Compounds that inhibit AROMATASE in order to reduce production of estrogenic steroid hormones.
Organic compounds containing the -CN radical. The concept is distinguished from CYANIDES, which denotes inorganic salts of HYDROGEN CYANIDE.
A selective aromatase inhibitor effective in the treatment of estrogen-dependent disease including breast cancer.
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.
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.
Derivatives of the steroid androstane having three double bonds at any site in any of the rings.
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.
Tumors or cancer of the human BREAST.
An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.
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.
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.
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)
One of the SELECTIVE ESTROGEN RECEPTOR MODULATORS with tissue-specific activities. Tamoxifen acts as an anti-estrogen (inhibiting agent) in the mammary tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and cell proliferation in the ENDOMETRIUM.
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.
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.
Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds.
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.
Enlargement of the BREAST in the males, caused by an excess of ESTROGENS. Physiological gynecomastia is normally observed in NEWBORNS; ADOLESCENT; and AGING males.
The physiological period following the MENOPAUSE, the permanent cessation of the menstrual life.
Supporting cells for the developing female gamete in the OVARY. They are derived from the coelomic epithelial cells of the gonadal ridge. Granulosa cells form a single layer around the OOCYTE in the primordial ovarian follicle and advance to form a multilayered cumulus oophorus surrounding the OVUM in the Graafian follicle. The major functions of granulosa cells include the production of steroids and LH receptors (RECEPTORS, LH).
An antineoplastic agent that is a derivative of progesterone and used to treat advanced breast cancer.
Derivatives of the steroid androstane having two double bonds at any site in any of the rings.
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.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
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.
The gamete-producing glands, OVARY or TESTIS.
A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.
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.
A highly vascularized mammalian fetal-maternal organ and major site of transport of oxygen, nutrients, and fetal waste products. It includes a fetal portion (CHORIONIC VILLI) derived from TROPHOBLASTS and a maternal portion (DECIDUA) derived from the uterine ENDOMETRIUM. The placenta produces an array of steroid, protein and peptide hormones (PLACENTAL HORMONES).
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.
Substances that possess antiestrogenic actions but can also produce estrogenic effects as well. They act as complete or partial agonist or as antagonist. They can be either steroidal or nonsteroidal in structure.
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.
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.
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.
A cyclic nucleotide formed from CYTIDINE TRIPHOSPHATE by the action of cytidylate cyclase. It is a potential cyclic nucleotide intracellular mediator of signal transductions.
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.
A transcription factor and member of the nuclear receptor family NR5 that is expressed throughout the adrenal and reproductive axes during development. It plays an important role in sexual differentiation, formation of primary steroidogenic tissues, and their functions in post-natal and adult life. It regulates the expression of key steroidogenic enzymes.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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)
Specific proteins found in or on cells of progesterone target tissues that specifically combine with progesterone. The cytosol progesterone-receptor complex then associates with the nucleic acids to initiate protein synthesis. There are two kinds of progesterone receptors, A and B. Both are induced by estrogen and have short half-lives.
A condition in which functional endometrial tissue is present outside the UTERUS. It is often confined to the PELVIS involving the OVARY, the ligaments, cul-de-sac, and the uterovesical peritoneum.
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.
Region of hypothalamus between the ANTERIOR COMMISSURE and OPTIC CHIASM.
An OOCYTE-containing structure in the cortex of the OVARY. The oocyte is enclosed by a layer of GRANULOSA CELLS providing a nourishing microenvironment (FOLLICULAR FLUID). The number and size of follicles vary depending on the age and reproductive state of the female. The growing follicles are divided into five stages: primary, secondary, tertiary, Graafian, and atretic. Follicular growth and steroidogenesis depend on the presence of GONADOTROPINS.
A potent androgenic metabolite of TESTOSTERONE. It is produced by the action of the enzyme 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE.
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.
A malignant metastatic form of trophoblastic tumors. Unlike the HYDATIDIFORM MOLE, choriocarcinoma contains no CHORIONIC VILLI but rather sheets of undifferentiated cytotrophoblasts and syncytiotrophoblasts (TROPHOBLASTS). It is characterized by the large amounts of CHORIONIC GONADOTROPIN produced. Tissue origins can be determined by DNA analyses: placental (fetal) origin or non-placental origin (CHORIOCARCINOMA, NON-GESTATIONAL).
A triazine herbicide.
Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.
Drug therapy given to augment or stimulate some other form of treatment such as surgery or radiation therapy. Adjuvant chemotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.
A structurally diverse group of compounds distinguished from ESTROGENS by their ability to bind and activate ESTROGEN RECEPTORS but act as either an agonist or antagonist depending on the tissue type and hormonal milieu. They are classified as either first generation because they demonstrate estrogen agonist properties in the ENDOMETRIUM or second generation based on their patterns of tissue specificity. (Horm Res 1997;48:155-63)
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.
A mitochondrial cytochrome P450 enzyme that catalyzes the side-chain cleavage of C27 cholesterol to C21 pregnenolone in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11A1 gene, catalyzes the breakage between C20 and C22 which is the initial and rate-limiting step in the biosynthesis of various gonadal and adrenal steroid hormones.
The fluid surrounding the OVUM and GRANULOSA CELLS in the Graafian follicle (OVARIAN FOLLICLE). The follicular fluid contains sex steroids, glycoprotein hormones, plasma proteins, mucopolysaccharides, and enzymes.
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.
Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Animals and plants which have, as their normal mode of reproduction, both male and female sex organs in the same individual.
Luciferases from RENILLA that oxidizes certain LUMINESCENT AGENTS to cause emission of PHOTONS.
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.
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.
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.
A plant genus of the family LILIACEAE with roots that contain VERATRUM ALKALOIDS used as emetics, parasiticides, antihypertensives. It is the main ingredient of Boicil.
In humans, one of the paired regions in the anterior portion of the THORAX. The breasts consist of the MAMMARY GLANDS, the SKIN, the MUSCLES, the ADIPOSE TISSUE, and the CONNECTIVE TISSUES.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Hormones produced in the testis.
Hormones that stimulate gonadal functions such as GAMETOGENESIS and sex steroid hormone production in the OVARY and the TESTIS. Major gonadotropins are glycoproteins produced primarily by the adenohypophysis (GONADOTROPINS, PITUITARY) and the placenta (CHORIONIC GONADOTROPIN). In some species, pituitary PROLACTIN and PLACENTAL LACTOGEN exert some luteotropic activities.
A selective triazine herbicide. Inhalation hazard is low and there are no apparent skin manifestations or other toxicity in humans. Acutely poisoned sheep and cattle may show muscular spasms, fasciculations, stiff gait, increased respiratory rates, adrenal degeneration, and congestion of the lungs, liver, and kidneys. (From The Merck Index, 11th ed)
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Exogenous agents, synthetic and naturally occurring, which are capable of disrupting the functions of the ENDOCRINE SYSTEM including the maintenance of HOMEOSTASIS and the regulation of developmental processes. Endocrine disruptors are compounds that can mimic HORMONES, or enhance or block the binding of hormones to their receptors, or otherwise lead to activating or inhibiting the endocrine signaling pathways and hormone metabolism.
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.
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.
Sexual activities of animals.
Gonadal interstitial or stromal cell neoplasm composed of only LEYDIG CELLS. These tumors may produce one or more of the steroid hormones such as ANDROGENS; ESTROGENS; and CORTICOSTEROIDS. Clinical symptoms include testicular swelling, GYNECOMASTIA, sexual precocity in children, or virilization (VIRILISM) in females.
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.
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
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.
Those protein complexes or molecular sites on the surfaces of gonadal and other sensitive cells that bind gonadotropins and thereby modify the functions of those cells; hCG, LH, and FOLLICLE STIMULATING HORMONE are the major specific gonadotropins.
A cell line derived from cultured tumor cells.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The surgical removal of one or both ovaries.
Pain in the joint.
Development of male secondary SEX CHARACTERISTICS in the FEMALE. It is due to the effects of androgenic metabolites of precursors from endogenous or exogenous sources, such as ADRENAL GLANDS or therapeutic drugs.
The period of the MENSTRUAL CYCLE representing follicular growth, increase in ovarian estrogen (ESTROGENS) production, and epithelial proliferation of the ENDOMETRIUM. Follicular phase begins with the onset of MENSTRUATION and ends with OVULATION.
Those protein complexes or molecular sites on the surfaces and cytoplasm of gonadal cells that bind luteinizing or chorionic gonadotropic hormones and thereby cause the gonadal cells to synthesize and secrete sex steroids. The hormone-receptor complex is internalized from the plasma membrane and initiates steroid synthesis.
An order of bottom fishes with short, small, spinous dorsal fins. It is comprised of one family (Batrachoididae) and about 70 species.
Tumors or cancers of the ADRENAL CORTEX.
A genus of BIRDS in the family Phasianidae, order GALLIFORMES, containing the common European and other Old World QUAIL.
Pathological processes involving any part of the UTERUS.
The mechanisms by which the SEX of an individual's GONADS are fixed.
Enzymes that catalyze the oxidation of estradiol at the 17-hydroxyl group in the presence of NAD+ or NADP+ to yield estrone and NADH or NADPH. The 17-hydroxyl group can be in the alpha- or beta-configuration. EC 1.1.1.62
Large, long-tailed reptiles, including caimans, of the order Loricata.
Cell surface proteins that bind FOLLICLE STIMULATING HORMONE with high affinity and trigger intracellular changes influencing the behavior of cells.
Organometallic compounds which contain tin and three alkyl groups.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Megestrol acetate is a progestogen with actions and uses similar to those of the progestogens in general. It also has anti-androgenic properties. It is given by mouth in the palliative treatment or as an adjunct to other therapy in endometrial carcinoma and in breast cancer. Megestrol acetate has been approved to treat anorexia and cachexia. (From Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
The surgical removal of one or both testicles.
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
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.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The most diversified of all fish orders and the largest vertebrate order. It includes many of the commonly known fish such as porgies, croakers, sunfishes, dolphin fish, mackerels, TUNA, etc.
Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.
The mucous membrane lining of the uterine cavity that is hormonally responsive during the MENSTRUAL CYCLE and PREGNANCY. The endometrium undergoes cyclic changes that characterize MENSTRUATION. After successful FERTILIZATION, it serves to sustain the developing embryo.
An enzyme that catalyzes the reduction of TESTOSTERONE to 5-ALPHA DIHYDROTESTOSTERONE.
Fushi tarazu transcription factors were originally identified in DROSOPHILA. They are found throughout ARTHROPODS and play important roles in segmentation and CENTRAL NERVOUS SYSTEM development.
A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.
Common name for small PASSERIFORMES in the family Fringillidae. They have a short stout bill (BEAK) adapted for crushing SEEDS. Some species of Old World finches are called CANARIES.
Development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of PUBERTY in the population. This early maturation of the hypothalamic-pituitary-gonadal axis results in sexual precocity, elevated serum levels of GONADOTROPINS and GONADAL STEROID HORMONES such as ESTRADIOL and TESTOSTERONE.
A species of baboon in the family CERCOPITHECIDAE with a somewhat different social structure than PAPIO HAMADRYAS. They inhabit several areas in Africa south of the Sahara.
Conditions of sexual ambiguity in which the individual possesses gonadal tissues of both sexes, tissues from the OVARY and the TESTIS. There can be a testis on one side and an ovary on the other (lateral), or there may be combined ovarian and testicular tissue (ovotestes) on each side (bilateral). The karyotype may be 46,XX; 46,XY; or a mosaic of 46,XX/46,XY. These disorders have historically been called true hermaphroditism.
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.
Cytoplasmic proteins that bind estradiol, migrate to the nucleus, and regulate DNA transcription.
A family of freshwater fish comprising the minnows or CARPS.
The degeneration and resorption of an OVARIAN FOLLICLE before it reaches maturity and ruptures.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A gonadotropic glycoprotein hormone produced primarily by the PLACENTA. Similar to the pituitary LUTEINIZING HORMONE in structure and function, chorionic gonadotropin is involved in maintaining the CORPUS LUTEUM during pregnancy. CG consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is virtually identical to the alpha subunits of the three pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity (CHORIONIC GONADOTROPIN, BETA SUBUNIT, HUMAN).
The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
A monoamine oxidase inhibitor with antihypertensive properties.
The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the ENDOCRINE GLANDS, included are the CHROMAFFIN SYSTEM and the NEUROSECRETORY SYSTEMS.
The D-isomer of ASPARTIC ACID.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
A species of PERCIFORMES commonly used in saline aquaculture.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
A subclass of repressor proteins that do not directly bind DNA. Instead, co-repressors generally act via their interaction with DNA-BINDING PROTEINS such as a TRANSCRIPTIONAL SILENCING FACTORS or NUCLEAR RECEPTORS.
An estrogen responsive cell line derived from a patient with metastatic human breast ADENOCARCINOMA (at the Michigan Cancer Foundation.)
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.
A malignant neoplasm of the ADRENAL CORTEX. Adrenocortical carcinomas are unencapsulated anaplastic (ANAPLASIA) masses sometimes exceeding 20 cm or 200 g. They are more likely to be functional than nonfunctional, and produce ADRENAL CORTEX HORMONES that may result in hypercortisolism (CUSHING SYNDROME); HYPERALDOSTERONISM; and/or VIRILISM.
Sexual union of a male and a female in non-human species.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
A major gonadotropin secreted by the human adenohypophysis (PITUITARY GLAND, ANTERIOR). Follicle-stimulating hormone stimulates GAMETOGENESIS and the supporting cells such as the ovarian GRANULOSA CELLS, the testicular SERTOLI CELLS, and the LEYDIG CELLS. FSH consists of two noncovalently linked subunits, alpha and beta. The alpha subunit is common in the three human pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity.
A neoplasm composed entirely of GRANULOSA CELLS, occurring mostly in the OVARY. In the adult form, it may contain some THECA CELLS. This tumor often produces ESTRADIOL and INHIBIN. The excess estrogen exposure can lead to other malignancies in women and PRECOCIOUS PUBERTY in girls. In rare cases, granulosa cell tumors have been identified in the TESTES.
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.
Phospholipoglycoproteins produced in the fat body of egg-laying animals such as non-mammalian VERTEBRATES; ARTHROPODS; and others. Vitellogenins are secreted into the HEMOLYMPH, and taken into the OOCYTES by receptor-mediated ENDOCYTOSIS to form the major yolk proteins, VITELLINS. Vitellogenin production is under the regulation of steroid hormones, such as ESTRADIOL and JUVENILE HORMONES in insects.
Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.
Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.
Ventral part of the DIENCEPHALON extending from the region of the OPTIC CHIASM to the caudal border of the MAMMILLARY BODIES and forming the inferior and lateral walls of the THIRD VENTRICLE.
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.
The inferior and superior venae cavae.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Hormones produced by the GONADS, including both steroid and peptide hormones. The major steroid hormones include ESTRADIOL and PROGESTERONE from the OVARY, and TESTOSTERONE from the TESTIS. The major peptide hormones include ACTIVINS and INHIBINS.
A cyclic nucleotide derivative that mimics the action of endogenous CYCLIC AMP and is capable of permeating the cell membrane. It has vasodilator properties and is used as a cardiac stimulant. (From Merck Index, 11th ed)
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.
A sudden, temporary sensation of heat predominantly experienced by some women during MENOPAUSE. (Random House Unabridged Dictionary, 2d ed)
Glycoproteins that inhibit pituitary FOLLICLE STIMULATING HORMONE secretion. Inhibins are secreted by the Sertoli cells of the testes, the granulosa cells of the ovarian follicles, the placenta, and other tissues. Inhibins and ACTIVINS are modulators of FOLLICLE STIMULATING HORMONE secretions; both groups belong to the TGF-beta superfamily, as the TRANSFORMING GROWTH FACTOR BETA. Inhibins consist of a disulfide-linked heterodimer with a unique alpha linked to either a beta A or a beta B subunit to form inhibin A or inhibin B, respectively
PLANT EXTRACTS and compounds, primarily ISOFLAVONES, that mimic or modulate endogenous estrogens, usually by binding to ESTROGEN RECEPTORS.

