the production of testosterone (a type of androgen or male sex hormone) in a person's body. (
  • Hormone Therapy for Prostate Cancer (Androgen Deprivation Therapy, or ADT). (
  • In a small study, high-dose testosterone given intermittently with androgen deprivation therapy lowered PSA levels without serious adverse effects. (
  • All patients received a 6-month androgen deprivation therapy (ADT) lead-in. (
  • Early androgen deprivation for prostate cancer? (
  • Background: Androgens are key regulators of prostate gland maintenance and prostate cancer growth, and androgen deprivation therapy has been the mainstay of treatment for advanced prostate cancer for many years. (
  • THURSDAY, May 28, 2015 (HealthDay News) - Primary androgen deprivation therapy increases diabetes risk, particularly in men under 70 years of age, according to research published in the June issue of The Journal of Urology . (
  • Primary androgen deprivation therapy was characterized as occurring within one year of diagnosis. (
  • The respective incidence rates were 2.5 and 1.6 events per 100 person-years in the primary androgen deprivation therapy and nonprimary androgen deprivation therapy groups. (
  • There was a 1.61-fold increase in diabetes risk with primary androgen deprivation therapy. (
  • Primary androgen deprivation therapy may increase diabetes risk by 60 percent and should be used with caution when managing localized prostate cancer," the authors write. (
  • Because of the consistent association between androgen deprivation therapy and greater diabetes risk across disease states, we recommend routine screening and lifestyle interventions to reduce the risk of diabetes in men receiving androgen deprivation therapy. (
  • Some men who are initially responsive to potent androgen-deprivation therapy develop gradually progressive disease with bone and lymph node metastases and rising PSA," she said. (
  • They may even become worse on potent androgen-deprivation therapy. (
  • And while it rarely arises de novo, the amount of neuroendocrine differentiation of prostate adenocarcinoma increases with disease progression and in response to androgen-deprivation therapy. (
  • Beltran and colleagues have written that treatment-related neuroendocrine prostate cancer should be suspected in patients with castration-resistant prostate cancer who experience rapid progression with a low serum PSA, especially in the setting of potent androgen deprivation therapies ( JCO 2012;36:e386-e389 ). (
  • The Phase III study ARASENS will evaluate the compound in combination with standard androgen deprivation therapy (ADT) and the chemotherapy docetaxel in men with newly diagnosed metastatic hormone-sensitive prostate cancer (mHSPC), who are starting first line hormone therapy. (
  • ARASENS (A Randomized, double-blind, placebo-controlled Phase III study of ODM-201 versus placebo in addition to standard Androgen deprivation therapy and docetaxel in patients with metastatic castration SENSitive prostate cancer) is planned to be initiated towards the end of 2016. (
  • Androgen deprivation therapy and other therapies targeting the androgen pathway may result in changes in the uptake of gallium Ga 68 PSMA-11 in prostate cancer. (
  • Although androgen deprivation therapy (ADT) has been the standard treatment, Concepcion noted that new evidence suggests this patient could benefit from a more aggressive approach. (
  • Ovarian overproduction of androgens is a condition in which the ovaries make too much testosterone . (
  • Exogenous androgen (testosterone) is the treatment of choice for many aspects of Klinefelter syndrome. (
  • Children with PAIS will be brought up either as girls or boys, depending mostly on the extent to which their body responds to hormones (androgens), including testosterone. (
  • In spite of this evidence, postmenopausal androgen replacement therapy with dehydroepiandrosterone (DHEA) or testosterone has been advocated for the prevention of osteoporosis and improved sexual well-being. (
  • For the androgens, relative risk estimates (95% confidence intervals) between the top and bottom quintiles of the exposure distribution were: DHEAS 1.69 (1.23-2.33), androstenedione 1.94 (1.40-2.69), testosterone 1.85 (1.33-2.57) and free testosterone 2.50 (1.76-3.55). (
  • Androgen replacement therapy or low testosterone therapy is commonly called as hormone replacement therapy for men. (
  • A free androgen index (FAI) is a ratio figured out after a blood test for testosterone. (
  • Both men and women make male hormones called androgens, which include testosterone. (
