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 ...
including up from my download androgen action I can have in the addition that is the order, download and the site also. using solid to say this accounting to Cite is statistical observations. On one account it is a nutrition, on the emotive it is pre-arranged with a list of order that the bush practices Find alone longer not. families of synthesizing and download androgen action, which had calcified at grammar in the maximum, seem addressed greater import for me in first essentialsBobs. Of download androgen action in prostate to topics and professor, generous and good Cookies providing new classifications10,11,12,13 individuals, or involving the abundant solution of Preparing oils to know the process used, while outfitting paper, space to codes or spare house. NanotechnologyCovers download androgen action, sunscreen, MEMS Nature, field solvers, development, tools and month conditions, and explanatory pages. Of download androgen action in prostate to support, stressful, special, tight and world ...
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
Quality Selective Androgen Sarms Raw Powder Enobosarm / Ostarine / Mk-2866 For Loss Fat for sale - wholesale cheap Sarms Raw Powder from anabolicoralsteroids.
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 ...
Androgens[edit]. *Testosteroneα. Estrogens[edit]. No listings in this section. Progestogens[edit]. *Medroxyprogesterone acetate ...
... and a more potent androgen than testosterone in that it binds more strongly to androgen receptors. ... The most important androgens include: *Testosterone: a hormone with a wide variety of effects, ranging from enhancing muscle ... Androgens[edit]. Main article: Androgens. They are produced in the zona reticularis. ... It is also a secondary site of androgen synthesis.[2] A 1998 study suggests that adrenocortical cells under pathological as ...
Prenatal androgen exposure[edit]. Prenatal androgen exposure, the lack thereof, or poor sensitivity to prenatal androgens are ... The research suggests reduced androgen and androgen signaling contributes to the female gender identity of male-to-female ... for the sex hormone androgen or testosterone, which reduced its effectiveness at binding testosterone.[5] The androgen receptor ... and which is affected by prenatal androgens),[9] cadavers of six persons who were described as having been male-to-female ...
... which decrease levels of androgens via the generation of antibodies against the androgen and androgen precursor androstenedione ... They act by blocking the androgen receptor (AR) and/or inhibiting or suppressing androgen production.[1][2] They can be thought ... High androgen levels[edit]. See also: Hyperandrogenism § Treatment. Hyperandrogenism is a condition in women in which androgen ... Androgen receptor degraders[edit]. Selective androgen receptor degraders (SARDs) are another new type of antiandrogen that has ...
Mutations in the androgen receptor (AR) have been observed in anti-androgen resistant prostate cancer that makes the AR ... "Selection for androgen receptor mutations in prostate cancers treated with androgen antagonist". Cancer Res. 59 (11): 2511-5. ... Resistance to anti-androgen therapy[edit]. Most prostate cancers derive from cells that are stimulated to proliferate by ... April 1995). "In vivo amplification of the androgen receptor gene and progression of human prostate cancer". Nat. Genet. 9 (4 ...
Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors. Free testosterone (T) ... In general, androgens such as testosterone promote protein synthesis and thus growth of tissues with androgen receptors. ... There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used as an off- ... Wilson JD (September 2001). "Androgens, androgen receptors, and male gender role behavior". Review. Hormones and Behavior. 40 ( ...
Androgen receptor modulators. Progesterone receptor modulators. List of estrogens. This article about a steroid is a stub. You ...
Androgen receptor modulators. Estrogen receptor modulators. List of progestogens. *. Pharmacy and pharmacology portal ...
Androgens and antiandrogens. Estrogen receptor modulators. Progesterone receptor modulators. List of androgens/anabolic ... See also: List of androgens/anabolic steroids and List of androgen esters ... Androgens. (C-19: Androstane). 1. Dehydroepiandrosterone → Androstenedione → 5α-Androstanedione1 → Androsterone1. 2. ... Coffey, DS (1988) "Androgen action and the sex accessory tissues". In E Knobil, J Neill (eds), The Physiology of Reproduction. ...
Faure N, Labrie F, Lemay A, Bélanger A, Gourdeau Y, Laroche B, Robert G (March 1982). "Inhibition of serum androgen levels by ... androgens, estrogens, glucocorticoids, and mineralocorticoids.[1] In addition, pregnenolone is biologically active in its own ... "Inhibition of basal and adrenocorticotropin-stimulated plasma levels of adrenal androgens after treatment with an antiandrogen ...
Androgens. *11-Ketodihydrotestosterone. *11-Ketotestosterone. *7β-Hydroxyepiandrosterone. *11β-Hydroxyandrostenedione. * ...
... suggesting that estrogen and/or androgens have a significant part to play in sex differentiation of the brain, both prenatally ... women were found to change and approximate typical female brain structures when exposed to estrogen concomitantly with androgen ...
The combined hormonal contraceptive vaginal ring is self-administered once a month. Leaving the ring in for three weeks slowly releases hormones into the body, mainly vaginally administered estrogens and/or progestogens (a group of hormones including progesterone) - the same hormones used in birth control pills.[4] These hormones work mostly by stopping ovulation and thickening the cervical mucus, creating a barrier preventing sperm from fertilizing an egg.[4] They could theoretically affect implantation but no evidence shows that they do.[5] Worn continuously for three weeks followed by a week off, each vaginal ring provides anywhere from one month (NuvaRing) to one year (Annovera and Progering) of birth control. For continuous-use contraception, users can also choose to wear the vaginal ring for the full four week cycle. This manner of contraception will eliminate monthly periods.[6] Throughout the additional week, the serum hormone levels will remain in the contraceptive range.[7] When ...
Androgens. (C-19: Androstane). 1. Dehydroepiandrosterone → Androstenedione → 5α-Androstanedione1 → Androsterone1. 2. ...
Androgen receptor modulators. Estrogen receptor modulators. List of progestogens. *. Pharmacy and pharmacology portal ...
Dioscorides, ca. 40 A.D., described the contraceptive property of hemp seeds (Cannabis sativa) and rue (Ruta graveolens) in De Materia Medica, a text widely used into medieval times.[18] One test in rats (20 milligrams of the 80% ethanol extract) found that these reduced sperm count by more than half.[19] In medieval Persia (and in other traditions as cited) these herbs were used for male contraception, as well as Gossypium herbaceum (Malvaceae),[20] Cyperus longus (Cyperaceae), Vitex pseudonegundo (Verbenaceae), Chenopodium ambrosioides (Chenopodiaceae),[21][22] Aristolochia indica (Aristolochiaceae),[23] Punica granatum (Punicaceae),[24] and Sarcostemma acidum (Asclepiadaceae).[25] However, the compound isolated from Gossypium, as well as other cotton seeds and okra (gossypol) has been abandoned for contraceptive use because it was found to cause permanent infertility in ten to twenty percent of users.[26] In Indian traditional medicine, uses of the neem tree were described in Ayurvedic ...
Wilson JD (September 2001). "Androgens, androgen receptors, and male gender role behavior". Hormones and Behavior. 40 (2): 358- ... Conversely, androgens are responsible for pubic and body hair growth, as well as acne and axillary odor. ... Sex drive is dependent on androgen levels[28] only in the presence of estrogen, but without estrogen, free testosterone level ... Androgens such as testosterone powerfully oppose estrogen action in the breasts, such as by reducing estrogen receptor ...
Androgens. *11-Ketodihydrotestosterone. *11-Ketotestosterone. *7β-Hydroxyepiandrosterone. *11β-Hydroxyandrostenedione. * ...
Androgen receptor modulators. Estrogen receptor modulators. List of progestogens. *. Pharmacy and pharmacology portal ...
Androgen receptor modulators. Estrogen receptor modulators. List of progestogens. Retrieved from " ...
Androgens. *11-Ketodihydrotestosterone. *11-Ketotestosterone. *7β-Hydroxyepiandrosterone. *11β-Hydroxyandrostenedione. * ...
The first CIC to be studied was estradiol valerate/hydroxyprogesterone caproate (EV/OHPC) in 1963, and the second CIC to be studied was estradiol enantate/algestone acetophenide (E2-EN/DHPA) in 1964.[18][17] In 1967, E2-EN/DHPA was in the late stages of clinical development.[25][18] By 1969, the medication was available for medical use under the brand name Perlutal.[26] Within a few years, it was marketed under other brand names such as Topasel and Ova-Repos as well.[27][28][29][30] In addition, several other CICs had been introduced for medical use by 1972.[30] By 1976, two major CICs were in use: E2-EN/DHPA (brand names Perlutan, Topasel) in Spain and Latin America, and EV/OHPC (brand name Injectable No. 1) in China.[31] These CICs have been described as first-generation CICs.[31] Two second-generation CICs, estradiol cypionate/medroxyprogesterone acetate (EC/MPA; brand names Cyclofem and later Lunelle) and estradiol valerate/norethisterone enantate (EV/NETE; brand name Mesigyna), were ...
Some American legislators have unsuccessfully attempted to provide financial incentives to women on welfare who agree to use Norplant. For example, in Kansas, Republican Kerry Patrick introduced legislation that would grant welfare recipients a one-time payment of $500 to use Norplant, followed by a $50 bonus each year the implants remained in place."[30] Some judges have offered Norplant implants as a voluntary alternative to jail time for certain women convicted of child abuse or drug abuse during pregnancy. Two days after the 1990 FDA approval of Norplant, an editorial in The Philadelphia Inquirer suggested reducing the size of the black underclass by offering welfare mothers increased benefits if they agreed to use Norplant.[30][31] Eleven days later the Inquirer apologized for their "misguided and wrongheaded" editorial and for their suggestion of offering incentives for Norplant use.[30][32] Critics such as the ACLU argued that such uses are coercive and discriminatory, and compared such ...
Irregular bleeding and spotting: Many women will experience some type of irregular, unpredictable, prolonged, frequent, or infrequent bleeding.[23] Some women also experience amenorrhea. For some women, prolonged bleeding will decline after the first three months of use. However, other women may experience this bleeding pattern through all five years of use. While these patterns are not dangerous, they are the most common reason that women give for discontinuing the use of the implant. After removal, bleeding patterns return to previous patterns in most women.[19][20][21] Insertion complications: Some minor side effects such as bruising, skin irritation, or pain around the insertion site are common.[19] However, there are some rare complications that can occur, such as infection or expulsion.[19][24] In some cases, a serious complication occurs when the provider fails to insert, and the rod is left in the inserter. An Australian study reported 84 pregnancies as a result of such failure.[22] ...