Constitutional genetic variation at the human aromatase gene (Cyp19) and breast cancer risk. (1/1297)

The activity of the aromatase enzyme, which converts androgens into oestrogens and has a major role in regulating oestrogen levels in the breast, is thought to be a contributing factor in the development of breast cancer. We undertook this study to assess the role of constitutional genetic variation in the human aromatase gene (Cyp19) in the development of this disease. Our genotyping of 348 cases with breast cancer and 145 controls (all Caucasian women) for a published tetranucleotide repeat polymorphism at intron 4 of the Cyp19 gene revealed the presence of six common and two rare alleles. Contingency table analysis revealed a significant difference in allelic distribution between cases and controls (chi2 5df = 13.52, P = 0.019). The allele measuring 171 bp was over-represented in cases; of 14 individuals homozygous for this allele, 13 were cases. These individuals had a higher incidence of cancer in family members and an earlier age at diagnosis than other cases. In sequencing Cyp19's coding exons and regulatory regions, we discovered a perfect association between a silent polymorphism (G-->A at Val80) and the high-risk genotype. Our conclusion is that constitutional genetic variation at the Cyp19 locus is associated with the risk of developing breast cancer, with the 171-bp allele serving as the high-risk allele.  (+info)

Endometriosis: a dysfunction and disease of the archimetra. (2/1297)

Endometriosis is considered primarily a disease of the endometrial-subendometrial unit or archimetra. The clinical picture of endometriosis characterises this disease as a hyperactivation of genuine archimetrial functions such as proliferation, inflammatory defence and peristalsis. While the aetiology of the disease remains to be elucidated, a key event appears to consist in the local production of extraovarian oestrogen by a pathological expression of the P450 aromatase. The starting event may consist in a hyperactivity of the endometrial inflammatory defence, a hyperactivity of the endometrial oxytocin/oxytocin receptor system or in the pathological expression of the P450 aromatase system itself. Regardless of which of these levels the starting event is localized in, they influence each other on both the level of the archimetra and the endometriotic lesions. Locally elevated oestrogen levels inevitably up-regulate the endometrial oxytocin mRNA and increased levels of oxytocin result in uterine hyperperistalsis, increased transtubal seeding of endometrial tissue fragments and finally subfertility and infertility by impairment of the uterine mechanism of rapid and sustained sperm transport. Locally increased levels of oestrogen lead, on both the level of the endometrial-subendometrial unit and the endometriotic lesion, to processes of hyperproliferation. These processes result, on the level of the uterus, in an infiltrative growth of elements of the archimetra into the neometra and, on the level of the endometriotic lesion, in infiltrative endometriosis. There is circumstantial evidence that trauma might be an important initial event that induces the specific biochemical and cellular responses of the archimetra. This model is able to explain both the pleiomorphic appearance of endometriosis and the, up until now, enigmatic infertility associated with mild and moderate endometriosis.  (+info)

The aromatase inactivator 4-hydroxyandrostenedione (4-OH-A) inhibits tamoxifen metabolism by rat hepatic cytochrome P-450 3A: potential for drug-drug interaction of tamoxifen and 4-OH-A in combined anti-breast cancer therapy. (3/1297)

Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 microM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA.  (+info)

The mechanism of action of epidermal growth factor and transforming growth factor alpha on aromatase activity in granulosa cells from polycystic ovaries. (4/1297)

We investigated aromatization and the mechanism of action of epidermal growth factor (EGF) and transforming growth factor alpha (TGFalpha) on oestradiol biosynthesis in freshly prepared granulosa cells from polycystic ovaries. Freshly prepared granulosa cells from polycystic ovaries incubated for only 3 h under basal conditions secreted significantly (P< 0.001) greater amounts of oestradiol-17beta than that of granulosa cells from normal ovaries. 8-Bromo-cyclic adenosine monophosphate (8-Br-cAMP), but not follicle stimulating hormone (FSH) or luteinizing hormone (LH), further enhanced this activity. Both EGF and TGFalpha inhibited gonadotrophinor 8-Br-cAMP-stimulated, but not basal, oestradiol production. LH receptor (LHR) binding, estimated by immunolabelling the bound LH, was significantly (P< 0.001) reduced in granulosa cells from polycystic ovaries when compared with cells from normal ovaries. EGF or TGFalpha significantly reduced the binding in cultured cells from all patient groups (P< 0.05). More interestingly, a further increase of the inhibitory effect was seen in granulosa cells from polycystic ovaries (P < 0.001). In conclusion, granulosa cells from polycystic ovaries contain high levels of basal aromatase activity in vitro, which is probably inherited from the in-vivo condition. EGF and TGFalpha suppress oestradiol synthesis at a step beyond the production of cAMP and also LHR binding with more effect in granulosa cells from polycystic ovaries.  (+info)

Effect of labor induction on the expression of oxytocin receptor, cytochrome P450 aromatase, and estradiol receptor in the reproductive tract of the late-pregnant ewe. (5/1297)

In this study, we investigated the timing of changes in aromatase, estradiol receptor, and oxytocin receptor expression in ovine uterine and placental tissues before parturition. Labor was induced by betamethasone injection into the fetus on Days 130-132 of pregnancy. Tissue samples were collected at injection and then every 14 h until labor (56 h) from four ewes at each time point. Samples were analyzed for aromatase, estradiol receptor, and oxytocin receptor expression by in situ hybridization; for oxytocin binding to its receptor using a specific antagonist; and for estradiol receptor quantitation by immunocytochemistry. Aromatase mRNA expression increased by 14 h postinjection (p < 0.02) in the fetal villi and remained high until labor. Expression of estradiol and oxytocin receptor mRNAs was unchanged in myometrium but increased in the endometrial luminal epithelium by 28 h (p < 0.05) and remained high until labor. Estradiol receptor protein concentration increased modestly at labor while oxytocin receptor binding in the luminal epithelium changed in parallel to the mRNA concentration. IN CONCLUSION: 1) induction of aromatase may facilitate the expression of endometrial estradiol and oxytocin receptors in the placentome, 2) changes in endometrial rather than myometrial oxytocin receptor may be important in inducing parturition, and 3) the transcription of estradiol receptor and oxytocin receptor in the uterine epithelium are positively correlated during parturition.  (+info)

A 500-bp region, approximately 40 kb upstream of the human CYP19 (aromatase) gene, mediates placenta-specific expression in transgenic mice. (6/1297)