  • A free androgen index measures testosterone in your blood and compares it with the total amount of testosterone and SHBG in your body. (
  • This is an androgen deficiency that causes testosterone levels to drop. (
  • The primary and most well-known androgen is testosterone. (
  • While androstenediones are converted metabolically to testosterone and other androgens, they are also the parent structure of estrone. (
  • Androsterone: a chemical by-product created during the breakdown of androgens, or derived from progesterone, that also exerts minor masculinising effects, but with one-seventh the intensity of testosterone. (
  • Dihydrotestosterone (DHT): a metabolite of testosterone that is actually a more potent androgen in that it binds more strongly to androgen receptors. (
  • Androgen action in target tissues often involves conversion of testosterone to 5α-dihydrotestosterone (Dihydrotestosterone). (
  • Androgens, in particular testosterone, produced during pregnancy act on the brain to produce permanent gender differences in structure and function. (
  • About 90% of a man's androgens are made in the testicles, so removing these organs causes testosterone levels to drop. (
  • Bipolar androgen therapy (BAT)-the intermittent use of high-dose testosterone therapy-is safe and possibly effective in patients with advanced hormone-sensitive prostate cancer (PCa) , according to findings of a small study that will be presented at the 2016 Genitourinary Cancers Symposium. (
  • Abiraterone inhibits cytochrome P450 17A1 (CYP17A1), an enzyme responsible for the synthesis of testosterone that, after conversion to dihydrotestosterone (DHT), binds to the androgen binding site (ABS) of the AR and activates the AR signaling axis. (
  • The androgen testosterone (17 -hydroxyandrostenone) has a molecular weight of 288 daltons. (
  • Androgens are the male sex hormones, and Testosterone is the benchmark when it comes to androgenic and anabolic rating. (
  • Testosterone belongs to the class of medications called androgens (male hormones). (
  • Androgens are male sex hormones, such as testosterone, that are present in both men and women, but men naturally have much higher levels than women. (
  • Androgen is the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates by binding to androgen receptors. (
  • James Mohler, MD, Roswell Park Cancer Institute, explains the progress needed to better understand androgen receptors. (
  • James Mohler, MD, Associate Director and Senior-Vice President for Translational Research, Chair, Department of Urology, Professor of Oncology, Roswell Park Cancer Institute, explains the progress needed to better understand androgen receptors. (
  • Steroid receptors and hormone action: physiological and synthetic androgens and progestins can mediate inappropriate biological effects. (
  • In the present study, we examine whether blockade of androgen receptors at the target musculature would prevent the neuroprotective effects of exercise on dendrites following partial motoneuron depletion. (
  • While all SARMs work by targeting the androgen receptors, some have somewhat different outcomes that might be better matched for weight loss, muscle gain, healing , endurance or hunger. (
  • Tabb , JS et al "Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors. (
  • Androgen replacement therapy is used to correct androgen deficiency, to provide appropriate virilization, and to improve psychosocial status. (
  • Since the landmark discovery by Huggins and Hodges, gonadal depletion of androgens has remained a mainstay of therapy for advanced disease. (
  • The results from this study caution against the use of DHEA(S), or other androgens, for postmenopausal androgen replacement therapy. (
  • 𝐂𝐨𝐡𝐞𝐫𝐞𝐧𝐭 𝐌𝐚𝐫𝐤𝐞𝐭 𝐈𝐧𝐬𝐢𝐠𝐡𝐭𝐬 launched a new market study on the 2022-2028 Androgen Replacement Therapy market that includes easy-to-understand detailed analysis and 100+ market data tables, pie chats, graphs, and figures distributed across pages. (
  • The results of the Radiation Therapy Oncology Group (RTOG) 9910 trial suggest that an 8-week schedule of androgen suppression should remain the standard of care for these patients. (
  • The open-label trial randomized 1,489 prostate cancer patients 1:1 to either 8 weeks of androgen suppression then radiotherapy with an additional 8 weeks of concurrent androgen suppression for a total of 16 weeks of therapy or to 28 weeks of androgen suppression followed by radiotherapy plus an additional 8 weeks of androgen suppression for a total of 36 weeks. (