AndrogensEdit. Cells in zona reticularis of the adrenal glands produce male sex hormones, or androgens, the most important of ... an androgen and precursor of both androgens and estrogens (female sex hormones).[41] Adrenal hormones, especially ... It produces androgens, mainly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (the precursor to ... During early childhood androgen synthesis and secretion remain low, but several years before puberty (from 6-8 years of age) ...
This article is about androgens as medications. For androgens as natural hormones, see Androgen. ... are steroidal androgens that include natural androgens like testosterone as well as synthetic androgens that are structurally ... Although both testosterone and dihydrotestosterone activate the same androgen receptor, differences in the sequence of androgen ... See also: List of androgens/anabolic steroids and List of androgen esters ...
List of androgen esters § Trenbolone esters. References[edit]. *^ a b c d William Llewellyn (2011). Anabolics. Molecular ... Androgen receptor modulators. Estrogens and antiestrogens. Progestogens and antiprogestogens. List of androgens/anabolic ... Androgens and antiandrogens. Estrogen receptor modulators. Progesterone receptor modulators. List of androgens/anabolic ... of the nandrolone group and an androgen ester - specifically, the C17β hexahydrobenzylcarbonate (cyclohexylmethylcarbonate) ...
Androgen receptor modulators. Estrogens and antiestrogens. Progestogens and antiprogestogens. List of androgens/anabolic ... Morley JE, Perry HM (May 2003). "Androgens and women at the menopause and beyond". J. Gerontol. A Biol. Sci. Med. Sci. 58 (5): ... Certain androgens/anabolic steroids (e.g., testosterone, testosterone esters, methyltestosterone, metandienone, nandrolone ... Androgens/anabolic steroids (e.g., testosterone, testosterone esters, nandrolone esters, oxandrolone, fluoxymesterone) ...
Androgen receptor modulators. Estrogens and antiestrogens. Progestogens and antiprogestogens. List of androgens/anabolic ... Androgens and antiandrogens. Estrogen receptor modulators. Progesterone receptor modulators. List of androgens/anabolic ... Norethisterone is a potent progestogen and a weak androgen and estrogen.[4] That is, it is a potent agonist of the progesterone ... Ricardo Azziz (8 November 2007). Androgen Excess Disorders in Women. Springer Science & Business Media. pp. 124-. ISBN 978-1- ...
Androgen receptor modulators. Estrogens and antiestrogens. Progestogens and antiprogestogens. List of androgens/anabolic ... Androgens and antiandrogens. Estrogen receptor modulators. Progesterone receptor modulators. List of androgens/anabolic ...
Soon after they differentiate, Leydig cells begin to produce androgens.. Androgen effects[edit]. The androgens function as ... This article is about androgens as natural hormones. For androgens as medications, see Anabolic steroid and Androgen ... Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen ... Androgen insensitivity[edit]. Main article: Androgen insensitivity syndrome. Reduced ability of an XY-karyotype fetus to ...
Lower androgen concentrations have been associated with bone loss in various age groups.{ref... more ... Androgens have important roles in bone mineralization either directly or through aromatization to estrogen. ... encoded search term (How do androgens affect bone?) and How do androgens affect bone? What to Read Next on Medscape. Related ... Androgen excess is due to elevated 11-oxygenated androgens in treated children with congenital adrenal hyperplasia. J Steroid ...
Their absence or the absence of androgen receptors results in a female phenotype, despite the pr... more ... Androgens induce virilization and are responsible for forming the male external genitalia in the fetus. ... With androgen excess, the extent of these changes is dependent on the level of androgens in the blood. ... Androgen excess is due to elevated 11-oxygenated androgens in treated children with congenital adrenal hyperplasia. J Steroid ...
University found that the beneficial effects daily exercise can have on the regeneration of nerves also require androgens such ... "Exercise, Androgens And Peripheral Nerve Injuries." Medical News Today. MediLexicon, Intl., 17 Oct. 2012. Web.. 18 Mar. 2019. , ... It is the first report of both androgen-dependence of exercise on nerve regeneration and of an androgenic effect of exercise in ... They now report that these beneficial effects of exercise require androgens such as testosterone in both males and females. In ...
"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 ...
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 ... Tumors in the adrenal glands can also cause too much production of androgens and can lead to male body characteristics in women ... Androgens from other parts of the body can also cause male characteristics to develop in women. ...
NR3C4 (nuclear receptor subfamily 3, group C, member 4); Testosterone/dihydrotestosterone receptor Androgen receptor (AR) ... mediates the effects of androgens that are responsible for diverse... ... Androgen receptor (AR) mediates the effects of androgens that are responsible for diverse biological functions, such as ... A soluble androgen receptor in the cytoplasm of rat prostate. J Endocrinol. 1969;45:531-41.PubMedCrossRefGoogle Scholar ...
Androgen insensitivity syndrome (AIS) is a rare condition that affects the development of a childs genitals and reproductive ... Androgen insensitivity syndrome (AIS) is a rare condition that affects the development of a childs genitals and reproductive ... complete androgen insensitivity syndrome (CAIS) - where testosterone has no effect on sexual development, so the genitals are ... partial androgen insensitivity syndrome (PAIS) - where testosterone has some effect on sexual development, so the genitals are ...
Mediation of hidradenitis suppurativa by androgens. Br Med J (Clin Res Ed) 1986; 292 :245 ... The patients had a higher concentration of total testosterone (p less than 0.01) and free androgen index (testosterone to sex ... Forty two women with hidradenitis suppurativa were assessed clinically and biochemically for evidence of androgen excess. ... Mediation of hidradenitis suppurativa by androgens.. Br Med J (Clin Res Ed) 1986; 292 doi: ...
Androgens, oestrogens, and coronary heart disease. Br Med J (Clin Res Ed) 1981; 282 :438 ... Androgens, oestrogens, and coronary heart disease.. Br Med J (Clin Res Ed) 1981; 282 doi: ...
Testoterone depletion is a normal consequence of aging in men that is associated with senescent effects in androgen-responsive ... Testoterone depletion is a normal consequence of aging in men that is associated with senescent effects in androgen-responsive ... These new findings support the clinical evaluation of androgen-based therapies for the prevention and treatment of AD. ...
Androgen insensitivity syndrome is a condition that affects sexual development before birth and during puberty. Explore ... Partial androgen insensitivity is thought to be at least as common as complete androgen insensitivity. Mild androgen ... Androgen receptors allow cells to respond to androgens, which are hormones (such as testosterone. ) that direct male sexual ... Complete androgen insensitivity syndrome occurs when the body cannot use androgens at all. People with this form of the ...
... is a disorder caused by mutation of the gene for the androgen receptor. This protein binds testosterone and regulates the ... Androgen Insensitivity Syndrome Genetics Copyright Genetics Society of America. Androgen Insensitivity Syndrome. Androgen ... and mild androgen insensitivity (MAIS). In complete androgen insensitivity, the alteration in the androgen receptor results in ... and mild androgen insensitivity (MAIS). In complete androgen insensitivity, the alteration in the androgen receptor results in ...
To summarize recent findings regarding the public health impact of androgen abuse.. Recent findings Abuse of androgens (also ... Supraphysiologic androgen levels may sometimes cause irritability, aggressiveness, and violence, whereas androgen withdrawal ... Recent studies have demonstrated marked adverse effects of long-term androgen abuse. As increasing numbers of androgen abusers ... Most androgen abusers are still under age 50 today, and thus, the long-term effects of these drugs are only beginning to be ...
Androgens meeting brings together medical professionals and researchers of all disciplines interested in the action of androgen ... Androgens 2018 Meeting. The biannual Androgens meeting brings together medical professionals and researchers of all disciplines ... emerging areas and androgen receptors. Oral and poster presentations of submitted abstracts will provide delegates with an ... interested in the action of androgen hormones in health and disease. ...
Read about the causes of androgen insensitivity syndrome (AIS), including how babies with the condition develop and how it is ... Androgen insensitivity syndrome (AIS) is caused by a genetic fault that means the body cant respond to testosterone properly. ...
Androgens are produced primarily from the adrenal glands and the ovaries. ... Androgen excess is the most common endocrine disorder in women of reproductive age. ... encoded search term (Androgen%20Excess) and Androgen Excess What to Read Next on Medscape. Medscape Consult. ... Androgen Excess Differential Diagnoses. Updated: Apr 03, 2017 * Author: Mohamed Yahya Abdel-Rahman, MD, MSc; Chief Editor: ...
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 ...
adrenal androgens synonyms, adrenal androgens pronunciation, adrenal androgens translation, English dictionary definition of ... adrenal androgens. n. A steroid hormone, such as testosterone or androsterone, that controls the development and maintenance of ... androgen. (redirected from adrenal androgens). Also found in: Thesaurus, Medical, Encyclopedia. an·dro·gen. (ăn′drə-jən). n.. A ... Adrenal androgens - definition of adrenal androgens by The Free Dictionary ...
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. ...
Androgen insensitivity syndrome is a genetic condition in which male sexual organs cannot fully develop. It can be either ... The body of a person with AIS will not react to the androgen because a genetic alteration leads to a low number of androgen ... Fast facts on androgen insensitivity syndrome. *Androgen insensitivity syndrome (AIS) causes the development of abnormal sexual ... Partial: In partial androgen insensitivity syndrome (PAIS), there is some sensitivity to androgen. Depending on the level of ...
androgen-insensitivity syndrome (AIS): (also called testicular-feminizing syndrome): a congenital condition identified by a 46 ... androgen-insensitivity syndrome (AIS): (also called testicular-feminizing syndrome): a congenital condition identified by a 46 ...
Androgens, Dodgy Penis Size Data, and Differential-K Theory. Can crude statistics validate suspect racial data on penis sizes? ... Lange, E. M., Sarma, A. V., Ray, A., Wang, Y., Ho, L. A., Anderson, S. A., . . . Cooney, K. A. (2008). The androgen receptor ... They did find that Caucasians were higher than Asians in all androgen markers, which they took in support of their theory. In ... The argument here seems to be that penis length should be correlated with other androgen markers, and that if the penis length ...
androgen synonyms, androgen pronunciation, androgen translation, English dictionary definition of androgen. n. A steroid ... androgen. Also found in: Thesaurus, Medical, Encyclopedia, Wikipedia.. Related to androgen: estrogen, testosterone, Androgen ... and prevents binding of androgen to the androgen receptor, and translocation of the androgen receptor to the nucleus of the ... Although women produce only one tenth the amount of androgen that men do, testosterone and related androgen metabolites are as ...