In humans, aromatase P450 (product of CYP19 gene), which catalyzes conversion of C19 steroids to estrogens, is expressed in a number of tissues, including ovary, adipose, and syncytiotrophoblast of the placenta. The 5' untranslated regions of CYP19 mRNA transcripts in these tissues are encoded by different tissue-specific first exons, which are spliced onto a common site just upstream of the translation initiation site in exon II. In placenta, the 5' untranslated region of CYP19 mRNA transcripts is encoded by exon I.1, which lies approximately 40 kb upstream of exon II. To map genomic sequences required for placenta-specific CYP19 expression, fusion genes containing 2,400 and 501 bp of placenta-specific exon I.1 5' flanking DNA linked to the human growth hormone gene (hGH), as reporter, were introduced into transgenic mice. Expression of CYP19(I.1):hGH fusion genes containing as little as 501 bp of 5' flanking DNA was placenta-specific and developmentally regulated. Furthermore, transgene expression occurred specifically in the labyrinthine trophoblast of the mouse placenta, which contains syncytial cells that may be analogous to the human syncytiotrophoblast. We show that a relatively small segment of DNA (approximately 500 bp) >40 kb upstream of the protein coding region of a human gene is able to direct expression in an appropriate tissue- and cell-specific manner in transgenic mice. These findings suggest that 5' flanking DNA within 501 bp of exon I.1 of the human CYP19 gene contains cis-acting elements that bind placenta-specific transcription factors that are conserved between humans and mice.  (+info)

Intrafollicular content of luteinizing hormone receptor, alpha-inhibin, and aromatase in relation to follicular growth, estrous cycle stage, and oocyte competence for in vitro maturation in the mare. (7/1297)

The intrafollicular content of LH receptor, alpha-inhibin, and aromatase are known good indicators of follicular status. We investigated the amounts of these proteins in granulosa and cumulus cells in relation to oocyte competence for in vitro maturation, follicular growth, and estrous cycle stage in the mare. Follicular punctures were performed 34 h after an injection of crude equine gonadotropins, either during the follicular phase, at the end of the follicular phase, or during the luteal phase. The cumulus-oocyte complex, granulosa cells, and follicular fluid of follicles larger than 5 mm were collected. The nuclear stage of the oocytes after in vitro culture was determined microscopically. Granulosa and cumulus cell amounts of LH receptor, alpha-inhibin, and aromatase were assessed by the semiquantitative Western blot method and image analysis. Follicular fluids were assayed for progesterone (P4) and estradiol-17beta (E2). The three factors were expressed in mural granulosa and cumulus cells from all follicles from the gonadotropin-independent growth period until the preovulatory stage. Considering all the follicles punctured, the amounts of LH receptor and alpha-inhibin in granulosa cells were not different for the three physiological stages studied. The amounts of aromatase in granulosa cells, as well as the E2:P4 ratios, were higher for follicles punctured during the follicular phase than for the two other groups (p < 0.05). Considering the data from the three groups, the E2:P4 ratio and the LH receptor and aromatase contents, but not alpha-inhibin, in granulosa cells increased with an increase in follicular diameter (p < 0.01). The E2:P4 ratios and the amounts of LH receptor, alpha-inhibin, and aromatase in granulosa cells were lower in follicles 5-9 mm in diameter than in larger ones (p < 0.05). In cumulus cells, the amounts of the three factors were different neither between the three groups nor between the follicular diameters. Although we could not establish any obvious relationship to oocyte competence for in vitro maturation, the influence of the follicle diameter on the content of LH receptors, alpha-inhibin, and aromatase in granulosa cells was similar to the influence of follicle diameter on oocyte competence. Therefore, one can hypothesize that, in the mare, there is a link between the acquisition of oocyte competence and the expression of these factors in the follicular cells.  (+info)

Dynamics of periovulatory steroidogenesis in the rhesus monkey follicle after ovarian stimulation. (8/1297)

The temporal relationships and regulation of events in the primate follicle during the periovulatory interval are poorly understood. This study was designed to elucidate the dynamics of steroid synthesis in the macaque follicle during ovarian stimulation cycles in which serum/follicular fluid aspirates were collected at precise intervals before (0 h) and after (up to 36 h) administration of the ovulatory human chorionic gonadotrophin (HCG) bolus. Serum concentrations of progesterone increased (P < 0.05) within 30 min, and follicular fluid progesterone concentrations were elevated 180-fold within 12 h, of HCG injection, and remained elevated until the time of ovulation. In contrast, 17beta-oestradiol concentrations increased initially, but then declined (P < 0.05) by 36 h post-HCG. Acute incubation of granulosa cells with and without steroidogenic substrates demonstrated that: (i) 3beta-hydroxysteroid dehydrogenase and aromatase activities were present in equivalent amounts before and after HCG; whereas (ii) P450 side-chain cleavage activity increased (P < 0.05) within 12 h of HCG; and (iii) exogenous low-density lipoprotein and cholesterol were not utilized for steroidogenesis. This model should be useful for further studies on ovulation and luteinization in primates, and enable elucidation of the local actions of progesterone and other steroids at specific time points during the periovulatory interval.  (+info)

There are different types of Breast Neoplasms such as:

1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.

2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.

3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.

4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.

5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.

Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.

Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.

It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.

Examples of hormone-dependent neoplasms include:

1. Breast cancer: Many breast cancers are estrogen receptor-positive (ER+), meaning that they grow in response to estrogen. These cancers can be treated with selective estrogen receptor modulators (SERMs) or aromatase inhibitors, which block the effects of estrogen on cancer growth.
2. Prostate cancer: Some prostate cancers are androgen-dependent, meaning that they grow in response to androgens such as testosterone. These cancers can be treated with androgen deprivation therapy (ADT), which reduces the levels of androgens in the body to slow or stop cancer growth.
3. Uterine cancer: Some uterine cancers are estrogen-dependent, meaning that they grow in response to estrogen. These cancers can be treated with hormone therapy to reduce estrogen levels.

Hormone-dependent neoplasms are often characterized by the presence of hormone receptors on the surface of the cancer cells. These receptors can bind to specific hormones and trigger signals that promote cancer growth and progression. Targeting these hormone receptors with hormone therapy can be an effective way to slow or stop the growth of these cancers.

The term "gynecomastia" comes from the Greek words "gyneco," meaning "womanlike," and "mastos," meaning "breast." The condition can occur at any age, but it is most common in infants, teenagers, and older men.

Gynecomastia can be caused by a variety of factors, including:

1. Hormonal imbalance: An imbalance of testosterone and estrogen hormones can lead to breast tissue growth.
2. Medications: Certain medications, such as antidepressants, anti-anxiety drugs, and heart medications, can cause gynecomastia as a side effect.
3. Medical conditions: Conditions such as hypogonadism (low testosterone levels), hyperthyroidism (high thyroid hormone levels), and liver or kidney disease can contribute to gynecomastia.
4. Genetic factors: Some men may inherit a tendency to develop gynecomastia due to genetic mutations.
5. Other factors: Gynecomastia can also be caused by other factors such as obesity, alcohol consumption, and certain types of foods or supplements.

Symptoms of gynecomastia may include:

* Enlarged breasts
* Breast tenderness
* Nipple sensitivity
* Pain in the breasts
* Swelling in the armpits

Gynecomastia is usually diagnosed through a physical examination and medical history. Imaging tests such as mammography or ultrasound may also be used to help rule out other conditions.

Treatment for gynecomastia depends on the underlying cause of the condition. In some cases, medications may be prescribed to address hormonal imbalances or other medical conditions that are contributing to the development of gynecomastia. Surgery may also be an option to remove excess breast tissue and improve the appearance of the chest.

In conclusion, gynecomastia is a relatively common condition in men that can have a significant impact on their self-esteem and quality of life. Understanding the causes and symptoms of gynecomastia is essential for proper diagnosis and effective treatment.

In the medical field, the term is often used to describe various conditions that affect gender development or sexual differentiation in individuals with variations in sex chromosomes, hormones, or genitalia. Feminization can occur in individuals assigned male at birth but who exhibit female physical characteristics, such as those with congenital adrenal hyperplasia (CAH) or other intersex traits.

The term is also used to describe the effects of estrogen on the male body, particularly during puberty. For example, boys taking estrogen medication for hormone therapy may experience feminization of their physical features, such as breast tissue growth and a softer voice.

It's important to note that the term feminization is sometimes used in medical contexts to describe a process or outcome that is perceived as negative or undesirable, particularly when it comes to gender identity or expression. However, it's essential to recognize that all individuals, regardless of their gender identity or expression, deserve respect and support in their healthcare needs.

In summary, feminization within the medical field refers to a process or condition whereby male characteristics are acquired by an individual or group, often as a result of hormonal or genetic factors. The term is used to describe various conditions affecting gender development or sexual differentiation and the effects of estrogen on the male body. However, it's important to recognize that the term can be perceived as negative, and healthcare providers should approach patients with respect and sensitivity regardless of their gender identity or expression.

Endometriosis can cause a range of symptoms, including:

* Painful periods (dysmenorrhea)
* Heavy menstrual bleeding
* Pelvic pain or cramping
* Infertility or difficulty getting pregnant
* Abnormal bleeding or spotting
* Bowel or urinary symptoms such as constipation, diarrhea, or painful urination during menstruation

The exact cause of endometriosis is not known, but it is thought to involve a combination of genetic, hormonal, and environmental factors. Some possible causes include:

* Retrograde menstruation: The backflow of endometrial tissue through the fallopian tubes into the pelvic cavity during menstruation
* Coelomic metaplasia: The transformation of cells that line the abdominal cavity (coelom) into endometrial cells
* Immunological factors: Abnormal immune responses that lead to the growth and accumulation of endometrial cells outside of the uterus
* Hormonal factors: Fluctuations in estrogen levels, which can stimulate the growth of endometrial cells
* Genetic factors: Inherited traits that increase the risk of developing endometriosis

There are several risk factors for developing endometriosis, including:

* Family history: A woman's risk increases if she has a mother, sister, or daughter with endometriosis
* Early onset of menstruation: Women who start menstruating at a younger age may be more likely to develop endometriosis
* Frequent or heavy menstrual bleeding: Women who experience heavy or prolonged menstrual bleeding may be more likely to develop endometriosis
* Polycystic ovary syndrome (PCOS): Women with PCOS are at higher risk for developing endometriosis
* Obesity: Being overweight or obese may increase the risk of developing endometriosis

There is no cure for endometriosis, but there are several treatment options available to manage symptoms and improve quality of life. These may include:

* Hormonal therapies: Medications that reduce estrogen levels or block the effects of estrogen on the endometrium can help manage symptoms such as pain and heavy bleeding
* Surgery: Laparoscopic surgery can be used to remove endometrial tissue and scar tissue, and improve fertility
* Alternative therapies: Acupuncture, herbal remedies, and other alternative therapies may help manage symptoms and improve quality of life

It's important for women with endometriosis to work closely with their healthcare provider to find the best treatment plan for their individual needs. With proper diagnosis and treatment, many women with endometriosis can go on to lead fulfilling lives.

The symptoms of choriocarcinoma can vary depending on the location and size of the tumor, but they may include:

* Abnormal vaginal bleeding
* Pelvic pain
* Abdominal pain
* Weakness and fatigue
* Shortness of breath
* Nausea and vomiting

If choriocarcinoma is suspected, a variety of tests may be performed to confirm the diagnosis. These may include:

* Ultrasound: This imaging test uses high-frequency sound waves to create pictures of the uterus and ovaries. It can help doctors identify any abnormal growths or tumors in the area.
* Hysteroscopy: This procedure involves inserting a thin, lighted tube through the cervix to visualize the inside of the uterus. Doctors may use hysteroscopy to collect samples of tissue for testing.
* Laparoscopy: This procedure involves making small incisions in the abdomen and using a thin, lighted tube to visualize the inside of the pelvis. Doctors may use laparoscopy to collect samples of tissue for testing or to remove any tumors that are found.
* Biopsy: In this test, doctors take a small sample of tissue from the uterus and examine it under a microscope for cancer cells.