  • Prostate cancer cells which are not dependent on male hormones and therefore do not respond to hormonal therapy (also known as androgen-insensitive cells). (
  • The combination of radiation therapy plus long-term androgen suppression for two or more years has been shown to improve overall survival in patients with locally advanced prostate cancer. (
  • The study included 970 men who had received external beam radiation therapy along with six months of androgen suppression. (
  • Sometimes, ADT is also referred to as androgen suppression therapy or hormone therapy for prostate cancer. (
  • Unfortunately, patients with advanced PCa either do not respond to anti-androgen therapy due to pre-existing aberrations of CYP17, or AR or relapse to CRPC due to adaptive responses, or Darwinian selection of rare aberrations. (
  • Whether combined CsA with androgen therapy was superior to androgen therapy alone in NSAA remains controversial. (
  • This study aimed to assess the efficacy and safety of combined therapy versus androgen therapy for NSAA patients using a meta-analytic approach. (
  • This study found that combined CsA with androgen therapy was superior to androgen therapy alone for Chinese patients with NSAA, and the most common adverse of combined therapy included hirsutism , handshake, gingiva hyperplasia , liver function damage, and renal function damage. (
  • Tumors in the adrenal glands can also cause too much production of androgens and can lead to male body characteristics in women. (
  • Since DHEAS and androstenedione are largely of adrenal origin in postmenopausal women, our results indicated that elevated adrenal androgen synthesis is a risk factor for breast cancer. (
  • A subset of androgens, adrenal androgens, includes any of the 19-carbon steroids synthesized by the adrenal cortex, an adrenal gland, that function as weak steroids or steroid precursors, including dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione. (
  • An older study found that patients with elevated circulating levels of adrenal androgens responded better and longer to ketoconazole. (
  • It has been demonstrated that mutations in the ABS of the AR can lead to its activation by weak adrenal androgens, steroidal and non-steroidal ligands, and by mutation-driven conversion of AR inhibitors into agonists [ 13 ]. (
  • Tumors of the ovaries and polycystic ovary syndrome (PCOS) can both cause too much androgen production. (
  • Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome. (
  • OBJECTIVE: To investigate the effects of a low-dose ketoconazole on ovarian steroidogenesis and on serum androgen levels in polycystic ovary syndrome (PCOS). (
  • Positions statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. (
  • The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. (
  • We are particularly focused on understanding how brain wiring and communication is altered in Polycystic Ovary Syndrome (PCOS), a common endocrine disorder characterised by androgen excess. (
  • Many men with metastatic prostate cancer experience an indolent disease course with long-term survival following prolonged responses to systemic therapies, most of which are directed towards disrupting androgen receptor (AR) signaling. (
  • The exciting discov-ery that androgen deficiency seems to be associated with DED, along with other work in this area, may lead sci-entists to developing hormone-based treatments for DED. (
  • Other blood tests may be done to help tell the difference between AIS and androgen deficiency. (
  • Here, we edited the androgen receptor gene ( AR ), which is associated with male reproductive behavior in zebrafish, using TAL effector nucleases (TALENs), and tested whether modifications at the AR impacted courtship during mating trials. (
  • The RTOG 0815 trial will address whether 6 months of androgen suppression can reduce prostate cancer mortality in men with unfavorable intermediate-risk prostate cancer who are treated with high-dose radiotherapy, and whether high-dose radiotherapy alone is enough to minimize prostate cancer mortality. (
  • A second analysis, of the Grupo de Investigación ClÃ-nica en OncologÃ-a Radioterápica (GICOR) R17 trial will ask whether 4 months of androgen suppression along with high-dose radiotherapy can decrease prostate cancer mortality in men with intermediate-risk, unfavorable prostate cancer. (
  • Estrogens and androgens. (
  • This information profile on estrogens (57636) and androgens (57852) is part of a group of 46 such profiles that provide information about chemicals or industrial processes considered to be potential occupational hazards. (
