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.
An enzyme that catalyzes the desaturation (aromatization) of the ring A of C19 androgens and converts them to C18 estrogens. In this process, the 19-methyl is removed. This enzyme is membrane-bound, located in the endoplasmic reticulum of estrogen-producing cells of ovaries, placenta, testes, adipose, and brain tissues. Aromatase is encoded by the CYP19 gene, and functions in complex with NADPH-FERRIHEMOPROTEIN REDUCTASE in the cytochrome P-450 system.
Derivatives of the steroid androstane having three double bonds at any site in any of the rings.
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.
Tumors or cancer of the human BREAST.
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.
An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.
The physiological period following the MENOPAUSE, the permanent cessation of the menstrual life.
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.
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.
Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds.
Derivatives of the steroid androstane having two 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.
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.
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.
An antineoplastic agent that is a derivative of progesterone and used to treat advanced breast cancer.
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)
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.
Enlargement of the BREAST in the males, caused by an excess of ESTROGENS. Physiological gynecomastia is normally observed in NEWBORNS; ADOLESCENT; and AGING males.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
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.
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)
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.
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.
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.
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.
A monoamine oxidase inhibitor with antihypertensive properties.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
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.
A sudden, temporary sensation of heat predominantly experienced by some women during MENOPAUSE. (Random House Unabridged Dictionary, 2d ed)
Pain in the joint.
A potent androgenic metabolite of TESTOSTERONE. It is produced by the action of the enzyme 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE.
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.
Discomfort stemming from muscles, LIGAMENTS, tendons, and bones.
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 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.
The surgical removal of one or both ovaries.
A triphenyl ethylene stilbene derivative which is an estrogen agonist or antagonist depending on the target tissue. Note that ENCLOMIPHENE and ZUCLOMIPHENE are the (E) and (Z) isomers of Clomiphene respectively.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Preliminary cancer therapy (chemotherapy, radiation therapy, hormone/endocrine therapy, immunotherapy, hyperthermia, etc.) that precedes a necessary second modality of treatment.
The gamete-producing glands, OVARY or TESTIS.
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.
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 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.
A cell surface protein-tyrosine kinase receptor that is overexpressed in a variety of ADENOCARCINOMAS. It has extensive homology to and heterodimerizes with the EGF RECEPTOR, the ERBB-3 RECEPTOR, and the ERBB-4 RECEPTOR. Activation of the erbB-2 receptor occurs through heterodimer formation with a ligand-bound erbB receptor family member.
Works about clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table.
Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.
Techniques for the artifical induction of ovulation, the rupture of the follicle and release of the ovum.
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).
The lack of development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations above the mean age at onset of PUBERTY in a population. Delayed puberty can be classified by defects in the hypothalamic LHRH pulse generator, the PITUITARY GLAND, or the GONADS. These patients will undergo spontaneous but delayed puberty whereas patients with SEXUAL INFANTILISM will not.
FIBROUS DYSPLASIA OF BONE affecting several bones. When melanotic pigmentation (CAFE-AU-LAIT SPOTS) and multiple endocrine hyperfunction are additionally associated it is referred to as Albright syndrome.
Pathological processes involving any part of the UTERUS.
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)
Organic compounds which contain P-C-P bonds, where P stands for phosphonates or phosphonic acids. These compounds affect calcium metabolism. They inhibit ectopic calcification and slow down bone resorption and bone turnover. Technetium complexes of diphosphonates have been used successfully as bone scanning agents.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.
A family of freshwater fish comprising the minnows or CARPS.

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. (1/981)

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)

Inhibitory effects of nitric oxide on the expression and activity of aromatase in human granulosa cells. (2/981)

The aim of the present study was to explore the mechanisms by which nitric oxide (NO) may inhibit aromatase activity of human granulosa cells. Ovarian granulosa-luteal cells, obtained from patients undergoing in-vitro fertilization (IVF) were cultured in the presence of NO-related substances. After 24 h of culture, aromatase activity of the cells was significantly inhibited by treatment with the NO donors, SNAP or NOC12 at > or =10(-4) M in a dose-dependent manner. Treatment with NO catabolites or a peroxynitrite-releasing compound, SIN1, had no significant influence. Treatment with SNAP at 10(-3) M decreased relative aromatase mRNA values by 72% (P<0.05) and intracellular cyclic AMP concentrations by 53% (P<0.01). However, treatment with H89, an inhibitor of protein kinase A, did not inhibit aromatase activity. Since there were no significant effects of NO catabolites or peroxinitrite, the inhibitory action of NO donors on aromatase must be related to NO release. The action of NO is, in part, attributable to the down-regulation of aromatase gene transcription. Although NO decreased intracellular cAMP values, down-regulation of aromatase gene transcription may not be mediated by protein kinase A-dependent mechanisms.  (+info)