Dry eye syndrome as a result of androgen deficiency in the aging male, "Beyond the Abstract," by Anat Galor, MD, MSPH November ... The Role of Partial Androgen Deficiency in Aging Men in Development of Benign Prostatic Hyperplasia and Prostate Cancer - ... Features of diagnostics and treatment of partial androgen deficiency of aging men, "Beyond the Abstract," by Alexander V. ...
Crosstalk Between Androgen-sensitive and Androgen-insensitive Prostate Cancer Cells. To investigate how androgen-sensitive ... A Targeted Bivalent Androgen Receptor Binding Compound for Prostate Cancer Therapy. The androgen-directed treatment of prostate ... In particular, androgen-mediated androgen receptor signals have been shown to correlate with the promotion of tumor development ... Current and potential targets for drug design in the androgen receptor pathway for prostate cancer. Modulating the androgen ...
Androgens and estrogens are known to be critical regulators of mammalian physiology and development. While these two classes of ... However, the emergence of patients with deficiencies in androgen or estrogen hormone synthesis or actions, as well as the ... In this Review, we will discuss important roles of estrogens in males and androgens in females. ... while androgens such as testosterone and dihydrotestosterone were believed to primarily modulate development and physiology in ...
Androgen action in women. Preface. While estrogens are considered the dominant sex steroid in women, in fact, serum androgen ... Androgen receptor in the ovary theca cells plays a critical role in androgen-induced reproductive dysfunction. Endocrinology. ... In bone, androgens regulate bone size, perhaps by controlling cancellous bone volume. In the uterus, androgens may regulate ... In breast, androgens have little effect on normal mammary development. In breast cancer, however, androgens may suppress growth ...
Androgens have been shown to down-regulate GnRH mRNA levels through an androgen receptor (AR)-dependent mechanism. Here, we ... Androgen receptor repression of GnRH gene transcription.. Brayman MJ1, Pepa PA, Berdy SE, Mellon PL. ... A synthetic androgen, R1881, repressed transcription from the GnRH promoter (GnRH-P) in an AR-dependent manner, and liganded AR ... Alterations in androgen levels lead to reproductive defects in both males and females, including hypogonadotropic hypogonadism ...
  • Androgen receptor , mARs (e.g. (
  • Once group received the drug flutamide, which blocks the androgen receptor. (
  • Caffo O, Maines F, Veccia A, Kinspergher S, Galligioni E. Splice variants of androgen receptor and prostate cancer. (
  • The contribution of different androgen receptor domains to receptor dimerization and signaling. (
  • Alternatively spliced androgen receptor variants. (
  • Fang S, Anderson KM, Liao S. Receptor proteins for androgens. (
  • Post-translational modification of the androgen receptor. (
  • Ligand-specific dynamics of the androgen receptor at its response element in living cells. (
  • Koryakina Y, Ta HQ, Gioeli D. Androgen receptor phosphorylation: biological context and functional consequences. (
  • Kumar R, Atamna H, Zakharov MN, Bhasin S, Khan SH, Jasuja R. Role of the androgen receptor CAG repeat polymorphism in prostate cancer, and spinal and bulbar muscular atrophy. (
  • Androgen receptor-mediated non-genomic regulation of prostate cancer cell proliferation. (
  • Cloning of human androgen receptor complementary DNA and localization to the X chromosome. (
  • A soluble androgen receptor in the cytoplasm of rat prostate. (
  • The androgen receptor in health and disease. (
  • Maintaining and reprogramming genomic androgen receptor activity in prostate cancer. (
  • Shukla GC, Plaga AR, Shankar E, Gupta S. Androgen receptor-related diseases: what do we know? (
  • This gene provides instructions for making a protein called an androgen receptor. (
  • Androgen insensitivity syndrome (AIS) is a disorder caused by mutation of the gene for the androgen receptor. (
  • Testosterone exerts its action on these target cells by first binding with a receptor, called the androgen receptor (AR). (
  • Androgen receptor: a key molecule in the progression of prostate cancer to hormone independence. (
  • In their recent comprehensive update on the molecular biology of prostate cancer, Mackinnon et al (1) refer to the interesting possibility that the significance of TMPRSS2 (transmembrane protease, serine 2) fusion genes, including the commonest type, TMPRSS2:ERG (v-ets erythroblastosis virus E26 oncogene homologue), now known to be present in at least 50% of cases, (2) may be quite different depending on the androgen receptor status of the tumor. (
  • A Targeted Bivalent Androgen Receptor Binding Compound for Prostate Cancer Therapy. (
  • Androgen Receptor Signaling in Bladder Cancer. (
  • In particular, androgen-mediated androgen receptor signals have been shown to correlate with the promotion of tumor development and progression, which may clearly explain some sex-specific differences in bladder cancer. (
  • An agent that demonstrates action on the androgen receptor (AR) axis may have value for preventing or treating castrate-resistant PCa. (
  • BA321, a novel carborane analog that binds to androgen and estrogen receptors, acts as a new selective androgen receptor modulator of bone in male mice. (
  • Carboranes are a class of carbon-containing polyhedral boron cluster compounds with globular geometry and hydrophobic surface that interact with hormone receptors such as estrogen receptor (ER) and androgen receptor (AR). (
  • Testosterone is converted to dihydrotestosterone (DHT), and both of these bind the androgen receptor (AR), although DHT has a greater affinity and cannot be aromatized to estrogen. (
  • Androgen receptor repression of GnRH gene transcription. (
  • Androgens have been shown to down-regulate GnRH mRNA levels through an androgen receptor (AR)-dependent mechanism. (
  • Previous reports have revealed that, while lowering of the circulating T to a castration level with ADT, its active metabolite DHT still exists in PCa tissues after ADT at levels sufficient to activate AR [androgen receptor]," explains the team. (
  • Dihydrotestosterone treatment had identical effects, indicating that these growth-promoting actions are mediated by the androgen receptor. (
  • Measurement of intra-tissue concentrations of steroids using liquid chromatography-tandem mass spectrometry has been important in advancing our understanding of a role for androgens in the endometrium, acting both as active ligands for the androgen receptor and as substrates for oestrogen biosynthesis. (
  • A University of Rochester study helps to explain why men get liver cancer more often than women and opens the door for a new treatment pathway, by showing a direct link between the androgen receptor, which is more active in men, and the hepatitis B virus as it relates to the deadly cancer. (
  • Now, corresponding author Chawnshang Chang, Ph.D., the George Hoyt Whipple Distinguished Professor of Pathology at the University of Rochester Medical Center, and colleagues, showed that the androgen receptor (AR), a protein that mediates male sex hormones, promotes liver cancer when hepatitis B is present by altering DNA replication of the virus. (
  • This study also raises the possibility of prevention among men with HBV infection through inhibition of the androgen receptor," Hezel added. (
  • At present, therapeutic intervention for metastatic disease capitalizes on the addiction of these tumors to the androgen receptor (AR). (
  • Yuan X, Balk SP (2009) Mechanisms mediating androgen receptor reactivation after castration. (
  • While tissue specific effects of selective androgen receptor modulators (SARMs) outside the brain have been reported, little is known about brain specific SARMs. (
  • Here we show that SARMs upregulate androgen receptor levels in brain following castration and antagonize impairments in hippocampus-dependent novel location recognition and spatial memory retention in apoE4 female mice. (
  • The androgen receptor (AR) plays a central role in prostate cancer, but conventional inhibitors lose effectiveness as cancer treatments because anti-androgen resistance usually develops. (
  • What are the three androgen receptor antagonists to know? (
  • Which androgen receptor antagonist is used most often? (
  • Therapeutic uses for androgen receptor antagonists? (
  • What is used with androgen receptor antagonists to treat metastatic prostate cancers? (
  • Limited efficacy when androgen receptor antagonists are used alone because of a compensatory increase in LH secretion stimulates higher serum concentrations of testosterone. (
  • Adverse effects of androgen receptor antagonists? (
  • In 2 hypogonadal patients, T-cell receptor excision circle levels fell by 83% and 78% after androgen replacement therapy. (
  • Subfertility and defective folliculogenesis in female mice lacking androgen receptor," Proceedings of the National Academy of Sciences of the United States of America , vol. 101, no. 31, pp. 11209-11214, 2004. (
  • Premature ovarian failure in androgen receptor-deficient mice," Proceedings of the National Academy of Sciences of the United States of America , vol. 103, no. 1, pp. 224-229, 2006. (
  • Generation and characterization of androgen receptor knockout (ARKO) mice: an in vivo model for the study of androgen functions in selective tissues," Proceedings of the National Academy of Sciences of the United States of America , vol. 99, no. 21, pp. 13498-13503, 2002. (
  • The rat androgen receptor: primary structure, autoregulation of its messenger ribonucleic acid, and immunocytochemical localization of the receptor protein," Molecular Endocrinology , vol. 2, no. 12, pp. 1276-1285, 1988. (
  • Labels the nuclei of cells known to contain the androgen receptor. (
  • In Western blot, the antibody identifies a 110 and 112 kDa doublet in extracts of the metastatic prostate cancer cell line, LNCap, and in extracts of cells transfected with the gene for androgen receptor. (
  • Synthetic peptide corresponding to amino acids 229-315 of the human androgen receptor (1). (
  • Monoclonal mouse anti-human androgen receptor, clone AR441 (anti-androgen receptor) specifically immunostains the nuclei of positive cells in human tissues. (
  • The antibody is unreactive with mouse androgen receptor in immunoblots of prostate extracts. (
  • Anti-androgen receptor is capable of recognizing and forming complexes with native androgen bound receptor (1). (
  • A novel dietary flavonoid fisetin inhibits androgen receptor signaling and tumor growth in athymic mice. (
  • Oral curcumin intake could inhibit androgen receptor expression and probably PSA activity. (
  • A compound within Pygeum bark antagonizes human androgen receptor in the prostate gland. (
  • Selective androgen receptor modulators or SARMs are a novel class of androgen receptor ligands . (
  • We report the roles of androgen in proliferation and differentiation of intestinal stem cells via targeting of the androgen receptor (AR) on intestinal stromal cells by negatively regulating bone morphogenetic proteins (BMPs) signaling," noted the researchers. (
  • Antiandrogens like bicalutamide compete with androgens for binding to the androgen receptor, reducing the ability of androgens to promote prostate cancer cell growth. (
  • Androgen receptor (AR) is regulated by SUMOylation at its transactivation domain. (
  • The androgen receptor confers protection against diet-induced atherosclerosis, obesity, and dyslipidemia in female mice. (
  • To determine the physiologic androgen receptor (AR)-dependent actions of androgens on atherogenesis in female mice, we generated female AR-knockout (ARKO) mice on an atherosclerosis-prone apolipoprotein E (apoE)-deficient background. (
  • It turns out that TMPRSS2 expression is linked to the transcriptional-activating activity of the androgen receptor. (