If choriocarcinoma is confirmed, treatment may involve a combination of surgery, chemotherapy, and radiation therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as the patient's overall health.

Prognosis for choriocarcinoma varies depending on the stage of the cancer when it is diagnosed. In general, the prognosis is good if the cancer is caught early and treated promptly. However, if the cancer has spread to other parts of the body (metastasized), the prognosis may be poorer.

It's important for women who have had a molar pregnancy or choriocarcinoma to follow up with their healthcare provider regularly to ensure that any remaining tissue is removed and to monitor for any signs of recurrence.

These tumors typically affect adult men and are relatively slow-growing. They can cause symptoms such as painless testicular swelling, difficulty urinating, or abdominal discomfort due to pressure on surrounding organs.

Leydig cell tumors are relatively rare, accounting for less than 1% of all testicular tumors. They are usually benign (non-cancerous), but in some cases can be malignant (cancerous). Treatment typically involves surgical removal of the affected testicle (orchiectomy) and may also involve hormone therapy to reduce levels of male hormones, such as testosterone.

Leydig cell tumors are classified into two main types: Leydig cell adenoma and Leydig cell carcinoma. Leydig cell adenoma is the more common type and typically grows slowly, while Leydig cell carcinoma is less common but can grow faster and be more aggressive.

Overall, Leydig cell tumors are rare and often slow-growing, but they can cause significant symptoms and may require surgical intervention to treat.

The word "arthralgia" comes from the Greek words "arthron," meaning joint, and "algos," meaning pain. It is often used interchangeably with the term "joint pain," but arthralgia specifically refers to a type of pain that is not caused by inflammation or injury.

Arthralgia can manifest in different ways, including:

1. Aching or dull pain in one or more joints
2. Sharp or stabbing pain in one or more joints
3. Pain that worsens with movement or weight-bearing activity
4. Pain that improves with rest
5. Pain that is localized to one joint or multiple joints
6. Pain that is accompanied by stiffness or limited range of motion
7. Pain that is worse in the morning or after periods of rest
8. Pain that is triggered by certain activities or movements

The diagnosis of arthralgia typically involves a comprehensive medical history and physical examination, as well as diagnostic tests such as X-rays, blood tests, or imaging studies. Treatment for arthralgia depends on the underlying cause and may include medications, lifestyle modifications, or other interventions.

The causes of virilism can be due to various factors including:

1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive levels of androgens such as testosterone.
2. Androgen insensitivity syndrome (AIS): A condition where the body is unable to respond to androgens, leading to virilization.
3. 5-alpha-reductase deficiency: A rare genetic disorder that affects the production of the enzyme 5-alpha-reductase, which is important for the development of male characteristics.
4. Genetic mutations: Some individuals may have genetic mutations that lead to the overproduction of androgens or the underproduction of anti-androgens.
5. Hormonal imbalances: Imbalances in hormone levels, such as high testosterone and low estrogen, can also cause virilism.

Virilism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as hormone level measurements. Treatment options for virilism depend on the underlying cause and may include hormone replacement therapy, surgery, or psychological counseling.

In summary, virilism is a condition characterized by the excessive development of male characteristics in individuals who are not biologically male, and it can be caused by various genetic or hormonal factors. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can improve outcomes.

Types of Adrenal Cortex Neoplasms:

1. Adrenocortical carcinoma (ACC): A rare and aggressive malignant tumor that originates in the adrenal cortex. It is often associated with virilization (excessive masculinization) in women.
2. Adrenocortical adenoma (ACA): A benign tumor that originates in the adrenal cortex. It is less common than ACC and may not cause any symptoms.
3. Pheochromocytoma: A rare tumor that originates in the adrenal medulla, which is the inner part of the adrenal gland. It can secrete excessive amounts of hormones that regulate blood pressure and heart rate.
4. Paraganglioma: A rare tumor that originates in the paraganglia, which are clusters of cells located near the adrenal glands. These tumors can produce excessive amounts of hormones and cause similar symptoms as pheochromocytoma.

Symptoms of Adrenal Cortex Neoplasms:

1. Virilization (excessive masculinization) in women, such as deepening of the voice, excessive body hair growth, and clitoral enlargement.
2. Headache, fatigue, and weight gain due to excessive production of steroid hormones.
3. High blood pressure and heart rate due to excessive production of catecholamines (hormones that regulate blood pressure and heart rate).
4. Abdominal pain, nausea, and vomiting due to the tumor's size and location.

Diagnosis of Adrenal Cortex Neoplasms:

1. Imaging tests such as CT scans or MRI to visualize the tumor and determine its size and location.
2. Laboratory tests to measure hormone levels in the blood, including cortisol, aldosterone, and catecholamines.
3. Biopsy to obtain a tissue sample for further examination under a microscope.

Treatment of Adrenal Cortex Neoplasms:

1. Surgery to remove the tumor, which is usually curative.
2. Medications to control symptoms such as high blood pressure and hormone levels.
3. Radiation therapy may be used in cases where surgery is not feasible or if there is a risk of recurrence.

Prognosis of Adrenal Cortex Neoplasms:

The prognosis for adrenal cortex neoplasms depends on the type and size of the tumor, as well as the extent of hormone production. In general, the prognosis is good for patients with benign tumors that are removed surgically. However, malignant tumors can have a poorer prognosis and may require additional treatments such as radiation therapy or chemotherapy.

Prevention of Adrenal Cortex Neoplasms:

There is no known prevention for adrenal cortex neoplasms, but early detection and treatment can improve outcomes. Regular monitoring of hormone levels and imaging tests can help detect tumors at an early stage.

Lifestyle Changes:

1. Reduce stress: High levels of cortisol can be caused by stress, so finding ways to manage stress can help prevent adrenal cortex neoplasms.
2. Maintain a healthy diet: Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains can help support overall health and well-being.
3. Exercise regularly: Regular physical activity can help reduce stress and improve overall health.
4. Get enough sleep: Aim for 7-8 hours of sleep per night to help regulate hormone levels.
5. Limit caffeine and alcohol: Both substances can disrupt hormone levels and contribute to the development of adrenal cortex neoplasms.

Some common types of uterine diseases include:

1. Endometriosis: A condition in which tissue similar to the lining of the uterus grows outside the uterus, causing pain, inflammation, and infertility.
2. Fibroids: Noncancerous growths that develop in the uterus, often causing heavy menstrual bleeding, pelvic pain, and infertility.
3. Adenomyosis: A condition where tissue similar to the lining of the uterus grows into the muscle wall of the uterus, leading to heavy menstrual bleeding, pain, and infertility.
4. Uterine polyps: Growths that develop on the inner lining of the uterus, often causing abnormal bleeding or spots on the uterine lining.
5. Uterine cancer: Cancer that develops in the cells of the uterus, often caused by factors such as obesity, hormonal imbalances, or family history of cancer.
6. Endometrial hyperplasia: A condition where the lining of the uterus becomes thicker than normal, often due to hormonal imbalances or excessive estrogen exposure.
7. Asherman's syndrome: Scar tissue that develops inside the uterus, often after a D&C procedure, leading to infertility and irregular menstrual bleeding.
8. Uterine septum: A congenital condition where a wall of tissue divides the uterus into two compartments, often causing irregular menstrual bleeding and fertility problems.
9. Endometrial cysts: Fluid-filled sacs that develop on the inner lining of the uterus, often causing abnormal bleeding or pelvic pain.
10. Uterine tuberculosis: A rare condition where the uterus becomes infected with tuberculosis bacteria, often caused by poor sanitation and hygiene.

These are just a few of the many conditions that can affect the uterus and cause abnormal bleeding. It's important to consult with a healthcare provider if you experience any unusual or persistent vaginal bleeding to determine the underlying cause and receive proper treatment.

Precocious puberty is a condition wherein children under the age of 8 or 9 experience early onset of pubertal changes, such as breast development, menstruation, or enlargement of the testes and scrotum. It is also known as central precocious puberty (CPP) when it is caused by premature activation of the hypothalamic-pituitary-gonadal axis, resulting in early release of sex hormones.

Precocious Puberty: Causes

The exact cause of precocious puberty is not known; however, several factors have been implicated, including:

1. Genetics: In some cases, precocious puberty may be inherited, with a family history of early puberty or other hormonal disorders.
2. Brain tumors: Tumors in the hypothalamus or pituitary gland can cause early activation of the HPG axis and result in precocious puberty.
3. Congenital anomalies: Some children may be born with abnormalities in the HPG axis, leading to early puberty.
4. Trauma: Traumatic brain injury or stroke may trigger premature activation of the HPG axis and result in precocious puberty.
5. Infections: Certain infections, such as meningitis or encephalitis, can cause inflammation in the hypothalamus or pituitary gland, leading to early puberty.
6. Nutritional factors: Malnutrition or rapid weight gain may contribute to early puberty.
7. Hormonal imbalance: Some children may have an imbalance of sex hormones, such as estrogen or testosterone, which can lead to early puberty.
8. Thyroid disorders: Hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid) can cause early puberty.
9. Chronic diseases: Certain chronic diseases, such as type 1 diabetes mellitus or inflammatory bowel disease, may increase the risk of early puberty.

It is important to note that in many cases, the exact cause of precocious puberty cannot be determined. If you suspect that your child is experiencing early puberty, it is essential to consult with a healthcare professional for proper evaluation and treatment.

The term "ovotesticular" refers to the presence of both ovarian and testicular tissue, while "disorders of sex development" (DSD) is a broader category that encompasses a wide range of conditions that affect the development of sex characteristics. OSDS are considered to be a subset of DSDs.

Examples of OSDS include:

1. Androgen insensitivity syndrome (AIS): A condition in which individuals with XY chromosomes do not respond to androgens, leading to the development of female physical characteristics.
2. Complete and partial ovary-testis duplication: Conditions in which there is an extra ovary and/or testis present in addition to the normal ovary and testis.
3. Mixed gonadal dysgenesis (MGD): A condition in which there is a combination of ovarian and testicular tissue, but the exact combination can vary.
4. Swyer syndrome: A condition in which individuals with XY chromosomes have a normal appearing ovary and uterus, but do not produce sperm.

The management of OSDS is complex and requires a multidisciplinary approach, including endocrinologists, geneticists, gynecologists, and psychologists. Treatment options may include hormone therapy, surgery, and/or gender confirmation surgeries. The goal of treatment is to help individuals with OSDS achieve optimal physical and emotional well-being, as well as to provide support and counseling for families and individuals affected by these conditions.

Adrenocortical carcinoma can be subdivided into three main types based on their histological features:

1. Typical adrenocortical carcinoma: This is the most common type and accounts for about 70% of all cases. It is characterized by a large, irregular tumor that grows in the cortex of the adrenal gland.
2. Adenomatous adrenocortical carcinoma: This type is less aggressive than typical adrenocortical carcinoma and accounts for about 20% of cases. It is characterized by a small, well-circumscribed tumor that grows in the cortex of the adrenal gland.
3. Adrenocortical sarcoma: This is the least common type and accounts for about 10% of cases. It is characterized by a rare, malignant tumor that grows in the cortex of the adrenal gland.

Adrenocortical carcinoma can cause a variety of symptoms, including abdominal pain, weight loss, fatigue, and skin changes. The diagnosis is typically made through a combination of imaging studies, such as CT scans and MRI, and tissue biopsy. Treatment options include surgery, chemotherapy, and radiation therapy, and the prognosis depends on the stage and aggressiveness of the tumor.