Evidence of sex reversal in the gonads of chicken embryos after oestrogen treatment as detected by expression of lutropin receptor. (3/981)

In chicken embryos, there is a difference between the sexes in the onset of lutropin receptor mRNA expression in the gonads. The effects of oestrogen on lutropin receptor expression were studied to investigate the mechanism controlling this difference. Lutropin receptor mRNA expression was detected in the ovaries of sesame oil-treated control female embryos on day 12 of incubation, while no expression was found in the testes of the male controls. Oestradiol administration to genetically male embryos before sexual differentiation resulted in gonadal sex reversal which was characterized histologically by the proliferation of cortical cords and the presence of lacunae. Lutropin receptor expression was detected in the feminizing testis on day 12 of incubation. Administration of aromatase inhibitor (CGS 16949 A) to genetically female embryos before sexual differentiation inhibited the formation of cortical cords, although a relatively weak expression of lutropin receptor was detected. These results indicate that early expression of the lutropin receptor is regulated by oestrogen.  (+info)

Presence of an aromatase inhibitor, possibly heat shock protein 90, in dominant follicles of cattle. (4/981)

In cattle, it has been suggested that follicular fluid has direct modulatory effects on follicular growth and maturation. In the first part of this study, an in vitro test using aromatase activity of follicular wall fragments as an end point was validated for cattle follicles and was used to test whether follicular fluid (from dominant or non-dominant follicles) modulates aromatase activity. Fluid from dominant follicles at a concentration of 24 or 12% (obtained during the luteal and follicular phases, respectively) significantly inhibited aromatase activity. Inhibitory activity was low or absent in fluid from non-dominant follicles. FSH-stimulated aromatase activity was also reduced by fluid from dominant follicles, but not to a greater extent than in basal conditions. Finally, charcoal-treated fluid from dominant follicles retained its inhibitory activity. In contrast, ovarian venous serum draining a dominant follicle had no activity at the three concentrations tested (6, 12 and 24%). In the second part of the study, identification of the compounds involved in this modulatory activity was attempted using SDS-PAGE. Comparison of the fluorographs from de novo synthesized proteins stored in follicular fluid (inhibitory medium) with those secreted in incubation medium (inactive medium) demonstrated that one protein (90 kDa, pI 5.8) was significantly (P < 0.05) more abundant in fluid from dominant follicles (2.0 +/- 0.09%) than in the culture medium (1.3 +/- 0.1% of the total proteins). This protein had characteristics similar to those of heat shock protein 90 (hsp 90). Therefore, in the final part of the study, the presence of hsp 90 in ovarian cells and follicular fluid was investigated using immunohistochemistry and western blot analysis. After immunohistochemistry, a positive signal was detected mainly in the granulosa cells of larger follicles and to a smaller extent in thecal cells and oocytes. Western blot analysis also demonstrated the presence of hsp 90 in follicular wall fragments and fluid. When blotting was achieved on a sample of follicular fluid resolved by two-dimensional PAGE, the spot detected had a similar location to that at 90 kDa and pI 5.8. Addition of purified hsp 90 to bovine follicles in vitro depressed aromatase activity by altering the K(m) value (and possibly the Vmax value) of the enzyme. It is proposed that hsp 90 is a functional regulator of follicular maturation through its action on aromatase.  (+info)

The third-generation non-steroidal aromatase inhibitors: a review of their clinical benefits in the second-line hormonal treatment of advanced breast cancer. (5/981)