  • Androgens are also the original anabolic steroids. (
  • its prevalence amongst young men and teenagers using androgens and/or anabolic steroids (AASs) is rising fast, and those affected can experience significant symptoms. (
  • Before the production of the pituitary hormone LH by the embryo starting at about weeks 11-12, human chorionic gonadotrophin (hCG) promotes the differentiation of Leydig cells and their production of androgens. (
  • In a baby with XY chromosomes, high levels of androgens are made in the testes. (
  • Thought to carry an X linked recessive inheritance 3 where multiple mutations in the androgen receptor (AR) gene has been localized to the long arm of the X chromosome (i.e. (
  • Along-standing hypothesis has been that inherited variation in the androgen receptor (AR) gene plays a role in prostate cancer initiation. (
  • Mutation analysis of the androgen receptor gene is now commercially available. (
  • Altered Theca and Cumulus Oocyte Complex Gene Expression, Follicular Arrest and Reduced Fertility in Cows with Dominant Follicle Follicular Fluid Androgen Excess Summers et al. (
  • This happens because a mutation on the X chromosome causes the body to resist androgen, the hormones that produce a male appearance. (
  • When a woman makes too many androgen hormones, she may develop extra body and facial hair. (
  • With too little androgen hormones, a woman may become very tired, lose bone mass, or have little interest in sex. (
  • Androgens, which were first discovered in 1936, are also called androgenic hormones or testoids. (
  • The Leydig cells can be viewed as producers of androgens that function as paracrine hormones required by the Sertoli cells in order to support sperm production. (
  • Describes the ability of tumor cells to grow in the absence of androgens (hormones that promote the development and maintenance of male sex characteristics). (
  • Extending the duration of androgen suppression in men with intermediate-risk prostate cancer prior to radiotherapy led to more adverse events and did not improve outcomes. (
  • The current trial was a clinical follow-up on the observation in animal models that prolonged androgen suppression prior to radiotherapy can improve prostate cancer outcomes. (
  • In an accompanying editorial , Anthony V. D'Amico, MD, of the Brigham and Women's Hospital and Dana-Farber Cancer Institute in Boston, noted that the question of whether the shorter androgen suppression regimen is sufficient or whether any androgen suppression is necessary in men with either favorable or unfavorable intermediate-risk prostate cancer is still an open question. (
  • Short-term androgen suppression produces inferior survival compared with long-term androgen suppression in the treatment of locally advanced prostate cancer, according to the results of a study published in the New England Journal of Medicine . (
  • However, long-term androgen suppression can also reduce quality of life and cause side effects such as impotence, hot flashes, and an increased risk of bone fractures. (
  • Researchers affiliated with the European Organization for Research and Treatment of Cancer (EORTC) conducted a study to evaluate whether short-term androgen suppression would achieve the same survival as long-term androgen suppression yet preserve quality of life. (
  • The men were then randomly assigned to receive either no further treatment (short-term suppression) or to receive 2.5 more years of androgen suppression (long-term suppression). (
  • They concluded that radiation plus short-term androgen suppression is inferior to radiation plus long-term androgen suppression for the treatment of locally advanced prostate cancer. (
  • Duration of androgen suppression in the treatment of prostate cancer. (
  • All current non-steroidal AR antagonists, such as hydroxyflutamide, bicalutamide, and enzalutamide, target the androgen binding site of the receptor, competing with endogenous androgenic steroids. (
  • [ 6 ] Moreover, mainstream academic endocrinology rather lost credibility with the 'performance-enhancement community' in the 1980s and 1990s, by persisting overlong in (a) doubting whether further enhancement of athletic performance could be achieved through raising serum T levels above the physiological reference range and (b) questioning whether any therapeutic separation of androgenic and anabolic actions was achievable, due to the single androgen receptor. (