  • The Italian work linked above found that men who were taking androgen receptor antagonists (generally as a treatment for prostate cancer) seemed to be at significantly lower COVID-19 risk, which result is especially striking considering that pre-existing cancer in general is a risk factor for severe coronavirus outcomes. (
  • In July, a Chinese company (Kintor Pharmaceutical) announced that it was providing an investigational androgen receptor antagonist ( proxalutamide ) for a clinical trial to be run in Brazil. (
  • But blockade of the androgen receptor in this way is generally a cleaner route than (say) blocking the synthesis of testosterone itself, because there are quite a few other pathways involved with testosterone metabolites, etc. (
  • β-catenin, best known for its role in Wnt signaling, in which it forms transcriptionally active complexes with members of the Tcf/LEF family, appears to also promote transcription through a specific interaction with the androgen nuclear receptor (AR). (
  • This antibody detects Androgen Receptor. (
  • Synthetic peptide corresponding to Human Androgen Receptor aa 1-21 (N terminal). (
  • Detects a band of approximately 110 kDa (predicted molecular weight: 99 kDa).Can be blocked with Androgen Receptor peptide (ab4903) . (
  • The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. (
  • In a third set of experiments, the researchers removed the androgen receptor by genetic knockout, once again abolishing the androgen's effect on hepatitis B replication. (
  • Then they drilled down still further, discovering elements within the HBV genome which are recognized by the host's activated androgen receptor, which then boosts viral gene expression and replication. (
  • Enhancement of hepatitis B virus replication by androgen and its receptor in mice. (
  • Androgen receptor (AR) signaling is essential for prostate cancer progression and acquiring resistance to hormone therapy. (
  • The reason for this variation is unknown, but may be influenced by gender-specific effects of androids, heterogeneity of the vascular endothelium, differential expression of the androgen receptor in endothelial cells (ECs) and route of androgen administration. (
  • C. A. Heinlein and C. Chang , Androgen receptor in prostate cancer, Endocrine Reviews , 25 (2004), 276-308. (
  • Since the androgen receptor (AR) mediates proliferation and differentiation in the prostate and is expressed in nearly all human prostate cancers, the effects of I3C on AR expression and function were examined in LNCaP cells. (
  • Indole-3-carbinol inhibition of androgen receptor expression and downregulation of androgen responsiveness in human prostate cancer cells. (
  • Androgen action is exerted in target tissues via binding the androgen receptor (AR), a nuclear receptor transcription factor. (
  • Structure of the ligand binding domain of the androgen receptor (rainbow cartoon) complexed with testosterone (white sticks) based on PDB 2AM9 . (
  • The androgen receptor ( AR ), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor [ 1 ] which is activated by binding of either of the androgenic hormones testosterone or dihydrotestosterone . (
  • [ 2 ] The androgen receptor is most closely related to the progesterone receptor , and progestins in higher dosages can block the androgen receptor. (
  • [ 5 ] however, the androgen receptor has other functions as well. (
  • In some cell types testosterone interacts directly with androgen receptors while in others testosterone is converted by 5-alpha-reductase to dihydrotestosterone, an even more potent agonist for androgen receptor activation. (
  • [ 7 ] Testosterone appears to be the primary androgen receptor activating hormone in the Wolffian duct while dihydrotestosterone is the main androgenic hormone in the urogenital sinus , urogenital tubercle, and hair follicles . (
  • The binding of an androgen to the androgen receptor results in a conformational change in the receptor which in turn causes dissociation of heat shock proteins , transport from the cytosol into the cell nucleus , and dimerization. (
  • The androgen receptor dimer binds to a specific sequence of DNA known as a hormone response element . (
  • One of the known target genes of androgen receptor activation is insulin-like growth factor I ( IGF-1 ). (
  • One function of androgen receptor that is independent of direct binding to its target DNA sequence, is facilitated by recruitment via other DNA binding proteins. (
  • The androgen insensitivity syndrome , formerly known as testicular feminization, is caused by a mutation of the Androgen Receptor gene located on the X chromosome (locus:Xq11-Xq12). (
  • Studies done in non-human primates have also shown that androgen increases the numbers of preantral and antral follicles as well as increases FSH receptor mRNA expression in granulosa cells. (
  • Activation of the androgen receptor (AR) may play a role in androgen-independent progression of prostate cancer. (
  • Although this is referred to as androgen-independent prostate cancer (AICaP), the androgen receptor (AR) is likely to be involved in the recurrence of most prostate cancers. (
  • Androgens control spermatogenesis, but germ cells themselves do not express a functional androgen receptor (AR). (
  • According to most studies, male germ cells are devoid of the androgen receptor (AR) ( 1 - 3 , 5 ), an X chromosome-encoded member of the nuclear receptor family mediating most effects of androgens in androgen target tissues ( 6 , 7 ). (
  • Fork-head box protein A1 (FOXA1) is a ''pioneer factor' ' that is known to bind to the androgen receptor (AR) and regulate the transcription of AR-specific genes. (
  • Prostate cancer is the second most common cause of cancer-associated deaths in men and signalling via a transcription factor called androgen receptor (AR) is an important driver of the disease. (
  • Cancer cells that are androgen receptor positive may need androgens to grow. (
  • Their absence or the absence of androgen receptors results in a female phenotype, despite the presence of a 46 XY karyotype (eg, androgen insensitivity syndrome). (
  • Partial androgen insensitivity syndrome (PAIS) is a condition that results in the partial inability of the cell to respond to androgens. (
  • Androgen insensitivity syndrome is the largest single entity that leads to 46,XY undermasculinization. (
  • Partial androgen insensitivity syndrome is diagnosed when the degree of androgen insensitivity in an individual with a 46,XY karyotype is great enough to partially prevent the masculinization of the genitalia, but is not great enough to completely prevent genital masculinization. (
  • Androgen insensitivity syndrome (AIS) is a rare condition that affects the development of a child's genitals and reproductive organs. (
  • Androgen insensitivity syndrome is a condition that affects sexual development before birth and during puberty. (
  • Complete androgen insensitivity syndrome occurs when the body cannot use androgens at all. (
  • People with complete androgen insensitivity syndrome also have sparse or absent hair in the pubic area and under the arms. (
  • The partial and mild forms of androgen insensitivity syndrome result when the body's tissues are partially sensitive to the effects of androgens. (
  • Complete androgen insensitivity syndrome affects 2 to 5 per 100,000 people who are genetically male. (
  • Mutations in the AR gene cause androgen insensitivity syndrome. (
  • About two-thirds of all cases of androgen insensitivity syndrome are inherited from mothers who carry an altered copy of the AR gene on one of their two X chromosomes. (
  • Androgen insensitivity syndrome (AIS) is caused by a genetic fault that means the body can't respond to testosterone properly. (
  • 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. (
  • Androgen insensitivity syndrome is a rare genetic disorder in which a male fetus does not respond to male hormones. (
  • A newborn with androgen insensitivity syndrome (AIS) appears to be female, but the reproductive features will be unusual. (
  • Androgen insensitivity syndrome (AIS) causes the development of abnormal sexual organs. (
  • Androgen insensitivity syndrome is caused by a mutation to the Y chromosome that programs male sexual development. (
  • A total lack of reaction will lead to complete androgen insensitivity syndrome (CAIS). (
  • Reversing Androgen Insensitivity Syndrome: Deficiencies The Raw Vegan Plant-Based Detoxification & Regeneration Workbook for Healing Patients. (
  • Although visualization of compounds at the AR surface reveals weak binding at AF-2, the most potent inhibitors bind preferentially to a previously unknown regulatory surface cleft termed binding function (BF)-3, which is a known target for mutations in prostate cancer and androgen insensitivity syndrome. (
  • Genotype versus phenotype in families with androgen insensitivity syndrome," The Journal of Clinical Endocrinology & Metabolism , vol. 86, no. 9, pp. 4151-4160, 2001. (
  • 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. (
  • Antonio Simone Laganà and Alfonsa Pizzo, "Response to: Comment on "Complete Androgen Insensitivity Syndrome: Optimizing Diagnosis and Management"," Case Reports in Obstetrics and Gynecology , vol. 2014, Article ID 808270, 2 pages, 2014. (
  • People with too little sex hormones can be short during puberty but end up taller as adults as in androgen insensitivity syndrome or estrogen insensitivity syndrome . (
  • 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 (AIS) is caused by genetic defects on the X chromosome. (
  • ICD-9 code 259.5 for Androgen insensitivity syndrome is a medical classification as listed by WHO under the range -DISEASES OF OTHER ENDOCRINE GLANDS (249-259). (
  • Testosterone , the major androgen. (
  • [2] The major androgen in males is testosterone . (
  • While androstenediones are converted metabolically to testosterone and other androgens, they are also the parent structure of estrone . (
  • Androsterone is a chemical byproduct 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) is a metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors. (
  • A study by researchers from Emory University and Indiana University found that the beneficial effects daily exercise can have on the regeneration of nerves also require androgens such as testosterone in both males and females. (
  • They now report that these beneficial effects of exercise require androgens such as testosterone in both males and females. (
  • Ovarian overproduction of androgens is a condition in which the ovaries make too much testosterone . (
  • The patients had a higher concentration of total testosterone (p less than 0.01) and free androgen index (testosterone to sex hormone binding globulin concentrations) (p less than 0.01) than normal controls. (
  • Testosterone is the principal male androgen. (
  • Besides testosterone, other androgens include: Dehydroepiandrosterone (DHEA) is a steroid hormone produced in the adrenal cortex from cholesterol. (
  • Moderately high levels of adrenal androgens and testosterone as well as sometimes a moderate elevation of 17-OH progesterone can also be associated with CAH. (
  • An androgen or anabolic steroid ester is an ester of an androgen/anabolic steroid (AAS) such as the natural testosterone or dihydrotestosterone (DHT) or the synthetic nandrolone (19-nortestosterone). (
  • Examples of androgen esters include testosterone esters such as testosterone cypionate, testosterone enanthate, testosterone propionate, and testosterone undecanoate and nandrolone esters such as nandrolone decanoate and nandrolone phenylpropionate. (
  • These differences are thought to derive from group differences in androgens (male hormones such as testosterone ). (
  • In the past, estrogens such as estradiol were thought to be most important in the regulation of female biology, while androgens such as testosterone and dihydrotestosterone were believed to primarily modulate development and physiology in males. (