Overall, adrenocortical carcinoma is a rare and aggressive cancer that requires prompt diagnosis and treatment to improve patient outcomes.

The tumor usually grows slowly and may not cause any symptoms in its early stages. However, as it progresses, it can cause abdominal pain, bloating, and irregular vaginal bleeding. GCTs are generally diagnosed through a combination of pelvic examination, imaging studies such as ultrasound or computed tomography (CT), and biopsy.

There are several subtypes of GCT, including:

1. Granulosa cell tumor with stromal element (GCT-SE): This is the most common type of GCT and accounts for about 70% of all cases. It is characterized by the presence of stromal cells, which are connective tissue cells that provide support and structure to the tumor.
2. Granulosa cell tumor without stromal element (GCT-wSE): This type of GCT lacks stromal cells and accounts for about 30% of all cases. It tends to be more aggressive than GCT-SE and is more likely to spread to other parts of the body.
3. Mucinous granulosa cell tumor (MGCT): This is a rare subtype of GCT that produces mucin, a type of protein that is found in the ovary. MGCTs tend to be slower-growing than other types of GCT and have a better prognosis.

Treatment for GCT typically involves surgery to remove the tumor, followed by radiation therapy and/or chemotherapy to destroy any remaining cancer cells. The prognosis for GCT is generally good, with a 5-year survival rate of about 80% for women with early-stage disease. However, the prognosis can be poorer for women with more advanced stages of the disease.

In summary, granulosa cell tumor is a rare type of ovarian cancer that originates from the granulosa cells of the ovary. It can present in different forms and has a good prognosis if treated early. Treatment typically involves surgery, radiation therapy, and/or chemotherapy.

Examples of 'Mammary Neoplasms, Experimental' in a sentence:

1. The researchers studied the effects of hormone therapy on mammary neoplasms in experimental animals to better understand its potential role in human breast cancer.
2. The lab used mice with genetic mutations that predispose them to developing mammary neoplasms to test the efficacy of new cancer drugs.
3. In order to investigate the link between obesity and breast cancer, the researchers conducted experiments on mammary neoplasms in rats with diet-induced obesity.

There are several theories about the causes of hot flashes, including hormonal changes, neurotransmitter imbalances, and blood vessel dilation. Some risk factors for hot flashes include age, family history, and certain medical conditions such as hypertension and diabetes.

Treatment options for hot flashes include hormone therapy, selective serotonin reuptake inhibitors (SSRIs), and non-hormonal medications such as clonidine and gabapentin. Lifestyle modifications such as dressing in layers, using a fan, and avoiding triggers like spicy foods and alcohol can also help manage hot flashes.

In conclusion, hot flashes are a common symptom of menopause that can have a significant impact on quality of life. While their exact cause is still not fully understood, there are several effective treatment options available to manage their frequency and severity. By understanding the causes and risk factors for hot flashes, women can work with their healthcare providers to find the best course of treatment for their individual needs.