  • Although all genomic AAS actions are ultimately transduced by ligand binding to the androgen receptor, selectivity of signalling towards anabolic vs androgenic pathways is mediated by an interacting web of molecular chaperones, co-activators/-repressors and transcription factors. (
  • It is a rare recessive genetic disorder linked to the X chromosome that results in different mutations in the androgen receptor. (
  • For example, androgens play a role in making the female hormone estrogen. (
  • This action of androgens is supported by a hormone from Sertoli cells, AMH, which prevents the embryonic Müllerian ducts from developing into fallopian tubes and other female reproductive tract tissues in male embryos. (
  • Both prostate gland development and tumorigenesis rely on the activity of a steroid hormone receptor family member, the androgen receptor (AR). (
  • A Large Study of Androgen Receptor Germline Variants and Their Relation to Sex Hormone Levels and Prostate Cancer Risk. (
  • Neuroendocrine prostate cancer does not express the androgen receptor and it's considered clinically hormone refractory. (
  • One such example came early this year when a study of serum metabolites in a British popula-tion-based sample (n = 2,819) found an association between DED and decreased serum androgens. (
  • For all sex steroids -the androgens as well as the oestrogens - elevated serum levels were positively associated with breast cancer risk, while SHBG levels were inversely related to risk. (
  • Our results have shown that, among postmenopausal women, not only elevated serum oestrogens but also serum androgens are associated with increased breast cancer risk. (
  • Partial androgen insensitivity may be diagnosed at birth because of the presence of male and female sexual traits. (
  • Furthermore, systemic treatment with supplemental androgens is neuroprotective, and dendritic atrophy following partial motoneuron depletion is attenuated. (
  • We have recently shown that exercise is also neuroprotective on motoneuron dendrites following partial motoneuron depletion, and circulating levels of androgens have previously been shown to increase following exercise. (
  • Early data suggests that following partial motoneuron depletion, exercised males with androgen receptor blockade at the quadriceps show dendritic lengths that are significantly shorter than those of exercised males with no treatment, while dendritic lengths in exercised males with interscapular implants do not differ from those of exercised animals without implants. (
  • Mild, partial or complete clinical dysfunction2 and resistance of target tissues entities depend on the degree of androgen to the action of male hormones3. (
  • Efforts to understand the mechanisms behind CRPC have revealed new insights into dysregulated androgen signaling and intratumoral androgen synthesis, which has ultimately led to the development of several novel androgen receptor (AR)-directed therapies for CRPC. (
  • These cancers are resistant to therapies that target androgen receptor signaling, and there is a lack of alternative therapies effective against AIPC. (
  • Therapies for advanced prostate cancer aim to block androgen receptor (AR) action. (
  • Three other molecules involved in androgen metabolism were also lower in the subjects with DED but did not attain metabolome-wide statistical significance. (
  • Considerable experimental and epidemiological evidence suggests that elevated endogenous sex steroids - notably androgens and oestrogens - promote breast tumour development. (
  • Halotestin acts as an endogenous androgen. (
  • When the body is supplied with endogenous androgen, it promotes the growth of male sex organs and builds the sex characteristics in men. (
  • The study authors suggested that PCOS-specific factors like androgen excess could be driving increased metabolic risk in women with PCOS, rather than obesity alone. (
  • We found that women with PCOS and hirsutism, a clinical feature of androgen excess, had a further increased risk of dysglycaemia,' they noted. (
  • Excess facial and body hair in PCOS is usually the result of excess androgens in your body. (
  • Immunoprecipitation of Androgen Receptor from LNCaP cell extracts. (
  • We also show that higher concentrations of BPA block proliferation of AR-positive, androgen-dependent prostate adenocarcinoma cells (LNCaP and LAPC-4), with a more modest inhibitory effect on androgen-independent cells (22Rv-1). (
  • Enzalutamide is a potent anti-androgen that competes with DHT and binds to the ABS, preventing AR transcriptional activation. (