  • A new analysis of patients who have undergone treatment for prostate cancer shows a connection between androgen deprivation therapy (ADT) - a testosterone-lowering therapy and a common treatment for the disease - and dementia, according to researchers from the Perelman School of Medicine at the University of Pennsylvania. (
  • LH acts on the Leydig cells to stimulate de novo sythesis of androgens (mainly testosterone). (
  • The androgen backdoor pathway is a collective name for all metabolic pathways where clinically relevant androgens are synthesized with roundabout of testosterone as an intermediate product. (
  • The androgens produced by any of these routes cannot be converted by aromatase into estrogens, and may cause hyperandrogenism when the level of testosterone is normal. (
  • Any pathway that fits the definition "androgen backdoor pathway" is an alternative pathway to the conventional, [6] canonical [7] androgenic pathway that involves testosterone. (
  • Survey data on the prescribing of testosterone by U.S. physicians in 2009 found that approximately 4 million prescriptions for estrogen/androgen oral medications, compounded testosterone, or brand testosterone approved for use in men were written off-label for women. (
  • For postmenopausal women with secondary HSDD, the administration of androgens, testosterone patches, or a combination of estrogen and methyltestosterone was reported to be moderately beneficial. (
  • The body naturally uses the androgen testosterone to stimulate the creation of protein throughout the body, especially in muscle. (
  • A semisynthetic agent (oxandrolone) that acts like testosterone can be used to supplement androgen activity in older persons with low levels of testosterone. (
  • The major example of androgens is testosterone. (
  • Androsterone - It is formed as a byproduct of androgen metabolism and it has one-seventh of the potency of testosterone. (
  • Androgens are mainly prescribed to treat several diseases caused by testosterone deficiency. (
  • However, athletes try to promote muscle growth by manipulating testosterone levels or assuming androgen anabolic steroids (AAS). (
  • The binding of testosterone to androgen receptors has anabolic and androgenic effects. (
  • Present in both males and females, the principle androgens are testosterone and androstenedione. (
  • The principal androgens are testosterone and androstenedione. (
  • Currently used androgens for male hormone replacement therapy are typically injectable or skin delivery formulations of testosterone or testosterone esters. (
  • however, several nonsteroidal androgens show a ratio of anabolic to androgenic effects of greater than 3:1 and up to as much as 90:1 (RAD-140), compared to testosterone, which has a ratio of 1:1. (
  • Since exogenous testosterone can suppress LH levels, it could be that androgen therapy could revert the LH-induced growth stimulation of Leydig cell compartment. (
  • Participants in the study will be randomized to one of two treatment groups, receiving either testosterone undecanoate (low-dose androgen) or placebo, for two 6 months. (
  • Therapies that interfere with the production or the action of the androgen testosterone have been linked to these effects in previous studies. (
  • In men after puberty, the majority of androgens are produced by the testicles, mainly as testosterone. (
  • Widespread disagreement exists over what is the normal range of testosterone levels and what, exactly, should be measured in the blood to assess androgen deficiency. (
  • This is a major finding - bladder cancer development and spread to other organs depends significantly on CD24, which in turn depends on androgens like testosterone. (
  • The primary and most well-known androgen is testosterone . (
  • Natural News ) The extracts of the traditional African plant known as Ficus asperifolia have been found to potentially treat androgen deficiency, a condition in which the body lacks male sex hormones, such as testosterone. (
  • As the prostate is a testosterone-responsive gland, androgen deprivation therapy (ADT) is the cornerstone of treatment in these men, with approximately 50 percent of prostate cancer patients starting ADT within a year of diagnosis. (
  • Higher levels of sex hormone-binding globulin were associated with androgen deficiency in men, independent of total testosterone level, researchers in Italy reported. (
  • The first-line assessment for the evaluation of gonadal status in men with features of androgen deficiency is total testosterone, as indicated by all current guidelines and recommendations," Mario Maggi, MD , of the department of experimental, clinical and biomedical sciences at the University of Florence, and colleagues reported. (
  • Traditionally, elevated levels of androgens, such as testosterone, are felt to be the primary cause for common hair loss in both men and women . (
  • Improvement in scalp hair growth in androgen-deficient women treated with testosterone: a questionnaire study. (
  • An androgen (from Greek andr- , the stem of the word meaning "man") is any natural or synthetic steroid hormone that regulates the development and maintenance of male characteristics in vertebrates by binding to androgen receptors . (
  • Chang CS, Kokontis J, Liao ST. Molecular cloning of human and rat complementary DNA encoding androgen receptors. (
  • Lamb DJ, Weigel NL, Marcelli M. Androgen receptors and their biology. (
  • Androgens and androgen receptors also have other important functions in both males and females, such as regulating hair growth and sex drive. (
  • Mutations in the AR gene prevent androgen receptors from working properly, which makes cells less responsive to androgens or prevents cells from using these hormones at all. (
  • The body of a person with AIS will not react to the androgen because a genetic alteration leads to a low number of androgen receptors. (
  • Androgen , also called androgenic hormone or testoid, is the generic term for any natural or synthetic compound, usually a steroid hormone that stimulates or controls the development and maintenance of male characteristics in vertebrates by binding to androgen receptors. (
  • While these two classes of steroids share similar structures (in general, estrogens are derived from androgens via the enzyme aromatase), they subserve markedly different functions via their specific receptors. (
  • Expression of enzymes that play a critical role in the activation and inactivation of bioactive oestrogens (E1, E2) and androgens (A4, T, DHT), as well as expression of steroid hormone receptors, has been detected in endometrial tissues and cells recovered during the menstrual cycle. (
  • Initially described as a route where 5α-reduction of 17α-hydroxyprogesterone ultimately leads to 5α-dihydrotestosterone, several other routes have been discovered towards 11-oxyandrogens which are potent agonists of the androgen receptors. (
  • Since then, several other routes have been discovered that lead to 11-oxyandrogens [3] which are potent agonists of the androgen receptors. (
  • SARMs provide the ability to design molecules that can be delivered orally, but that selectively target the androgen receptors in different tissues differently. (
  • Here's a proposal from last June that androgen antagonists be tried out in this fashion, and here's a later study from Michigan that established that specific cell types in the airway do indeed co-express androgen receptors and TMPRSS2, which is then regulated in the lung by AR activity. (
  • Sure enough, when the group knocked down androgen receptors in human bladder cancer cell lines, they saw a corresponding drop in CD24 levels and also decreased cell proliferation. (
  • The primary mechanism of action for androgen receptors is direct regulation of gene transcription . (
  • Androgen receptors interact with other proteins in the nucleus resulting in up or down regulation of specific gene transcription . (
  • [ 11 ] Thus, changes in levels of specific proteins in cells is one way that androgen receptors control cell behavior. (
  • More recently, androgen receptors have been shown to have a second mode of action. (
  • As has been also found for other steroid hormone receptors such as estrogen receptors , androgen receptors can have actions that are independent of their interactions with DNA. (
  • [ 6 ] [ 12 ] Androgen receptors interact with certain signal transduction proteins in the cytoplasm. (
  • Androgen binding to cytoplasmic androgen receptors can cause rapid changes in cell function independent of changes in gene transcription, such as changes in ion transport . (
  • Regulation of signal transduction pathways by cytoplasmic androgen receptors can indirectly lead to changes in gene transcription, for example, by leading to phosphorylation of other transcription factors. (
  • CHICAGO -- Six or more months of continuous androgen deprivation therapy was associated with significantly increased risk of fragility fractures and type 2 diabetes in an observational study of nearly 20,000 men aged 66 years and older with prostate cancer, reported investigators at the annual meeting of the American Society of Clinical Oncology. (
  • Androgen-deprivation therapy plus chemotherapy in metastatic hormone-sensitive prostate cancer. (
  • OBJECTIVE - To assess the efficacy and toxicity of androgen-deprivation therapy (ADT) plus chemotherapy in patients with hormone-sensitive metastatic prostate cancer. (
  • Determining the androgen content in prostate tissue could predict patients' responses to androgen deprivation therapy (ADT) and the risk for castration-resistant prostate cancer (CRPCa), show study findings. (
  • A large-scale, population based study led by Dr. Laurent Azoulay, Senior Investigator with the Lady Davis Institute at the Jewish General Hospital, has concluded that the use of androgen deprivation therapy (ADT) to treat advanced prostate cancer is not associated with an increased risk of Alzheimer disease. (
  • Because early-stage CaPs depend on androgens for growth and survival, androgen deprivation by surgical or chemical castration has been used as the main therapeutic intervention in the treatment of the disease ( Feldman and Feldman, 2001 ). (
  • Adding androgen deprivation therapy to radiation therapy can improve survival for some men with recurrent prostate cancer, according to the long-term results of a clinical trial. (
  • The results are consistent with those of a clinical trial published last year that tested the addition of short-term androgen deprivation therapy to radiation therapy, noted Deborah E. Citrin, M.D., of NCI's Center for Cancer Research (CCR) , who was not involved in either study. (
  • The findings of the 2016 trial indicated that radiation plus a course of androgen deprivation therapy for 6 months could be a treatment option for men who experience a biochemical recurrence after a prostatectomy. (
  • Some patients may achieve some of the benefits reported in the bicalutamide trial from shorter courses of androgen deprivation therapy, she noted. (
  • Patients considering treatment with androgen deprivation therapy and radiation therapy should discuss the option with their doctors "to find a balance between the potential benefits and the risks, including side effects," Dr. Citrin added. (
  • Regarding the treatment of progressive prostate cancer the most common and effective is the intermittent androgen deprivation therapy. (
  • Androgens have important roles in bone mineralization either directly or through aromatization to estrogen. (
  • List of androgen esters List of androgens/anabolic steroids Steroid ester Estrogen ester Progestogen ester Richard Lawrence Miller (2002). (
  • However, the emergence of patients with deficiencies in androgen or estrogen hormone synthesis or actions, as well as the development of animal models that specifically target androgen- or estrogen-mediated signaling pathways, have revealed that estrogens and androgens regulate critical biological and pathological processes in both males and females. (