In particular, aromatase is responsible for the aromatization of androgens into estrogens. The enzyme aromatase can be found in ... Aromatase activity is decreased or antagonized by prolactin, anti-Müllerian hormone and glyphosate. Aromatase is generally ... "Aromatase Inhibitors". Breastcancer.org. 29 October 2020. Attar E, Bulun SE (May 2006). "Aromatase inhibitors: the next ... Despite the fact that data suggest temperature controls aromatase quantities, other studies have shown that aromatase can ...
Aromatase deficient female cannot synthesize estrone or estradiol in the absence of aromatase. The amount of androgen will ... RORA is the gene for aromatase, an enzyme that converts male to female hormones. Thus, RORA deficiency is linked to aromatase ... Aromatase deficient males experience a normal growth into adulthood. With a very low level of circulating estrogen (. ... Aromatase deficiency is an exceedingly rare condition characterized by extremely low levels or complete absence of the enzyme ...
... s work by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens by a ... Chen S, Kao YC, Laughton CA (1997). "Binding characteristics of aromatase inhibitors and phytoestrogens to human aromatase". J ... The heightened gonadotropin levels also upregulate the aromatase promoter, increasing aromatase production in the setting of ... some natural elements have aromatase inhibiting effects, such as damiana leaves. The development of aromatase inhibitors was ...
... s irreversibly inhibit the enzyme by binding covalently to the binding site of aromatase so the ... If nonsteroidal aromatase Inhibitors are not working or patients are relapsing, then the use of steroidal aromatase inhibitors ... Aromatase inhibitors stops this conversion and lowers the levels of estrogen. Treating breast cancer with aromatase inhibitors ... Exemestane is the first oral aromatase inactivator. Clinical use of steroidal aromatase inhibitors today is more or less ...
... (AES or AEXS) is a rare genetic and endocrine syndrome which is characterized by an overexpression of ... Excessive levels of aromatase P450arom and its transcripts in breast adipose tissue of a girl with pubertal macromastia [ ... In one study, cellular aromatase mRNA expression was found to be at least 10 times higher in a female patient compared to the ... "Aromatase excess syndrome - Conditions - GTR - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2022-02-08. Shozu, Makio; Sebastian, Siby ...
Aromatase inhibitors Steroidal aromatase inhibitors Chumsri, Saranya (2015-05-06). "Clinical utilities of aromatase inhibitors ... Aromatase is an enzyme that belongs to the cytochrome P450 family located on chromosome 15. In the human body, the aromatase ... When aromatase inhibitors (AIs) are used to treat breast cancer the main target is the aromatase enzyme which is responsible ... Non-Steroidal Aromatase Inhibitors (NSAIs) are one of two categories of aromatase inhibitors (AIs). AIs are divided into two ...
It can be used at a dosage of up to 500 mg four times per day (2,000 mg/day). It is used as an aromatase inhibitor to inhibit ... Maximal aromatase inhibition is said to occur between dosages of 250 to 500 mg per day. The side effects of AG are less ... AG can inhibit aromatase by 74 to 92% and decrease circulating estradiol levels by 58 to 76% in men and postmenopausal women. ... In any case, AG is also used by bodybuilders and other men for its actions as an aromatase inhibitor in order to decrease ...
Aromatase inhibitors like exemestane (which forms a permanent and deactivating bond with the aromatase enzyme) and anastrozole ... Lephart, E. D. (1996). "A Review of Brain Aromatase Cytochrome P450". Brain Res. Rev. 22 (1): 1-26. doi:10.1016/0165-0173(96) ... Avendaño, C.; Menéndez, J. C. (2008). "Aromatase Inhibitors". Medicinal Chemistry of Anticancer Drugs. Elsevier. pp. 65-73. doi ... A related aromatization process includes dehydroisomerization of methylcyclopentane to benzene: Aromatases are enzymes that ...
ASL Aromatase deficiency; 613546; CYP19A1 Aromatase excess syndrome; 139300; CYP19A1 Aromatic L-amino acid decarboxylase ...
... aromatase, on breast cancer. Brodie managed to get an aromatase inhibitor into a limited clinical trial in breast cancer ... aromatase. They developed several steroidal aromatase inhibitors, she focused on 4-OHA. In 1979, she moved to Maryland, ... Santen, R. J.; Brodie, H.; Simpson, E. R.; Siiteri P. K.; Brodie, A. (1 July 2013). "History of Aromatase: Saga of an Important ... She never intended to retire, and collaborated with Vincent Njar on aromatase inhibitors in prostate cancer for the rest of her ...
Examples of aromatase inhibitors include anastrozole and letrozole. Evidence for aromatase inhibitors is confirmed by numerous ... Aromatase inhibitors are medications that block the formation of estrogen and have become of interest for researchers who are ... December 2020). "Aromatase inhibitors for the treatment of endometriosis: a systematic review about efficacy, safety and early ... Bulun SE, Zeitoun K, Sasano H, Simpson ER (1999). "Aromatase in aging women". Seminars in Reproductive Endocrinology. 17 (4): ...
Medications such as aromatase inhibitors have been found to be effective and even in rare cases of gynecomastia from disorders ... Aromatase excess syndrome is a rare genetic disorder that leads to increased conversion of androgens to estrogens in the body. ... Aromatase inhibitors (AIs) such as anastrozole have been used off-label for cases of gynecomastia occurring during puberty but ... Obesity is another common cause of excess serum estrogens due to the presence of aromatase in peripheral tissue, which is a ...
ISBN 978-1-84816-959-3. Balthazart J, Ball G (15 November 2012). Brain Aromatase, Estrogens, and Behavior. OUP USA. pp. 161-. ...
Chen S, Zhou D, Yang C, Okubo T, Kinoshita Y, Yu B, Kao YC, Itoh T (December 2001). "Modulation of aromatase expression in ... Bulun SE, Yang S, Fang Z, Gurates B, Tamura M, Zhou J, Sebastian S (December 2001). "Role of aromatase in endometrial disease ... Modugno F, Weissfeld JL, Trump DL, Zmuda JM, Shea P, Cauley JA, Ferrell RE (October 2001). "Allelic variants of aromatase and ... Mutations in this gene can result in either increased or decreased aromatase activity; the associated phenotypes suggest that ...
Bulun SE (2014). "Aromatase and estrogen receptor α deficiency". Fertil. Steril. 101 (2): 323-9. doi:10.1016/j.fertnstert. ... Congenital estrogen deficiency can alternatively be caused by a defect in aromatase, the enzyme responsible for the ... for instance that seen in aromatase excess syndrome. In 1994, a 28-year-old man with EIS was reported. He was fully ... biosynthesis of estrogens, a condition which is referred to as aromatase deficiency and is similar in symptomatology to EIS. ...
His lab has synthesized a number of aromatase inhibitors using equine aromatase as a model.[non-primary source needed] His ... Lemazurier E, Sourdaine P, Nativelle C, Plainfossé B, Séralini G (June 2001). "Aromatase gene expression in the stallion". ... The general area of his lab's research focuses on the endocrine system, in particular the enzyme aromatase. ... Séralini G, Moslemi S (June 2001). "Aromatase inhibitors: past, present and future". Molecular and Cellular Endocrinology. 178 ...
Experience from experimental aromatase inhibitor treatment of endometriosis indicates that aromatase inhibitors might be ... Aromatase inhibitors have been used experimentally to reduce fibroids. The effect is believed to be due partially by lowering ... Bulun SE, Yang S, Fang Z, Gurates B, Tamura M, Zhou J, Sebastian S (2001). "Role of aromatase in endometrial disease". The ... Aromatase inhibitors are currently considered for treatment, at certain doses they would completely inhibit estrogen production ...
It inhibits aromatase seven fold more potently than nicotine. It also releases dopamine in adult but not adolescent rats. ... Doering IL, Richter E (April 2009). "Inhibition of human aromatase by myosmine". Drug Metabolism Letters. 3 (2): 83-6. doi: ...
... is a major peripheral source of aromatase in both males and females, contributing to the production of estradiol ... Stocco C (January 2012). "Tissue physiology and pathology of aromatase". Steroids. 77 (1-2): 27-35. doi:10.1016/j.steroids. ...
... is an aromatase (CYP19A1) inhibitor. Huuskonen, P; Myllynen, P; Storvik, M; Pasanen, M (2013). "The effects of ... Aromatase inhibitors, Nitriles, Triazoles, Fluoroarenes, All stub articles, Antineoplastic and immunomodulating drug stubs). ...
Chalcones are also natural aromatase inhibitors. Chalcones are aromatic ketones with two phenyl rings that are also ... "Chalcones are potent inhibitors of aromatase and 17β-hydroxysteroid dehydrogenase activities". Life Sciences. 68 (7): 751-61. ...
... and aromatase inhibitors. As of 2016 the only marketed SERD was fulvestrant (brand name Faslodex). As of November 2016 other ... Aromatase inhibitor Estrogen deprivation therapy Lee, CI; Goodwin, A; Wilcken, N (3 January 2017). "Fulvestrant for hormone- ...
The brain is also affected by this sexual differentiation; the enzyme aromatase converts testosterone into estradiol that is ... Fat cells synthesize the enzyme aromatase, which converts testosterone, the male sex hormone, into estradiol, the female sex ... Meinhardt U, Mullis PE (August 2002). "The essential role of the aromatase/p450arom". Seminars in Reproductive Medicine. 20 (3 ... and brain and aromatase is highly expressed in adipose tissue, bone, and the brain. As much as 90% of testosterone is converted ...
June 1994). "Novel aromatase and 5 alpha-reductase inhibitors". The Journal of Steroid Biochemistry and Molecular Biology. 49 ( ... Unlike other steroidal aromatase inhibitors such as formestane and exemestane, minamestane does not have androgenic properties ... Minamestane (INN (former developmental code name FCE-24,928) is a steroidal aromatase inhibitor which was under development by ... Combs, Donald W (1995). "Review Oncologic, Endocrine & Metabolic: Recent developments in aromatase inhibitors". Expert Opinion ...
Aromatase is an enzyme that synthesizes estrogen. Aromatase inhibitors block the synthesis of estrogen. This lowers the ... Type II aromatase inhibitors such as anastrozole and letrozole, by contrast, are not steroids and work by interfering with the ... Maximal aromatase inhibition occurs after two to three days. 90% of the absorbed substance are bound to plasma proteins. The ... Along with other aromatase inhibitors, exemestane is on the World Anti-Doping Agency's list of prohibited substances. Oral ...
361-. ISBN 978-0-12-815676-6. Vanden Bossche HV, Moereels H, Koymans LM (1994). "Aromatase inhibitors--mechanisms for non- ... Aromatase inhibitors, Glutarimides, 4-Pyridyl compounds, All stub articles, Antineoplastic and immunomodulating drug stubs). ... but instead has pharmacological activity as a selective aromatase inhibitor similar to the related drug aminoglutethimide and ...
Lephart, E. D. (1996). "A Review of Brain Aromatase Cytochrome P450". Brain Res. Rev. 22 (1): 1-26. doi:10.1016/0165-0173(96) ... These conversions are catalyzed by aromatase enzymes using O2 as the oxidant. Specific conversions include testosterone to ...
Hata S, Miki Y, Saito R, Ishida K, Watanabe M, Sasano H (June 2013). "Aromatase in human liver and its diseases". Cancer Med. 2 ... It was reported in 2002 that tibolone or its metabolite δ4-tibolone is transformed by aromatase into the potent estrogen 7α- ... In accordance, a 2009 study found that an aromatase inhibitor had no effect on the estrogenic potencies of tibolone or its ... despite the absence of aromatase in the adult human liver. Tibolone and δ4-tibolone act as agonists of the progesterone ...
... by the enzyme aromatase. Minor endogenous estrogens, the biosyntheses of which do not involve aromatase, include 27- ... aromatase deficiency, and aromatase excess syndrome. High estrogen can amplify stress-hormone responses in stressful situations ... Aromatase deficiency is ultimately suspected which is involved in the synthesis of estrogen in humans and has therapeutic ... When estrogen levels were raised through the increased activity of the enzyme aromatase in male lab mice, OCD rituals were ...
... has been found to act as a weak aromatase inhibitor in vitro (Ki = 10 μM), though there is evidence to suggest that ... Kao YC, Zhou C, Sherman M, Laughton CA, Chen S (1998). "Molecular basis of the inhibition of human aromatase (estrogen ... Le Bail JC, Laroche T, Marre-Fournier F, Habrioux G (November 1998). "Aromatase and 17beta-hydroxysteroid dehydrogenase ... though similarly to the case of aromatase, these activities have not yet been confirmed in vivo. Unlike many other flavonoids, ...
Find symptoms and other information about Aromatase excess syndrome. ... Aromatase excess syndrome is a genetic disease, which means that it is caused by one or more genes not working correctly. ... When Do Symptoms of Aromatase excess syndrome Begin?. Symptoms of this disease may start to appear as a Child and as a Teenager ... About Aromatase excess syndrome. Many rare diseases have limited information. Currently GARD aims to provide the following ...
Aromatase excess syndrome is a condition characterized by elevated levels of the female sex hormone estrogen in both males and ... Aromatase excess syndrome is a condition characterized by elevated levels of the female sex hormone estrogen in both males and ... The prevalence of aromatase excess syndrome is unknown; more than 20 cases have been described in the medical literature. ... Rearrangements of genetic material involving the CYP19A1 gene cause aromatase excess syndrome. The CYP19A1 gene provides ...
SEARCH RESULTS for: Aromatase Inhibitors [Drug Class] (92 results) *Share : JavaScript needed for Sharing tools. Bookmark & ...
... hormone-receptor-positive breast cancer who got 5 years of an aromatase inhibitor seem to be more likely to have heart problems ...
The aromatase inhibitors block estrogen synthesis and are used as therapy of estrogen receptor positive breast cancer, usually ... Are all aromatase inhibitors the same? A review of controlled clinical trials in breast cancer. Berry J. Berry J. Clin Ther. ... Aromatase Inhibitors No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet ... The effect of combining aromatase inhibitors with antiestrogens on tumor growth in a nude mouse model for breast cancer. Lu Q, ...
The aromatase inhibitors block estrogen synthesis and are used as therapy of estrogen receptor positive breast cancer, usually ... Are all aromatase inhibitors the same? A review of controlled clinical trials in breast cancer. Berry J. Berry J. Clin Ther. ... Aromatase Inhibitors No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet ... The effect of combining aromatase inhibitors with antiestrogens on tumor growth in a nude mouse model for breast cancer. Lu Q, ...