  • With the introduction of new highly potent androgen receptor-targeted agents into the clinic, such as abiraterone acetate, treatment-related neuroendocrine prostate cancer is becoming an even more important disease to recognize. (
  • In this new era of potent androgen receptor-targeted drugs, there is an evolving change in the clinical landscape of advanced prostate cancer, and we believe there is potential to drive tumors toward this more virulent form of prostate cancer. (
  • Androgens have diverse effects at both a physiological and behavioral level. (
  • In physiological concentrations, androgens have no specific effects in women. (
  • During puberty, androgen, LH and FSH production increase and the sex cords hollow out, forming the seminiferous tubules, and the germ cells start to differentiate into sperm. (
  • Studies have also found that losing weight helps improve insulin resistance (the main driver of ovarian androgen production). (
  • Androgens from other parts of the body can also cause male characteristics to develop in women. (
  • Male-typical courtship, spawning behavior, and olfactory sensitivity are induced to different extents by androgens in the goldfish suggesting they are controlled by different neuroendocrine mechanisms. (
  • Soon after they differentiate, Leydig cells begin to produce androgens which are required for masculinization of the developing male fetus (including penis and scrotum formation). (
  • IR leads to high insulin levels which trigger the ovaries to over-produce androgens. (
  • Simultaneously, some saporin-injected rats were given implants of the androgen receptor antagonist hydroxyflutamide, either directly at the quadriceps musculature or interscapularly as a systemic control. (
  • We analyzed by immunohistochemistry the expression of B7-H3, PD-L1/B7-H1, and androgen receptor (AR) in tissue samples from 120 prostate adenocarcinoma patients treated with radical prostatectomy in Spain, and from 206 prostate adenocarcinoma patients treated with radical prostatectomy in Norway. (
  • The efficacy and safety of cyclosporine A plus androgen versus androgen alone for adult patients with non-severe aplastic anemia in China: a meta-analysis of randomized controlled trials. (
  • Androgen excess in women: experience with over 1000 consecutive patients. (
  • It also depends on the levels of androgens. (
  • In a baby with XX chromosomes, there are no testes and the levels of androgens are very low. (
  • and the relationship between androgen levels and diverse cognitive abilities and social behavior in childhood. (
  • It's used to see whether you have abnormal androgen levels. (
  • You may need this test if you show signs of abnormal androgen levels, which differ in women and men. (
  • Theoretically, Mohler says, an oncologist could biopsy a patient's prostate gland, measure tissue levels of androgens, and determine which anti-androgen agent would work best. (
  • Here, we show that BPA cooperates with androgen to activate AR-T877A as shown by both reporter assays and increased levels of prostate-specific antigen expression. (
  • Chronic use of opiates has long been associated with multiple side effects, many of which are due to lower levels of androgens in this patient population. (
  • WHIPPANY, N.J., June 3, 2016 -- (Healthcare Sales & Marketing Network) -- Bayer and Orion Corp oration today announced the expansion of the global clinical development program for the investigational androgen receptor (AR) antagonist BAY-1841788 (ODM-201) in the area of prostate cancer. (
  • However, progression to castration-resistant prostate cancer (CRPC) typically follows and is largely the result of restored androgen signaling. (
  • Blockade of the androgen receptor at the target muscle prevents the neuroprotective effects on motoneuron dendrites in rats treated with supplemental androgens. (
  • A novel dietary flavonoid fisetin inhibits androgen receptor signaling and tumor growth in athymic mice. (
  • We have shown previously that a known xenoestrogen, bisphenol A (BPA), activates a tumor-derived AR mutant ( T877A ), leading to androgen-independent prostate cancer cell proliferation. (
  • Anna C. Ferrari, MD, Co-Director of the Genitourinary Cancer Program at NYU Langone Medical Center, who was co-moderator of the GU oncology session at the meeting, said that it is becoming apparent that as a prostate cancer tumor evolves to become castration resistant, it then evolves beyond the targeting of the androgen- receptor agents. (