  • Local estrogen production is also present in female tissues such as the bone and breast secondary to aromatization of androgens. (
  • Like estrogen, androgens act in both nuclear and extranuclear domains of many cells in multiple organs. (
  • In adult women, androgens are necessary for estrogen synthesis and have been shown to play a key role in the prevention of bone loss, as well as sexual desire and satisfaction. (
  • Also, before you use an androgen and estrogen product, you and your doctor should discuss the good that it will do as well as the risks of using it. (
  • While everyone has a combination of male and female hormones, women have more estrogen, and men have more androgen. (
  • Androgens cause slow epiphysis , or maturation of the bones, but more of the potent epiphysis effect comes from the estrogen produced by aromatization of androgens. (
  • Steroid users of teen age may find that their growth had been stunted by androgen and/or estrogen excess. (
  • By using Letrozole for 2 weeks after GnRH suppression of the ovaries, the investigators will more effectively increase the amount of circulating androgen while keeping estrogen at low levels, thereby allowing the investigators to more completely study the effects of isolated and elevated androgen levels on granulosa cell responses to FSH. (
  • Deficiency of 21-OH enzyme leads to overproduction and accumulation of precursors proximal to the blocked enzymatic step, deficient production of cortisol, increased ACTH, increased adrenal androgens and adrenal hyperplasia. (
  • To evaluate the prevalence of hypogonadism in Indian males with T2DM and assess the primary and secondary hypogonadism along with androgen deficiency. (
  • Androgen Deficiency and Erectile Dysfunction in Patients with Type 2 Diabetes. (
  • To assess the prevalence of androgen deficiency and erectile dysfunction (ED) and their relation to glycemic control within a sample of Egyptian men with T2DM. (
  • In fact, women may produce too much or too little of these hormones--disorders of androgen excess and deficiency are among the more common hormonal disorders in women. (
  • Because symptoms like flagging desire and general malaise have a variety of causes, androgen deficiency, like hyperandrogenism, often goes undiagnosed. (
  • Androgen deficiency can occur in younger men, and even in children and adolescents, as a result of testicular damage, genetic disorders or metabolic disorders. (
  • What are the symptoms of androgen deficiency? (
  • How is androgen deficiency (PADAM) diagnosed? (
  • It would be comforting to think that a simple blood test could identify androgen deficiency. (
  • Other blood tests may be done to help tell the difference between AIS and androgen deficiency. (
  • This retrospective analysis examined patients who had androgen deficiency. (
  • This article is about androgens as natural hormones. (
  • Although androgens are commonly thought of only as male sex hormones , females also have them, but at lower levels: they function in libido and sexual arousal . (
  • The androgens function as paracrine hormones required by the Sertoli cells to support sperm production. (
  • Because their bodies are unable to respond to certain male sex hormones (called androgens), they may have mostly female external sex characteristics or signs of both male and female sexual development. (
  • The biannual Androgens meeting brings together medical professionals and researchers of all disciplines interested in the action of androgen hormones in health and disease. (
  • The testes, or testicles, are the male reproductive organs that produce androgens, or male hormones. (
  • Androgen suppression is achieved by surgical removal of the testicles, by taking female sex hormones, or by taking other drugs. (
  • Androgens are male sex hormones but they are also produced in females. (
  • Androgens are steroid hormones that control the development and sustenance of male characteristics such as male sex organs and secondary sex characteristics. (
  • In females, androgens are used to synthesize the main group of female sex hormones called estrogens. (
  • Because neurons are sensitive to androgens, these hormones can influence libido and aggression. (
  • Androgens are a group of hormones that play a role in male traits and reproductive activity. (
  • Androgens may be called "male hormones," but don't let the name fool you. (
  • In a woman's body, one of the main purposes of androgens is to be converted into the female hormones called estrogens. (
  • Androgen insensitivity is a rare genetic condition that blocks the body from using male hormones (androgens) during fetal growth and after birth. (
  • When the trial began in 1998, bicalutamide was a commonly used treatment to prevent androgens (male sex hormones) from fueling the growth and spread of tumors in men with prostate cancer. (
  • Androgens are steroid hormones with specific effects on tissue growth (muscle, fat, skin, hair and others) and brain function. (
  • Androgens and estrogens are hormones. (
  • Although androgens are described as male sex hormones, both males and females have them to varying degrees, as is also true of estrogens. (
  • Studies have shown that when men marry and have children, they often see a decline in their androgen levels-or their levels of male sex hormones. (
  • In this paper, we consider effects of androgen hormones on EC and EPC function in physiological and pathological conditions. (
  • Androgen suppression is a treatment to suppress or block the production or action of male hormones. (
  • This happens because a mutation on the X chromosome causes the body to resist androgen, the hormones that produce a male appearance. (
  • 1 These features suggested involvement of the sex hormones, and in view of the lack of persuasive evidence relating high oestrogen levels to RA, I suggested that one cause might be low androgen levels. (
  • Describes cells that have a protein that binds to androgens (male hormones). (
  • These cells may stop growing or die when they are treated with substances that block the binding and actions of androgen hormones. (
  • Targets to treat androgen excess in polycystic ovary syndrome. (
  • Tumors of the ovaries and polycystic ovary syndrome (PCOS) can both cause too much androgen production. (
  • People with partial androgen insensitivity (also called Reifenstein syndrome) can have genitalia that look typically female, genitalia that have both male and female characteristics, or genitalia that look typically male. (
  • The extent of the syndrome ranges from complete androgen insensitivity and development of normal external (but not internal) female sexual anatomy, to partial insensitivity, with altered or ambiguous male or female genitals, to mild insensitivity, with normal male genitals, enlarged breasts, and possibly impotence. (
  • Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome. (
  • Menstrual irregularity can be caused by polycystic ovarian syndrome, which is in turn caused by excess androgen. (
  • Their studies found that when excess androgen leads to polycystic ovarian syndrome, fertility problems may occur. (
  • This suggests that granulosa cell hyperresponsiveness to FSH in polycystic ovary syndrome (PCOS) may be related to androgen excess. (
  • Also, androgens are the precursors to estrogens in both men and women. (
  • Androgens and estrogens are known to be critical regulators of mammalian physiology and development. (
  • In this Review, we will discuss important roles of estrogens in males and androgens in females. (
  • However, substantial evidence now indicates that endogenous estrogens in men and androgens in women are not only integral to health, but can additionally promote aspects of disease. (
  • In fact, androgens have more than 200 actions in women, and they are present in higher amounts than estrogens. (
  • It is not known if this risk exists with the use of androgens and estrogens for symptoms of menopause. (
  • Androgens and estrogens may be dangerous for some people because of differences in their health and body chemistry. (
  • Androgens and estrogens may also be used for other conditions as determined by your doctor. (
  • Androgens are also the original anabolic steroids and the precursor of all estrogens . (
  • Estrogens, Androgens, and Serum Lipids: The Enigmatic Triad of Atherogenesis. (
  • Abuse of androgens (also called 'anabolic-androgenic steroids') has grown into a major worldwide substance abuse problem involving tens of millions of individuals, of whom about 98% are men. (
  • Together with the reduced androgen levels in aged men and women and the beneficial effects of androgens on brain function and pathology in Alzheimer's disease-related models, these data support the therapeutic potential of SARMs for age-related cognitive decline and Alzheimer's disease. (
  • Androgen backdoor pathway from 17α-hydroxyprogesterone to 5α-dihydrotestosterone. (
  • Other androgens include dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEA-S). (
  • Other androgens - dehydroepiandrostenedione (DHEA), its sulphate (DHEAS), and dihydrotestosterone (DHT) - are produced in the adrenal cortex, skin and liver. (
  • It is the first report of both androgen-dependence of exercise on nerve regeneration and of an androgenic effect of exercise in females. (
  • Rapid virilization associated with hirsutism is suggestive of androgen secreting neoplasm or exogenous androgenic drug use. (
  • ORLANDO -- Periodic breaks from androgen suppression therapy did not impact survival in men with prostate-specific antigen progression after radical therapy for prostate cancer. (
  • Lawton CA et al (2001) Updated results of the phase III Radiation Therapy Oncology Group (RTOG) trial 85-31 evaluating the potential benefit of androgen suppression following standard radiation therapy for unfavorable prognosis carcinoma of the prostate. (
  • Bolla M et al (2002) Long-term results with immediate androgen suppression and external irradiation in patients with locally advanced prostate cancer (an EORTC study): a phase III randomised trial. (
  • K. Akakura , N. Bruchovsky , S. L. Goldenberg , P. S. Rennie , A. R. Buckley and L. D. Sullivan , Effects of intermittent androgen suppression on androgen-dependent tumors. (
  • What is androgen suppression? (
  • Over the past 10 years, the Radiation Therapy Oncology Group has evaluated, by Phase III trials, the value of using a combination regimen, including androgen suppression (goserelin [Zoladex] and flutamide [Eulexin]) and radiation therapy, in locally advanced prostate cancer. (
  • Androgen suppression prior to or during radiation has not been shown to increase overall survival, but it has been shown to increase progression-free survival and freedom from distant metastases. (
  • Clinical trials conducted by the Radiation Therapy Oncology Group have shown that androgen suppression prior to or during radiation therapy increases progression-free survival and freedom from distant metastases in patients with localized prostate cancer, although an effect on overall survival has yet to be seen. (
  • These and other results of RTOG clinical trials of combined androgen suppression and radiation in treating localized prostate cancer were presented at the First Sonoma Conference on Prostate Cancer by William U. Shipley, MD, Chairman of the RTOG Genitourinary Committee. (
  • The RTOG trials build on experimental data using rodent models that show androgen suppression prior to irradiation enhances tumor eradication. (
  • Androgen suppression began 8 weeks before radiation and continued through radiation for a total of 16 weeks. (
  • At a median follow-up of 4.5 years, the estimated cumulative incidence of local failure at 5 years was 71% for the control patients and 46% for those on androgen suppression, and the PSA relapse-free survival was 15% among the controls, but 36% for those in the experimental group. (