Aromatase inhibitors in breast cancer: an overview. Oncologist 2006;11(6):553-62. CrossRefexternal icon PubMedexternal icon ... Aromatase inhibitor-associated arthralgia syndrome. Breast 2007;16(3):223-34. CrossRefexternal icon PubMedexternal icon ... Aromatase inhibitor-associated arthralgia and/or bone pain: frequency and characterization in non-clinical trial patients. Clin ... Adding aromatase inhibitors (AIs) to adjuvant treatment of postmenopausal women with hormone-receptor-positive breast cancer ...
The aromatase inhibitors (AI) have become a critical component of adjuvant therapy for breast cancer, but they cause bone pain ... Evaluation of the safety of vitamin D3 supplements in women treated with aromatase inhibitors is crucial. In vitro studies have ... To assure that vitamin D3 does not abrogate the clinical benefits of aromatase inhibitors, the effect of vitamin D3 supplements ... Project Title: Vitamin D3 Effects on Musculoskeletal Symptoms with Use of Aromatase Inhibitors. Abstract: DESCRIPTION (provided ...
There are three FDA approved aromatase inhibitors for all stages of breast cancer: Anastrozole (Arimidex and generic); ... Aromatase inhibitors interfere with the enzyme aromatase to decrease the female hormones in your body. It then can reduce the ... Who gets aromatase inhibitors. All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive ... How aromatase inhibitors are given. The AIs are all given as daily pills. In early-stage disease they are usually given after ...
Anne Hudson Blaes, MD, on Aromatase Inhibitors and Cardiovascular Disease 2016 San Antonio Breast Cancer Symposium. ... Anne Hudson Blaes, MD, of the University of Minnesota, discusses the association between aromatase inhibitors, endothelial ... aromatase inhibitor-treated, locally advanced or metastatic breast cancer, who progressed on or after mTOR inhibitor-based ...
... lower aromatase levels were a strong predictor of survival. Our findings implicate aromatase as an early-stage predictor of ... Aromatase expression predicts survival in women with early-stage non small cell lung cancer.. ... Within this population, the prognostic value of aromatase was greatest in earlier stage lung cancer (stage I/II). In addition, ... We predict that women whose lung cancers have higher levels of aromatase might be good candidates for targeted treatment with ...
WT1 and DAX-1 inhibit aromatase P450 expression in human endometrial and endometriotic stromal cells. In: Journal of Clinical ... WT1 and DAX-1 inhibit aromatase P450 expression in human endometrial and endometriotic stromal cells. Journal of Clinical ... Dive into the research topics of WT1 and DAX-1 inhibit aromatase P450 expression in human endometrial and endometriotic ... WT1 and DAX-1 inhibit aromatase P450 expression in human endometrial and endometriotic stromal cells. / Gurates, Bilgin; ...
SEARCH RESULTS for: Aromatase Inhibitors [Drug Class] (92 results) *Share : JavaScript needed for Sharing tools. Bookmark & ...
The Resveratrol competed with the aromatase and also inhibited the genes that create aromatase so it affected aromatase in two ... Thats why aromatase inhibitors work well in women after menopause. Currently the available aromatase inhibitors are Arimidex, ... These cells had aromatase added to them. Adding testosterone to the breast cancer cells increased the cell numbers by 50% ... Resveratrol has aromatase inhibiting activity - another important way that it may help curtail cancer. Tweet ...
Arimidex is a powerful drug suppressing aromatase, a third generation drug. Anastrozole belongs to the group of steroids, but ...
Aromatase. Aromatase is an enzyme which belongs to the cytochrome p450 superfamily. It localizes on the endoplasmic reticulum ...
Aromatase inhibitors work by blocking the enzyme aromatase, which turns the hormone androgen into small amounts of estrogen in ... Aromatase inhibitors stop the production of estrogen in postmenopausal women. ... Aromatase. Aromatase. Aromatase inhibitors stop the production of estrogen in postmenopausal women. Aromatase inhibitors work ... buy AstraZeneca Pharmaceuticals LP is a non-steroidal aromatase inhibitor, which reduces the amount of oestrogen (female sex ...
Clinical trial for Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated Musculoskeletal Pain in Breast ... The aim is to compare targeted individualized physiotherapeutic treatment and medical care with medical care alone on aromatase ... The aim is to compare targeted individualized physiotherapeutic treatment and medical care with medical care alone on aromatase ... Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated Musculoskeletal Pain in Breast Cancer Survivors - AIMSS ...
Aromatase inhibitors. Anastrozole was given to 86 patients, aged 11-18 years (27-29). In the testolactone study (30), there ... Aromatase inhibitors. Size reduction in patients treated with anastrozole occurred in 36.1%-72.2% (27-29) of patients, with a ... Treatment of PG with the specific aromatase inhibitor anastrozole. Horm Res. (2004) 62:113-8. doi: 10.1159/000079882 ... Drugs of interest included medications from the selective estrogen receptor modulator, aromatase inhibitors, and androgens ...
Aromatase inhibitors for sale: Anastrozole, Letrozole, Arimidex, Aromasin. ... Aromatase Inhibitors And Estradiol. Aromatase inhibitors - drugs that reduce activity of the enzyme aromatase. Such drugs to ... Aromatase - an enzyme that is responsible, not just for flavoring, in someone it is more active, in someone less active. How to ... Aromatase Inhibitors. In the lives of most serious athletes, sooner or later there comes a time when the reception of exogenous ...
... as well as the increased expression of aromatase. Similar results of low LKB1 expression in cells expressing aromatase were ... The aim of this study was to characterize the role of LKB1 in regulating the expression of aromatase in boys with PJS via ... Aromatase/biossíntese Ginecomastia/etiologia Perda de Heterozigosidade Síndrome de Peutz-Jeghers/genética Proteínas Serina- ... Loss of heterozygosity of the STK11 gene leads to an increase in aromatase expression associated with an increase in CRTC ...
... ... Aggarwal, N, AROMATASE ACTIVITY OF BRAIN AND OVARY IN RELATION TO ANNUAL REPRODUCTIVE CYCLE OF THE INDIAN CATFISH, ...
title = "Extending aromatase-inhibitor adjuvant therapy to 10 years",. abstract = "BACKGROUND: Treatment with an aromatase ... Extending aromatase-inhibitor adjuvant therapy to 10 years. P. E. Goss, J. N. Ingle, K. I. Pritchard, N. J. Robert, H. Muss, J ... Extending aromatase-inhibitor adjuvant therapy to 10 years. / Goss, P. E.; Ingle, J. N.; Pritchard, K. I. et al. In: New ... Extending aromatase-inhibitor adjuvant therapy to 10 years. In: New England Journal of Medicine. 2016 ; Vol. 375, No. 3. pp. ...
375 A MULTICENTER STUDY OF THE ASSOCIATION OF AROMATASE AND ESTROGEN RECEPTOR GENES WITH HIP AND KNEE OSTEOARTHRITIS ... 375 A MULTICENTER STUDY OF THE ASSOCIATION OF AROMATASE AND ESTROGEN RECEPTOR GENES WITH HIP AND KNEE OSTEOARTHRITIS ...
Aromatase/antagonists & inhibitors. Aromatase Inhibitors. Coproporphyrinogen Oxidase/deficiency. Porphyrias, Hepatics. Diabetes ...
Aromatase Expression in Health and Disease. / Simpson, Evan R.; Zhao, Ying; Agarwal, Veena R. et al. In: Recent progress in ... Aromatase Expression in Health and Disease. Evan R. Simpson, Ying Zhao, Veena R. Agarwal, M. Dodson Michael, Serdar E. Bulun, ... Aromatase Expression in Health and Disease. In: Recent progress in hormone research. 1997 ; Vol. 52. pp. 185-213. ... title = "Aromatase Expression in Health and Disease",. abstract = "Family 19 of the P450 superfamily is responsible for the ...
What Are Aromatase Inhibitors?. Aromatase inhibitors are a class of drugs that reduce the production of estrogen in the body. ...
Aromatase. [11C]VOR. Cox-1. [11C]PS13. FAAH. [11C]CURB. ...
These data are consistent with a concomitant decrease in aromatase activity. Aromatase content was reduced in response to low ... These data are consistent with a concomitant decrease in aromatase activity. Aromatase content was reduced in response to low ... These data are consistent with a concomitant decrease in aromatase activity. Aromatase content was reduced in response to low ... These data are consistent with a concomitant decrease in aromatase activity. Aromatase content was reduced in response to low ...
5α-reductase and aromatase cytochrome P-450 (P450arom) enzymes, are detected in the skeletal muscle, while testosterone, ...
  • The aromatase inhibitors include anastrozole, letrozole and exemestane, some of which have been implicated in causing rare instances of clinically apparent liver injury. (nih.gov)
  • Arimidex 1mg ( buy Anastrozole ) Arimidex 1mg ( buy Anastrozole ) buy AstraZeneca Pharmaceuticals LP is a non-steroidal aromatase inhibitor, which reduces the amount of oestrogen (female sex hormone) made by the body. (gradepharma.com)
  • Anastrozole is by far the most popular aromatase inhibitor, due to its accessibility. (steroidsforsale.biz)
  • 11. Formestane, a steroidal aromatase inhibitor after failure of non-steroidal aromatase inhibitors (anastrozole and letrozole): is a clinical benefit still achievable? (nih.gov)
  • The enzyme aromatase converts that hormone into estrogen. (lbbc.org)
  • Aromatase inhibitors interfere with the enzyme aromatase to decrease the female hormones in your body. (lbbc.org)
  • Aromatase inhibitors block the enzyme aromatase, which converts androgen hormone into small quantities of estrogen in the body. (newhealthguide.org)
  • instead they work by inhibiting a key enzyme aromatase, which converts other hormones into estrogen. (newhealthguide.org)
  • Aromatase inhibitors work by blocking the enzyme aromatase, which turns the hormone androgen into small amounts of estrogen in the body. (gradepharma.com)
  • Aromatase inhibitors - drugs that reduce activity of the enzyme aromatase. (steroidsforsale.biz)
  • To assure that vitamin D3 does not abrogate the clinical benefits of aromatase inhibitors, the effect of vitamin D3 supplements on estrogen production and on serum levels of aromatase inhibitor needs to be evaluated. (nih.gov)
  • What Are the Benefits of Aromatase Inhibitors? (newhealthguide.org)
  • Evaluation of the safety of vitamin D3 supplements in women treated with aromatase inhibitors is crucial. (nih.gov)
  • These symptoms, referred to as aromatase inhibitor-associated musculoskeletal symptoms (AIMSS), decrease quality of life and medication adherence. (nih.gov)
  • The primary objective of this trial is to assess the efficacy of targeted individualised physiotherapeutic treatment on aromatase inhibitor-associated musculoskeletal pain. (inclinicaltrials.com)
  • The aim is to compare targeted individualized physiotherapeutic treatment and medical care with medical care alone on aromatase inhibitor associated musculoskeletal pain in female breast cancer survivors. (inclinicaltrials.com)
  • It is hypothesized that targeted physiotherapeutic treatment and medical care reduces musculoskeletal pain significantly in women with aromatase inhibitor associated musculoskeletal pain when compared to medical care alone. (inclinicaltrials.com)
  • Background: Adjuvant hormone treatment of postmenopausal breast cancer is mainly based on aromatase inhibitors. (who.int)
  • 4. The effect of second-line antiestrogen therapy on breast tumor growth after first-line treatment with the aromatase inhibitor letrozole: long-term studies using the intratumoral aromatase postmenopausal breast cancer model. (nih.gov)
  • In affected males, the increased aromatase and subsequent conversion of androgens to estrogen are responsible for the gynecomastia and limited bone growth characteristic of aromatase excess syndrome. (medlineplus.gov)
  • Aromatase cytochrome P450, the key enzyme of estrogen biosynthesis from androgens, is encoded by CYP19. (archives-ouvertes.fr)
  • Aromatase is the enzyme that changes androgens (testosterone) into estrogen. (invitehealth.com)
  • MEDLINE, Embase, and Cochrane CENTRAL were searched for the terms "gynecomastia", "pubertal", and "adolescent" in conjunction with medications from the Selective Estrogen Receptor Modulator (SERM), aromatase inhibitors (AI), and androgens groups in different combinations to optimize the search results. (frontiersin.org)
  • In human placenta androgens derived from the maternal and fetal adrenal glands are converted into estrogens by the enzymatic action of placental aromatase. (uandes.cl)
  • Aromatase content and estrogens and androgens concentrations were measured. (uandes.cl)
  • We used a human lung cancer xenograph model system to analyze the effect of aromatase or estradiol on tumor growth. (nih.gov)
  • In the present study, we used RT-PCR to characterize aromatase transcripts and real-time PCR to quantify the expression of the total aromatase mRNA at the different stages of the estrous cycle and from an ovariectomy and estradiol replacement model. (archives-ouvertes.fr)
  • After ovariectomy, we observed an increase of aromatase mRNA levels, and this effect was completely prevented by estradiol administration. (archives-ouvertes.fr)
  • To deal with increased levels of estradiol, aromatase inhibitors are used. (steroidsforsale.biz)
  • Recent studies have shown that sex steroidogenesis-related mRNA and protein expressions, such as for 17β-hydroxysteroid dehydrogenase (HSD), 3β-HSD, 5α-reductase and aromatase cytochrome P-450 (P450arom) enzymes, are detected in the skeletal muscle, while testosterone, estradiol, and 5α-dihydrotestosterone (DHT) were locally synthesized in skeletal muscle from dehydroepiandrosterone (DHEA). (nih.gov)
  • After menopause the ovaries no longer produce estrogen and at this point it is much more effective to block aromatase (since an aromatase inhibiting drug doesn't work well on the ovaries but efficiently blocks estrogen production by other tissues). (invitehealth.com)
  • Aromatase is an enzyme which belongs to the cytochrome p450 superfamily. (apexbt.com)
  • The aromatase inhibitors block estrogen synthesis and are used as therapy of estrogen receptor positive breast cancer, usually after resection and as a first line treatment or after failure of tamoxifen (another antiestrogen that acts by blocking the estrogen receptor). (nih.gov)
  • That's why aromatase inhibitors work well in women after menopause. (invitehealth.com)
  • Aromatase inhibitors are substances that inhibit the production of estrogen in women who have undergone menopause. (newhealthguide.org)