Three new aromatase inhibitors have recently completed phase III evaluation as treatment of metastatic breast cancer in post-menopausal women whose disease has progressed despite tamoxifen therapy: anastrozole (ARIMIDEX, Zeneca), letrozole (FEMARA, Novartis) and vorozole (RIVIZOR, Janssen). All belong to the third generation of non-steroidal aromatase inhibitors, and each is superior to previous generations in terms of potency and selectivity. The trials that have been performed compare each agent to megestrol acetate, and letrozole and vorozole to aminoglutethimide. Although the studies are not directly comparable due to differing study designs and patient populations, it has been demonstrated each of these drugs provides single agent, once-daily, oral palliation of hormone-responsive, post-menopausal metastatic breast cancer. Letrozole is clearly more effective than megestrol acetate, and anastrozole and vorozole are possibly so. All three are better tolerated than the progestin, particularly in terms of weight gain. Both letrozole and vorozole are significantly more effective, and better tolerated than aminoglutethimide. Overall, this most recent generation of aromatase inhibitors is a clear improvement on our current standard second-line therapies. In 1999, tamoxifen remains the first choice in the hormonal therapy of breast cancer. Following tamoxifen failure, the optimal second-line hormonal therapy remains undefined, but aminoglutethimide and megestrol acetate are no longer optimal therapy in this setting. The third-generation non-steroidal aromatase inhibitors must now be compared to each other, to the steroidal aromatase inhibitors, to the pure anti-oestrogens, and to tamoxifen.  (+info)

Estrogen-inducible, sex-specific expression of brain-derived neurotrophic factor mRNA in a forebrain song control nucleus of the juvenile zebra finch. (6/981)

The expression of brain-derived neurotrophic factor (BDNF) mRNA is increased significantly within the high vocal center (HVc) of male but not female zebra finches from posthatching day 30-35 on. The population of HVc cells expressing BDNF mRNA included 35% of the neurons projecting to the nucleus robustus of the archistriatum (RA). In the RA and in RA-projecting neurons of the lateral portion of the magnocellular nucleus of the anterior neostriatum, BDNF mRNA was expressed at very low levels in both sexes. The BDNF-receptor trkB mRNA was expressed in the RA, in RA-projecting neurons of lateral portion of the magnocellular nucleus of the anterior neostriatum, and in the HVc, except in most of its RA-projecting neurons. Premature stimulation and an inhibitory effect on the normal increase of the BDNF mRNA expression in juvenile males occurred after treatments with 17beta-estradiol and the aromatase inhibitor fadrozole, respectively. The up-regulation of the BDNF expression in the HVc could be a mechanism by which estrogen triggers the differentiation of cells within and connected to the HVc of male zebra finches.  (+info)

Mitogenic and antioxidant mechanisms of estradiol action in preovulatory ovine follicles: relevance to luteal function. (7/981)

The objectives of this investigation were to determine the intrafollicular mechanisms and physiological consequences of estradiol actions in preovulatory ovine follicles. Acute suppression of estradiol production in proestrous ewes by an aromatase inhibitor (Arimidex) was associated with follicular lipid peroxidation, testosterone accumulation, and a granulosa cell deficiency (decreased proliferation/increased apoptosis). Estradiol-17beta stimulated granulosa proliferating cell nuclear antigen (PCNA) and protected cells from oxidative (H(2)O(2)) stress-induced apoptosis in vitro; the PCNA, but not the antiapoptotic response, was negated by the transcriptional inhibitor actinomycin D. Thus, it appears that genomic/mitotic and cytoprotective (oxygen-scavenging) modes of estradiol action operate in preovulatory follicles. Luteal (large steroidogenic cell) function was diminished following ovulation induction of estradiol-deficient follicles. It is suggested that inadequate exposure of the preovulatory follicle to estradiol caused the granulosa lutein insufficiency.  (+info)

Gonadal stage-dependent effects of gonadal steroids on gonadotropin II secretion in the Atlantic croaker (Micropogonias undulatus). (8/981)

Involvement of gonadal steroids in the control of gonadotropin II (GTH II) (homologous to LH) secretion was investigated in the Atlantic croaker (Micropogonias undulatus) using gonadectomy (Gx) and steroid replacement paradigms. Gonadectomy in males and females during the late gonadal recrudescence phase elicited significant increases in the gonadotropin response to stimulation by an LHRH analog (LHRHa), without altering basal GTH II secretion. Slow-release silicone elastomer implants of testosterone or estradiol significantly inhibited LHRHa-induced GTH II secretion in gonad-intact and Gx males, and in Gx females, whereas 5alpha-dihydrotestosterone, a nonaromatizable androgen, was ineffective. Pretreatment of fish with an aromatase inhibitor, 1,4, 6-androstatrien-3,17-dione, 2 days before the administration of testosterone implants, completely blocked the negative effect of testosterone on LHRHa-induced GTH II secretion in males, but only partially restored it in females. This suggests that the negative feedback of testosterone in males is primarily mediated by its conversion to estradiol at the level of the hypothalamus and/or pituitary gland, while in females the androgen may also exert a direct inhibitory effect on GTH II secretion, probably mediated via an androgen receptor. In addition, estradiol and testosterone exerted positive effects on basal and LHRHa-induced GTH II secretion during the early-recrudescence phase of the gonadal cycle. The steroids switched to a negative effect on LHRHa-induced GTH II secretion once the fish had fully developed gonads, possibly as a mechanism that prevents a precocious surge in GTH II secretion and final gamete maturation until gametogenesis is complete and the environmental conditions are appropriate for spawning.  (+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.