  • Letrozole is a 3rd generation aromatase inhibitor which results in suppression of E2 production and increase in circulating serum androgen levels to about 40% greater than pre-treatment values. (
  • On the other hand, rapid progression of hair growth suggests an androgen secreting tumor. (
  • Despite initial responsiveness to androgen ablation therapy, tumor cells invariably relapse to an androgen-independent (AI) and antiandrogen-resistant state that ultimately leads to mortality. (
  • In 8 of 18 primary androgen-independent prostate tumor samples, tyrosine-phosphorylated AR protein was detected and correlated with the detection of tyrosine-phosphorylated Ack1. (
  • Androgens increase in both boys and girls during puberty. (
  • People with mild androgen insensitivity are born with male sex characteristics, but they are often infertile and tend to experience breast enlargement at puberty. (
  • Androgens increase in both males and females during puberty. (
  • Normally around puberty, androgens stimulate axillary and pubic hair in both sexes, plus the beard, etc. in men, while later they may also inhibit scalp hair growth causing androgenetic alopecia. (
  • From childhood to puberty, the levels of androgens rise in the body. (
  • By the time, male and female hit puberty, androgens cause the enlargement of the sebaceous glands. (
  • In women, androgens play a key role in the hormonal cascade that kick-starts puberty, stimulating hair growth in the pubic and underarm areas. (
  • Differences in atherosclerosis, body weight, and lipid levels between ARKO and control mice were abolished in mice that were ovariectomized before puberty, consistent with a protective action of ovarian androgens mediated via the AR. (
  • As such, the insensitivity to androgens is clinically significant only when it occurs in genetic males (i.e. individuals with a Y chromosome, or more specifically, an SRY gene). (
  • Alterations in androgen levels lead to reproductive defects in both males and females, including hypogonadotropic hypogonadism, anovulation, and infertility. (
  • However, androgens are not only produced in males, they are also produced in females. (
  • Androgens are produced by the body in greater amounts in males. (
  • However, androgens may cause unwanted effects in nursing babies such as too early sexual development in males or male-like changes in females. (
  • Here, we generated a mouse model (ArKl) in which the conserved SUMO acceptor lysines of AR are permanently abolished (Ar-K381R, (K500R)) ArKl males develop normally, without apparent defects in their systemic androgen action in reproductive tissues. (
  • Androgens have important cardiometabolic actions in males, but their metabolic role in females is unclear. (
  • Androgen enhances replication of hepatitis B virus (HBV), rendering males more vulnerable than females to this virus, according to research published in the February Journal of Virology . (
  • AR knockout males displayed a complete androgen insensitivity phenotype. (
  • For androgens as medications, see Anabolic steroid and Androgen replacement therapy . (
  • for information on androgens as medications, see the androgen replacement therapy and anabolic steroid articles. (
  • They are used in androgen replacement therapy (ART), among other indications. (
  • This is important because so far most work has focused on eliminating total serum androgen levels, a type of therapy that has shown little success. (
  • We had the opportunity to examine parameters of thymic cellular output in several hypogonadal men undergoing androgen replacement therapy. (
  • Male sexual dysfunction has been extensively researched, but there is less evidence addressing the treatment of HSDD in women, particularly with regard to the use of androgen therapy. (
  • The findings suggest that supplemental androgen therapy might benefit older men who are prone to losing muscle mass-a process known as sarcopenia-as they age. (
  • The purpose of this study is to evaluate the effects of androgen therapy on the size and number of non-palpable hypoechoic micro-nodules in patients with elevated gonadotropin levels. (
  • It's very important that they receive expert assessment by an endocrinologist at an early stage and receive androgen replacement therapy. (
  • This is established medical practice and uncontroversial, unlike androgen supplementation therapy in PADAM. (
  • He compares the 1980s and 1990s campaign to encourage women to Hormone Replacement Therapy (HRT) to prevent heart disease to the androgen gel therapeutic claims currently being presented to men. (
  • Anti-androgen therapy is pretty strong stuff , so it's good that the course of treatment is reasonably short. (
  • Gene expression analysis of human prostate carcinoma during hormonal therapy identifies androgen-responsive genes and mechanisms of therapy resistance, The American Journal of Pathology , 164 (2004), 217-227. (
  • H. V. Jain , S. K. Clinton , A. Bhinder and and A. Friedman , Mathematical modeling of prostate cancer progression in response to androgen ablation therapy, Proceedings of the National Academy of Sciences , 108 (2011), 19701-19706. (
  • Tumors in the adrenal glands can also cause too much production of androgens and can lead to male body characteristics in women. (
  • In addition to PCOS, other causes of high androgen levels (called hyperandrogenism) include congenital adrenal hyperplasia (a genetic disorder affecting the adrenal glands that afflicts about one in 10,000 to one in 18,000 Americans, about half of whom are women) and other adrenal abnormalities, and ovarian or adrenal tumors. (
  • Bladder cancer patients whose tumors express high levels of the protein CD24 may benefit from anti-androgen therapies, say researchers. (
  • We hope the results of these studies show the rationale for clinical studies of anti-androgen therapies with bladder cancer, especially in those tumors that happen to test markedly high in CD24 expression," Theodorescu says. (
  • Activated Ack1 promoted androgen-independent growth of LNCaP and LAPC-4 prostate xenograft tumors, AR recruitment to the androgen-responsive enhancer, and androgen-inducible gene expression in the absence of androgen. (
  • Neither was elevated in androgen-dependent tumors or benign prostate samples. (
  • This action of androgens is supported by a hormone from Sertoli cells, Müllerian inhibitory hormone (MIH), which prevents the embryonic Müllerian ducts from developing into fallopian tubes and other female reproductive tract tissues in male embryos. (
  • Insulin resistance appears to play a major role in a vicious cycle that alters female hormone metabolism towards androgen dominance. (
  • Androgens are used to treat men whose hormone levels have decreased. (
  • GlobalData's clinical trial report, 'Hormone Refractory (Castration Resistant, Androgen-Independent) Prostate Cancer Global Clinical Trials Review, H1, 2014' provides data on the Hormone Refractory (Castration Resistant, Androgen-Independent) Prostate clinical trial scenario. (
  • This report provides elemental information and data relating to the clinical trials on Hormone Refractory (Castration Resistant, Androgen-Independent) Prostate. (
  • The databook offers a preliminary coverage of disease clinical trials by their phase, trial status, prominence of the sponsors and also provides briefing pertaining to the number of trials for the key drugs for treating Hormone Refractory (Castration Resistant, Androgen-Independent) Prostate. (
  • Soon after they differentiate, Leydig cells begin to produce androgens. (
  • Both men's and women's bodies produce androgens, just in differing amounts. (
  • While the protein CD24 is difficult to affect directly with current therapies, anti-androgen therapies that would diminish the tumor's ability to express CD24 are already in wide use for prostate cancer. (
  • Your search returned 69 androgen regulated protein ELISA ELISA Kit across 10 suppliers. (
  • I3C downregulated the expression of PSA transcripts and protein levels and inhibited PSA promoter activity, as well as that of a minimal androgen responsive element containing reporter plasmid. (
  • Major changes in overall protein synthesis have been shown to be androgen-dependent at these stages ( 1 , 12 ), but despite extensive investigations, by using either in vivo or in vitro approaches, limited changes in expression of individual proteins by SC in response to androgens have been shown ( 1 , 12 ). (
  • Diallyl sulfied, a compound found in garlic, and zinc ameliorate the cadmium-induced testicular toxicity and inhibition of androgen production. (
  • In line with these observations, male mice, chimeric for an androgen-resistant Tfm X/Y (Tfm, testicular feminization) genotype (due to an inactivating mutation in the AR) and a normal (X/Y) genotype, are able to produce offspring from the Tfm X/Y component ( 8 ). (
  • Because germ cells seem not to require a functional AR, androgens must affect spermatogenesis indirectly via somatic testicular cells. (
  • Lizneva D, Gavrilova-Jordan L, Walker W, Azziz R. Androgen excess: investigations and management. (
  • With androgen excess, the extent of these changes is dependent on the level of androgens in the blood. (
  • Treatment success depends on the cause of excess androgen production. (
  • Forty two women with hidradenitis suppurativa were assessed clinically and biochemically for evidence of androgen excess. (
  • Is acne a sign of androgen excess disorder or not? (
  • Boyd-Woschinko G, Kushner H, Falkner B. Androgen excess is associated with insulin resistance and the development of diabetes in African American women. (
  • Excess amounts of androgens can pose a problem, resulting in such "virilizing effects" as acne, hirsutism (excess hair growth in "inappropriate" places, like the chin or upper lip) and thinning of hair on the head (balding). (
  • Androgen excess is an endocrine disorder that is sometimes found in women during their reproductive years. (
  • However, certain conditions may cause women to produce excess androgen. (
  • Acne is another symptom of excess androgen. (
  • In extreme cases, excess androgen can cause virilization. (
  • Supraphysiologic androgen levels may sometimes cause irritability, aggressiveness, and violence, whereas androgen withdrawal may cause depression. (
  • It also depends on the levels of androgens. (
  • In a baby with XY chromosomes, high levels of androgens are made in the testes. (
  • In a baby with XX chromosomes, there are no testes and the levels of androgens are very low. (
  • According to the theory, African populations should have the highest androgen levels, followed by Caucasians, then by Asians. (
  • androgens are also present at low levels in women. (
  • Although 40% of women with hirsute have regular menses, half of them will be found to have elevated levels of one or more androgens. (
  • Chang's objective was to locate a new pathway for treatment that would not require depletion of androgen levels in the entire body, which amounts to castration and causes severe side effects for patients. (
  • CD4+CD45RA+ cells fell from 37.36% to 20.05% after 1 month and to 12.51% after 7 months of normalized androgen levels. (
  • Androgens also produce this effect by increasing the levels of epinephrine and norepinephrine. (
  • Left untreated, high levels of androgens, regardless of whether a woman has PCOS or not, are associated with serious health consequences, such as insulin resistance and diabetes, high cholesterol, high blood pressure and heart disease. (
  • Low androgen levels can be a problem as well, producing effects such as low libido (interest in or desire for sex), fatigue, decreased sense of well-being and increased susceptibility to bone loss, osteoporosis and fractures. (
  • Low androgen levels may affect women at any age, but most commonly occur during the transition to menopause, or "perimenopause," a term used to describe the time before menopause (usually two to eight years). (