  • In human bone cells, intracrine mechanism through aromatase activity, together with a positive regulation of aromatase activity by glucocorticoid and VD 3 , may contribute to the local production of estrogens, thus leading to protective effect against osteoporosis especially after menopause. (elsevier.com)
  • Common questions at our breast cancer support group are about endocrine aromatase inhibitors, menopause, and estrogen hormone treatment. (ironwoodcrc.com)
  • The orphan nuclear receptor steroidogenic factor-1 (SF-1) induces the expression of Müllerian inhibiting substance (MIS) and many steroidogenic genes, including aromatase P450 (P450arom). (northwestern.edu)
  • Interestingly, DEX and 1α,25- dihydroxyvitamin D 3 (VD 3 ) synergistically enhanced aromatase activity as well as P450arom mRNA expression. (elsevier.com)
  • Total aromatase mRNA expression in the pituitary varied significantly during the estrous cycle, with the highest level occurring on the day of metestrus. (archives-ouvertes.fr)
  • These results suggest that pituitary aromatase mRNA expression is downregulated by estrogens. (archives-ouvertes.fr)
  • When Do Symptoms of Aromatase excess syndrome Begin? (nih.gov)
  • Aromatase excess syndrome is a genetic disease, which means that it is caused by one or more genes not working correctly. (nih.gov)
  • Aromatase excess syndrome is a condition characterized by elevated levels of the female sex hormone estrogen in both males and females. (medlineplus.gov)
  • Males with aromatase excess syndrome experience breast enlargement (gynecomastia) in late childhood or adolescence. (medlineplus.gov)
  • The ability to have children (fertility) is usually normal in both males and females with aromatase excess syndrome. (medlineplus.gov)
  • Rearrangements of genetic material involving the CYP19A1 gene cause aromatase excess syndrome. (medlineplus.gov)
  • Fukami M, Shozu M, Ogata T. Molecular bases and phenotypic determinants of aromatase excess syndrome. (medlineplus.gov)
  • Adding aromatase inhibitors (AIs) to adjuvant treatment of postmenopausal women with hormone-receptor-positive breast cancer significantly reduces cancer recurrence. (cdc.gov)
  • Conclusion: The VES-13 and the G-8 tools could be valuable predictors of the onset of toxicity associated with aromatase inhibitors in the adjuvant treatment of breast cancer in elderly patients aged ?70. (who.int)
  • Immunohistochemistry studies in the rat have shown that pituitary aromatase expression is sex-dependent and varies across the estrous cycle, suggesting that estrogens might be involved in the regulation of aromatase activity and might act locally as a paracrine or autocrine factor in the pituitary. (archives-ouvertes.fr)
  • The Resveratrol competed with the aromatase and also inhibited the genes that create aromatase so it affected aromatase in two ways. (invitehealth.com)
  • The gene encoding human aromatase has been cloned and characterized and shown to be unusual compared to genes encoding other P450 enzymes, since there are a number of untranslated first exons that occur in aromatase transcripts in a tissue-specific fashion, due to differential splicing as a consequence of the use of tissue-specific promoters. (elsevierpure.com)
  • The aromatase activity in cultured human osteoblast cells was significantly increased by dexamethasone (DEX). (elsevier.com)
  • CONCLUSIONS: The extension of treatment with an adjuvant aromatase inhibitor to 10 years resulted in significantly higher rates of disease-free survival and a lower incidence of contralateral breast cancer than those with placebo, but the rate of overall survival was not higher with the aromatase inhibitor than with placebo. (arizona.edu)
  • Results The protein and mRNA content of placental aromatase significantly diminished in placentae obtained from preeclamptic patients compared to controls. (uandes.cl)
  • 3. Biology of aromatase inhibitors: pharmacology/endocrinology within the breast. (nih.gov)
  • Abstract: DESCRIPTION (provided by applicant): This project will determine the efficacy and safety of vitamin D3 supplements for reducing side effects of treatment with aromatase inhibitors in women with breast cancer. (nih.gov)
  • Anne Hudson Blaes, MD , of the University of Minnesota, discusses the association between aromatase inhibitors, endothelial function, and early heart disease (Abstract S5-07). (ascopost.com)
  • Ruth O'Regan, MD , of the University of Wisconsin, discusses study findings on buparlisib plus fulvestrant in postmenopausal women with HR-positive, HER2-positive, aromatase inhibitor-treated, locally advanced or metastatic breast cancer, who progressed on or after mTOR inhibitor-based treatment (Abstract S4-07). (ascopost.com)
  • The working of aromatase inhibitors is different from the working of tamoxifen and raloxifene. (newhealthguide.org)
  • Numerous studies have been done to compare the effects of aromatase inhibitors and tamoxifen in the treatment of early-stage HR+ breast cancer in postmenopausal females. (newhealthguide.org)
  • Aromatase inhibitors are the best form of hormonal therapy to treat early-stage, HR+ breast cancer as they have more benefits and lesser side effects in comparison to tamoxifen therapy. (newhealthguide.org)
  • Giving aromatase inhibitors after 2-3 years of tamoxifen therapy is more beneficial than taking tamoxifen for 5 years. (newhealthguide.org)
  • Taking aromatase inhibitors for a period of 5 years after the completion of 5 years of tamoxifen therapy reduces the risk of recurrence in comparison to taking no treatment after tamoxifen therapy. (newhealthguide.org)
  • Fewer side effects are produced from taking aromatase inhibitors in comparison to taking tamoxifen, which increases the risk of stroke, blood clots and endometrial cancer. (newhealthguide.org)
  • Aromatase inhibitors are also associated with causing increased heart problems, increased bone loss leading to osteoporosis and more incidences of fractures in comparison to tamoxifen. (newhealthguide.org)
  • BACKGROUND: Treatment with an aromatase inhibitor for 5 years as up-front monotherapy or after tamoxifen therapy is the treatment of choice for hormone-receptor-positive early breast cancer in postmenopausal women. (arizona.edu)
  • P = 0.01 by a two-sided log-rank test stratified according to nodal status, prior adjuvant chemotherapy, the interval from the last dose of aromatase-inhibitor therapy, and the duration of treatment with tamoxifen). (arizona.edu)
  • Being a drug to regulate your hormones, side effects of aromatase inhibitors come along with benefits. (newhealthguide.org)
  • Any of the AIs may be the first or primary hormonal therapy your doctor prescribes if you have early- stage disease because aromatase inhibitors are the standard hormonal therapy for postmenopausal women. (lbbc.org)
  • Aromatase inhibitors stop the production of estrogen in postmenopausal women. (gradepharma.com)
  • Aromatase expression predicts survival in women with early-stage non small cell lung cancer. (nih.gov)
  • We further examined the level of protein expression of aromatase in 422 patients with NSCLC using a high-density tissue microarray. (nih.gov)
  • PGE 2 is also an important regulator of aromatase expression in adipose mesenchymal cells via cAMP and PGE 2 appears to be a major factor produced by breast rumors that stimulates estrogen biosynthesis in local mesenchymal sites. (elsevierpure.com)
  • Conclusions Placental aromatase expression and functionality are diminished in pregnancies complicated by preeclampsia in comparison with healthy pregnant controls. (uandes.cl)
  • For women with this tumor type, standard adjuvant (postsurgery chemotherapy and/or radiation) treatment generally includes an aromatase inhibitor (AI) to reduce the chances for cancer recurrence (4,5). (cdc.gov)
  • All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive breast cancer. (lbbc.org)
  • If you have metastatic breast cancer, you may receive any of the three aromatase inhibitors as a first treatment after your stage IV diagnosis . (lbbc.org)
  • The aromatase inhibitors (AI) have become a critical component of adjuvant therapy for breast cancer, but they cause bone pain, joint pain, joint stiffness, and muscle weakness in approximately 40% of patients. (nih.gov)
  • Within this population, the prognostic value of aromatase was greatest in earlier stage lung cancer (stage I/II). (nih.gov)
  • Adding testosterone to the breast cancer cells increased the cell numbers by 50% because aromatase changed the testosterone to estrogen. (invitehealth.com)
  • Aromatase inhibitors are a type of new drugs that are used in the treatment of breast cancer in some cases or to help prevent the recurrence of breast cancer post initial surgery. (newhealthguide.org)
  • This trial asks a critical, previously unaddressed, question of clinical importance about management of musculoskeletal (MSK) pain secondary to aromatase inhibitor (AI) treatment of hormone receptor-positive breast cancer. (inclinicaltrials.com)
  • Extending treatment with an aromatase inhibitor to 10 years may further reduce the risk of breast-cancer recurrence. (arizona.edu)
  • Methods: In light of national and international oncological guidelines recommending the use of screening tests for multidimensional geriatric assessment in elderly patients aged ?70 years and eligible for active cancer treatment, we assessed whether the Vulnerable Elder Survey (VES)-13 and the Geriatric (G)-8 could be predictors of toxicity associated with aromatase inhibitors. (who.int)
  • Seventy?seven consecutive patients aged ?70 diagnosed with non?metastatic hormone?responsive breast cancer and therefore eligible for adjuvant hormone therapy with aromatase inhibitors, were screened with the VES-13 and the G-8, and underwent a six-monthly clinical and instrumental follow-up in our medical oncology unit, from September 2016 to March 2019 (30 months). (who.int)
  • 5. Aromatase, its inhibitors and their use in breast cancer treatment. (nih.gov)
  • 6. Aromatase inhibitors for breast cancer in postmenopausal women. (nih.gov)
  • 9. An overview of the use of non-steroidal aromatase inhibitors in the treatment of breast cancer. (nih.gov)
  • 10. Aromatase and its inhibitors in breast cancer treatment--overview and perspective. (nih.gov)
  • 12. Use of aromatase inhibitors in postmenopausal women with advanced breast cancer. (nih.gov)
  • 13. New aromatase inhibitors in the treatment of advanced breast cancer. (nih.gov)
  • 17. The evolving role of aromatase inhibitors in breast cancer. (nih.gov)
  • 19. Aromatase inhibitors and inactivators in breast cancer. (nih.gov)
  • Recent attempts to model the three-dimensional structure of aromatase have permitted a model that accounts for the reaction mechanism and predicts the location of aromatase inhibitors. (elsevierpure.com)
  • Its structure shows some peculiarities: exons II to X encode the protein, while multiple alternative exons I encode unique 5'-untranslated regions of the aromatase mRNA transcripts. (archives-ouvertes.fr)
  • We identified the two previously described aromatase transcripts with a specific 5'untranslated region of the brain 1f and the gonadal PII transcripts. (archives-ouvertes.fr)
  • promote clinical resistance to alpelisib plus aromatase inhibitors. (bvsalud.org)
  • Alterations in PTEN and ESR1 promote clinical resistance to alpelisib plus aromatase inhibitors. (bvsalud.org)
  • Lower levels of aromatase predicted a greater chance of survival in women 65 years and older. (nih.gov)
  • In addition, for women with no history of smoking, lower aromatase levels were a strong predictor of survival. (nih.gov)
  • Our findings implicate aromatase as an early-stage predictor of survival in some women with NSCLC. (nih.gov)
  • We predict that women whose lung cancers have higher levels of aromatase might be good candidates for targeted treatment with aromatase inhibitors. (nih.gov)
  • Because of the role of vitamin D in muscle cell physiology and musculoskeletal pain, there is reason to believe that vitamin D3 may decrease symptoms associated with the use of aromatase inhibitors. (nih.gov)
  • These data are consistent with a concomitant decrease in aromatase activity. (uandes.cl)
  • A rare, genetic endocrine disease characterized by increased levels of estrogen due to elevated extraglandular aromatase activity. (nih.gov)
  • If you are considering therapy with aromatase inhibitors, you can ask your doctor to perform a bone densitometry to determine if you will require a bone strengthening medicine along with the aromatase inhibitor. (newhealthguide.org)
  • So, if there is differing amounts of aromatization occurring at different points of this cycle, as well as saturation levels increasing at different rates and heavily aromatizing compounds being swapped in and out of the cycle, does it make sense to be using the exact same dose of Aromatase Inhibitor for the entirety of this cycle? (moreplatesmoredates.com)
  • 18. Aromatase inhibitors: a dose-response effect? (nih.gov)
  • The Virtual Lunch & Learn " Endocrine Aromatase Inhibitors" was recorded live on Tuesday, March 28, 2023. (ironwoodcrc.com)
  • These rearrangements alter the activity of the gene and lead to an increase in aromatase production. (medlineplus.gov)
  • The two most important of them is the activity of aromatase enzyme and body fat. (steroidsforsale.biz)
  • Actually, in cultured human osteoblast cells, DHEA was found to convert to androstenedione by 3β-hydroxysteroid dehydrogenase (3β-HSD) activity and then androstenedione to estrone through the apparent aromatase activity. (elsevier.com)
  • A little stronger induction of aromatase activity by DEX and VD 3 was observed in cultured human fibroblasts. (elsevier.com)
  • The increase of the aromatase activity by DEX and VD 3 was accompanied with the increase of luciferase activity of fibroblast cells transfected with Exon 1b-promoter-luciferase construct, but not of osteoblasts transfected with the same construct, suggesting a different regulatory mechanism of aromatase by DEX and 1α,25-dihydroxyvitamin D 3 (VD 3 ) between these two cells despite the same promotor usuage. (elsevier.com)
  • Aromatase content was reduced in response to low oxygen tension in the choriocarcinoma JEG-3 cell line and in rabbit placentae in response to partial ligation of uterine spiral arteries, suggesting that reduced placental aromatase activity in preeclamptic patients may be associated with chronic placental ischemia and hypoxia later in gestation. (uandes.cl)
  • 14. Steroidal aromatase inhibitors in elderly patients. (nih.gov)
  • How can you expect to keep your Estrogen levels in the sweet spot with a predetermined dosage of your Aromatase Inhibitor? (moreplatesmoredates.com)

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