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.

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.

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.

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.

Musculoskeletal pain can have a significant impact on an individual's quality of life, making it difficult to perform daily activities and enjoy leisure time. It can also lead to sleep disturbances, mood changes, and decreased productivity. Treatment options for musculoskeletal pain vary depending on the underlying cause but may include physical therapy, medication, or lifestyle modifications such as exercise and stress management.

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.

Delayed puberty, also known as constitutional delay of growth and development, is a condition in which a child's physical development and sexual maturation are significantly later than their peers. This can be due to a variety of factors, including genetics, hormonal imbalances, chronic illnesses, and nutritional deficiencies.

Delayed puberty can have both physical and emotional effects on a child. Physically, it may cause a child's body to appear younger than their age, and they may experience delayed growth spurts and the development of secondary sex characteristics such as breast development in girls or testicular enlargement in boys. Emotionally, delayed puberty can lead to feelings of isolation, low self-esteem, and anxiety about not fitting in with their peers.

It is important to note that some children may experience a delay in puberty due to normal variations in growth and development, while others may have a more serious underlying medical condition that needs to be evaluated by a healthcare provider. If you suspect that your child is experiencing delayed puberty, it is important to consult with their pediatrician or an endocrinologist for proper evaluation and treatment.

The exact cause of fibrous dysplasia is unknown, but genetic factors are suspected to play a role. It can occur sporadically or as part of certain inherited medical conditions. Fibrous dysplasia is more common in males than females and typically affects children and young adults.

The symptoms of fibrous dysplasia depend on the bones affected and may include pain, limb deformity, and difficulty moving or using affected limbs. Diagnosis is based on a combination of clinical evaluation, imaging studies such as X-rays, CT scans or MRI, and biopsy to confirm the presence of fibrous tissue in affected bones.

Treatment for fibrous dysplasia depends on the severity of symptoms and the specific bones involved, but may include medications such as bisphosphonates to slow bone growth, surgery to remove affected bone tissue or correct deformities, or radiation therapy to reduce pain and improve function. In some cases, surgical removal of affected bone tissue may be necessary.

Prognosis for fibrous dysplasia varies depending on the severity of symptoms and the specific bones involved, but in general, with appropriate treatment, most individuals with this condition can achieve significant improvement in symptoms and function. However, some individuals may experience chronic pain or disability despite treatment.

In summary, fibrous dysplasia is a developmental disorder that affects multiple bones in the body, causing pain, deformity, and impaired function of affected limbs. Diagnosis is based on clinical evaluation, imaging studies, and biopsy, and treatment options include medications, surgery, or radiation therapy. Prognosis varies depending on severity and specific bones involved.

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.