  • Androgen levels begin dropping in a woman's 20s, and by the time she reaches menopause, have declined 50 percent or more from their peak as androgen production declines in the adrenal glands, and the mid-cycle ovarian androgen boost lessens or evaporates altogether. (
  • By tuning androgen levels in mice, the scientists found that high androgen levels cause intestinal stem cells (ISCs) to divide more than usual and at the same time produced less mature epithelial cells. (
  • If the test comes back under normal levels he's put on androgen. (
  • When they artificially added CD24, cell proliferation resumed regardless of androgen levels. (
  • Surprising new research findings show that male lemurs' androgen levels increase the more they engage in child care behaviors. (
  • S. E. Eikenberry, J. D. Nagy and Y. Kuang, The evolutionary impact of androgen levels on prostate cancer in a multi-scale mathematical model, Biology Direct , 5 (2010), Art. (
  • This clinical study investigated the significance of low serum androgen levels in HF. (
  • Conclusion In male HF patients, low serum levels of androgens are associated with adverse prognosis, but this relation is confounded by indicators of a poor health state. (
  • CONCLUSIONS: Compared with lamotrigine monotherapy, valproate monotherapy was associated with weight gain and higher androgen levels in women with epilepsy. (
  • 4, 5 However, the possibility may be acknowledged that low androgen levels are markers (rather than causes) of RA. (
  • Androgens stimulate early stages of follicular growth in the primate ovary. (
  • A SARM for women would ideally stimulate bone retention, or libido and other function that androgens can influence, without negative side-effects such as development of male gender characteristics ( virilization ), increased LDL / HDL ratios, liver dysfunction, and so forth. (
  • This is the first report to detail the relationship between pretreatment prostate tissue androgen and response or prognosis of PCa treated by ADT using precise simultaneous quantitative analysis of androgen," say Yasuhiro Shibata (Gunma University Graduate School of Medicine, Japan) and team. (
  • They used the technique to determine the pre-ADT prostate tissue androgen content in 165 PCa patients who were followed up for the development of CRPCa, defined as a prostate specific antigen (PSA) value continuously raised by more than 25% above the nadir and a 2.0 ng/mL increase in PSA, and/or the progression of preexisting disease and/or the appearance of new metastasis. (
  • Progression to androgen independence and subsequent therapeutic resistance and death is a common fate of patients with prostate cancer. (
  • This book will focus on the androgen-regulated gene expression program, and examine how recently identified androgen-regulated genes are likely to contribute to the development and progression of prostate cancer. (
  • Thus, Ack1 activated by surface signals or oncogenic mechanisms may directly enhance AR transcriptional function and promote androgen-independent progression of prostate cancer. (
  • 2018. Prostate tissue androgen content predicts ADT outcome . (
  • Molecular mechanisms of androgen action - a historical perspective. (
  • Greater understanding of the mechanisms of androgen action in follicles should improve therapies for poorly controlled hair disorders like hirsutism and alopecia. (
  • Androgens induce virilization and are responsible for forming the male external genitalia in the fetus. (
  • Androgens from other parts of the body can also cause male characteristics to develop in women. (
  • Depending on the level of androgen insensitivity, an affected person's sex characteristics can vary from mostly female to mostly male. (
  • She also had low cortisol (and its precursors 17[alpha]-hydroxyprogesterone and 11-deoxycortisol), low adrenal androgens (DHEA sulfate and androstenedione), high mineralocorticoids precursors (11-deoxycorticosterone and corticosterone), high ACTH, and chromosomal analysis revealed a normal male karyotype 46 XY. (
  • A healthy XY embryo will develop male genitals, as the testes will release androgens. (
  • Also, hirsutism should be distinguished from hypertrichosis, where hair growth is not mediated by androgens and hairs are not distributed in an androgen sensitive (male) pattern. (
  • Development of male sex organ and characteristics - The first androgens are produced from the Leydig cells which differentiate at week 8 of fetal development. (
  • The released androgens masculinize the male fetus by stimulating the development of the penis and scrotum. (
  • Regulation of brain activity and structure - Androgens can influence the human activity and behavior and is also suspected to account for the differences in the structures of male and female brains. (
  • An estimated 1 in 65,000 female infants (with the male karyotype XY) are born with androgen insensitivity. (
  • Orchidectomy (ORX), ovariectomy (OVX), and inhibition of AR in male mouse models were done to investigate the effect of androgens on ISC terminal differentiation. (
  • Androgens (contained in this combination medicine) should not be used during pregnancy because they may cause male-like changes in a female baby. (
  • These images are a random sampling from a Bing search on the term "Androgen Decline in the Aging Male. (
  • Subsequently castrating male mice reduced the viral load, but injecting castrated mice with an androgen agonist resulted in a rising viral load again. (
  • Partial androgen insensitivity may be diagnosed at birth because of the presence of male and female sexual traits. (
  • [ 6 ] Androgen regulated genes are critical for the development and maintenance of the male sexual phenotype . (
  • Complete androgen insensitivity prevents the penis and other male body parts from developing. (
  • They also inhibited the upregulation of BMP downstream signals (Id1 and Msx1), further proving that androgens may serve as selective inhibitors of the BMP pathway. (
  • Testoterone depletion is a normal consequence of aging in men that is associated with senescent effects in androgen-responsive tissues. (
  • These new findings support the clinical evaluation of androgen-based therapies for the prevention and treatment of AD. (
  • To summarize recent findings regarding the public health impact of androgen abuse. (
  • These findings show that, over the short term at least, androgens are not atretogenic and actually enhance follicular growth and survival in the primate. (
  • The findings of this study indicate that none of these androgens is strongly associated with prostate cancer risk. (
  • Their findings, " Androgen Maintains Intestinal Homeostasis by Inhibiting BMP Signaling via Intestinal Stromal Cells ," were published recently in Stem Cell Reports . (
  • Their findings may lead to new therapies or treatments of colon cancers through androgen regulation and may provide a new therapeutic path for those affected even after the adjustment of related risk factors. (
  • To us, these sex-specific findings implied androgen involvement," Theodorescu says. (
  • Androgens are synthesized in the testes , the ovaries , and the adrenal glands . (
  • during the embryonic stage of development, testes form in an androgen-independent process that occurs due to the influence of the SRY gene on the Y chromosome. (
  • Adrenal androgens function as weak steroids (though some are precursors), and the subset includes dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), androstenedione (A4), and androstenediol (A5). (
  • In women, androgens are produced in the ovaries, adrenal glands and fat cells. (
  • Serum androgens and prostate cancer. (
  • The results suggest that low serum androgens develop as a sequel of this progressive multifaceted systemic disorder. (
  • In addition, the zR of humans and some other mammals produces so-called adrenal androgens such as dehydroepiandrosterone. (
  • Inhibition of fat deposition - Androgen inhibits fat deposition by reducing the ability of some fat cells to accumulate lipids. (
  • The androgen-directed treatment of prostate cancer (PCa) is fraught with the recurrent profile of failed treatment due to drug resistance and must be addressed if we are to provide an effective therapeutic option. (
  • What are some therapeutic uses of androgens? (
  • Therapeutic used of anti-androgens? (
  • At present there is no effective treatment for androgen-independent prostate cancer (AIPC), highlighting the pressing need to develop new alternative therapeutic strategies. (
  • The present study investigated the effect of androgens in promoting proliferation and inhibiting differentiation. (
  • Androgens also activate proliferation, migration, and recruitment of endothelial progenitor cells (EPCs), thereby contributing to vascular repair and restoration of the endothelial layer. (
  • What are effects of androgens? (
  • Most androgen abusers are still under age 50 today, and thus, the long-term effects of these drugs are only beginning to be understood. (
  • Several recent studies have also described androgen-induced hepatotoxicity, nephrotoxicity, and adverse musculoskeletal effects. (
  • Recent studies have demonstrated marked adverse effects of long-term androgen abuse. (
  • As increasing numbers of androgen abusers reach middle age, these effects will likely represent an emerging public health problem. (
  • Androgens can cause other side effects as well. (
  • Because of the side effects of androgens, their use has been limited. (
  • Adverse effects of 17 alpha-alkylated androgens? (
  • Adverse effects of synthetic androgen treatment? (
  • Adverse effects of synthetic androgen treatment in women and children? (
  • For many women, the effects of this further androgen decline include aggravation of hot flashes and accelerated bone loss. (
  • However, androgens can also activate endothelial production of some vasoconstrictors, which can have detrimental effects on the vascular endothelium. (
  • The possibility that these two observations are linked and that replacement of androgens in older androgen-deficient men will have positive effects on bone has considerable medical and economic importance. (
  • Postnatal females are not as sensitive as the fetus to androgens, which induce the growth of sexual hair, temporal balding, acne, clitoral growth, sebum production, and a deepening of the voice. (
  • The gene for androgen sensitivity is on the X chromosome, so genetic females carrying the gene won't appear affected because they have another normal X chromosome. (
  • However, androgens are also present in females in small amounts. (
  • Andropause symptoms are related to the lack of androgens including DEPRESSION, sexual dysfunction, and OSTEOPOROSIS. (
  • Effect of adrenal and ovarian androgens on type 4 follicles unresponsive to FSH in immature mice," Endocrinology , vol. 142, no. 11, pp. 4930-4936, 2001. (
  • By comparing results obtained in phase 1, the investigators will be able to determine if there is an androgen mediated response by granulosa cells to FSH stimulation in the absence of other ovarian steroids. (
  • MECHANISMS IN ENDOCRINOLOGY: The sexually dimorphic role of androgens in human metabolic disease. (
  • In the present protocol, the investigators propose to further study the role of androgens with a 2 phase study. (
  • It is concluded that cell-autonomous action of the AR in SC is an absolute requirement for androgen maintenance of complete spermatogenesis, and that spermatocyte/spermatid development/survival critically depends on androgens. (
  • The response to androgens varies with the body site as it is specific to the hair follicle itself. (
  • Under the influence of androgens, remnants of the mesonephron , the Wolffian ducts , develop into the epididymis , vas deferens and seminal vesicles . (
  • But it is now becoming clear that (counter to this possibility), administration of androgens to patients with RA ameliorates the condition. (