Non-substrate FAs can potentiate or attenuate PTGS (COX) inhibitors depending on the fatty acid and whether the inhibitor binds ... Brueggemeier RW, Díaz-Cruz ES (March 2006). "Relationship between aromatase and cyclooxygenases in breast cancer: potential for ... PTGSs are targets for NSAIDs and PTGS2 (COX-2) specific inhibitors called coxibs. PTGS-2 is a sequence homodimer. Each monomer ... Substrate and non-substrate fatty acid (FAs) and some PTGS (COX) inhibitors (e.g. naproxen) preferentially bind to the PTGS ( ...
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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 ... "Aromatase inhibitors: Are there differences between steroidal and nonsteroidal aromatase inhibitors and do they matter?". ... Steroidal aromatase inhibitors irreversibly inhibit the enzyme by binding covalently to the binding site of aromatase so the ...
The tamoxifen metabolite and aromatase inhibitor norendoxifen is also a TPE derivative. In addition to their estrogenic ... a new class of protein kinase C inhibitors". J. Natl. Cancer Inst. 76 (6): 1243-6. doi:10.1093/jnci/76.6.1243. PMID 3458960. ... activity, various TPE derivatives like tamoxifen and clomifene have been found to act as protein kinase C inhibitors. The ...
Aromatase inhibitors, Flavones, Neuroprotective agents, Nootropics, Phytoestrogens, Steroid sulfotransferase inhibitors, TrkB ... Tropoflavin 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 ...
... aromatase inhibitors are not without their own risks as well; there are concerns surrounding long-term aromatase inhibitor ... Aromatase inhibitors - such as Letrozole - can be used in place of testosterone to overcome reduced testosterone levels ...
... this was not the case in another study with a similar design that used the aromatase inhibitor testolactone. Men with aromatase ... with or without the aromatase inhibitor anastrozole, showed that prevention of the conversion of testosterone into estradiol ... 5α-Reductase inhibitors, which block the conversion of testosterone into DHT, result in a slightly increased risk of sexual ... However, estradiol supplementation in some men with aromatase deficiency increased sexual desire and activity but not in other ...
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Extracts are sold as bodybuilding supplements based on the assumption that aromatase inhibitors present in the plant might have ... "Isolation and characterization of aromatase inhibitors from Brassaiopsis glomerulata (Araliaceae)". Phytochemistry Letters. 2 ( ...
Crider A, Thakkar R, Ahmed AO, Pillai A (9 September 2014). "Dysregulation of estrogen receptor beta (ERβ), aromatase (CYP19A1 ... a potential inhibitor ofestrogen action in human". Nucleic Acids Research. 26 (15): 3505-3512. doi:10.1093/nar/26.15.3505. PMC ... relevance of estrogen receptor-beta expression to the antiproliferative effects observed with histone deacetylase inhibitors ...
... aromatase inhibitors), and generally have a better prognosis. Generally, prior to modern treatments, HER+ had a worse prognosis ... may overcome the resistance that can arise in BRCA cancers to PARP inhibitors or platinum-based chemotherapy. mTOR inhibitors ... August 2010). "6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance". Cancer Research ... Correction published at Correction: 6-Thioguanine Selectively Kills BRCA2-Defective Tumors and Overcomes PARP Inhibitor ...
... has been proposed that bicalutamide and other CYP27A1 inhibitors may be effective as adjuvant therapies to aromatase inhibitors ... However, a study found that a combination of bicalutamide and dutasteride, a 5α-reductase inhibitor and inhibitor of ... Bicalutamide, as well as enzalutamide, have been found to act as inhibitors of P-glycoprotein efflux and ATPase activity. This ... In fact, estradiol is a much stronger inhibitor of gonadotropin secretion than is testosterone, and even though circulating ...
TBT can locally disrupt aromatase regulation in the hypothalamus causing the responses of the HPA axis to hormones to become ... Selective serotonin reuptake inhibitors (SSRI) (e.g. paroxetine), tricyclic antidepressants (e.g. amitriptyline), tetracyclic ... Certain antidepressants, known as selective serotonin reuptake inhibitors (SSRIs), are potentially adding to the almost 100 ... selective serotonin reuptake inhibitors, and thiazolidinedione and as a result of unintentional exposure to environmental ...
Aromatase inhibitors, Belgian inventions, Chloroarenes, CYP17A1 inhibitors, CYP2C8 inhibitors, Phenylethanolamine ethers, ... Imidazole antifungals, Lanosterol 14α-demethylase inhibitors, Otologicals, World Health Organization essential medicines, ... Wikipedia medicine articles ready to translate, General cytochrome P450 inhibitors). ...
Aromatase inhibitors, AbbVie brands, Carboxylic acids, Endocrine disruptors, GABA analogues, GABA transaminase inhibitors, ... In addition, the drug has been identified as a potent aromatase inhibitor, and suppresses estrogen concentrations. These ... January 2009). "A phase I-II study of the histone deacetylase inhibitor valproic acid plus chemoimmunotherapy in patients with ... April 2009). "Clinical and biological effects of valproic acid as a histone deacetylase inhibitor on tumor and surrogate ...
Aromatase inhibitors, Circadian rhythm, Hormones of the pineal gland, Melatonin receptor agonists, Methoxy compounds, Mexamines ... Also acts as a growth inhibitor on fungal pathogens including Alternaria, Botrytis, and Fusarium spp. Decreases the speed of ...
... aromatase inhibitors such as anastrozole and exemestane, gonadotropin-releasing hormone (GnRH) analogues such as leuprorelin ... and aromatase excess syndrome. Such conditions may be treated with drugs with antiestrogen actions, including selective ...
Aromatase inhibitors, Circadian rhythm, Drugs acting on the nervous system, Melatonin receptor agonists, Methoxy compounds, ... As such, inhibitors and inducers of CYP1A enzymes, such as CYP1A2, can modify melatonin metabolism and exposure. As an example ... the CYP1A2 and CYP2C19 inhibitor fluvoxamine increases melatonin peak levels by 12-fold and overall exposure by 17-fold and ...
Aromatase inhibitors, Belgian inventions, Chloroarenes, Cholesterol side-chain cleavage enzyme inhibitors, CYP17A1 inhibitors, ... 7α-Hydroxylase inhibitors, 11β-Hydroxylase inhibitors, 21-Hydroxylase inhibitors, Acetamides, Aldosterone synthase inhibitors, ... Both isomers were relatively weak inhibitors of human placental aromatase. Oral ketoconazole has been used clinically as a ... Ketoconazole shampoo in conjunction with an oral 5α-reductase inhibitor such as finasteride or dutasteride has been used off ...
Acetylcholinesterase inhibitors, Amorphous solids, Antiemetics, AbbVie brands, Appetite stimulants, Aromatase inhibitors, ...
ASL Aromatase deficiency; 613546; CYP19A1 Aromatase excess syndrome; 139300; CYP19A1 Aromatic L-amino acid decarboxylase ... Lutheran inhibitor; 111150; KLF1 Bloom syndrome; 210900; RECQL3 Blue cone monochromacy; 303700; OPN1MW Blue cone monochromacy; ... KRT1 Plasminogen activator inhibitor, type I; 613329; PAI1 Platelet disorder, familial, with associated myeloid malignancy; ... response to tyrosine kinase inhibitor in; 211980; EGFR Nonsmall cell lung cancer, somatic; 211980; IRF1 Nonsmall cell lung ...
... putting aromatase inhibitors on the map (BIG 1-98), changing how we treat young women with breast cancer (SOFT), leading to a ...
Aromatase inhibitors, O-methylated flavanones, Flavonoids found in Rutaceae, 3-Hydroxypropenals). ...
Järvinen K, Vuolteenaho K, Nieminen R, Moilanen T, Knowles RG, Moilanen E (2008). "Selective iNOS inhibitor 1400W enhances anti ... and aromatase in women with hyperandrogenism, and polycystic ovary syndrome. While in vitro experiments have confirmed a ...
... an aromatase inhibitor. Follicle-stimulating hormone (FSH), directly stimulating the ovaries. In women with anovulation, it may ...
Franik, Sebastian; Eltrop, Stephanie M.; Kremer, Jan Am; Kiesel, Ludwig; Farquhar, Cindy (2018-05-24). "Aromatase inhibitors ( ... Other space occupying pituitary lesions can also cause amenorrhea due to the inhibition of dopamine, an inhibitor of prolactin ...
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... only occurs when a nonaromatizable testosterone or an aromatase inhibitor is administered, indicating that the enzyme ... particularly in regards to the effects of aromatase in each process. In some fish species, aromatase is in both the ovaries of ... of the coding sequences of each aromatase being identical, showing that aromatase is not unique to TSD and suggesting that ... Aromatase has also been shown to play a role in certain tumor development. The adaptive significance of TSD is currently not ...
... hormone-receptor-positive breast cancer who got 5 years of an aromatase inhibitor seem to be more likely to have heart problems ...
SEARCH RESULTS for: Aromatase Inhibitors [Drug Class] (92 results) *Share : JavaScript needed for Sharing tools. Bookmark & ...
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, ...
There are three FDA approved aromatase inhibitors for all stages of breast cancer: Anastrozole (Arimidex and generic); ... Who gets aromatase inhibitors. All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive ... Aromatase inhibitors interfere with the enzyme aromatase to decrease the female hormones in your body. It then can reduce the ... How aromatase inhibitors are given. The AIs are all given as daily pills. In early-stage disease they are usually given after ...
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 ...
However, half of patients develop aromatase-inhibitor-induced arthralgia (AIIA), which is characterized by inflammation of the ... Aromatase Inhibitors (AIs) block estrogen production and improve survival in patients with hormone-receptor-positive breast ... Keywords: aromatase inhibitor; aromatase-inhibitor-induced arthralgia (AIIA); breast cancer; estrogen; hormone-receptor- ... Aromatase inhibitors for treatment of advanced breast cancer in postmenopausal women. Gibson LJ, Dawson C, Lawrence DH, Bliss ...
Arimidex is a powerful drug suppressing aromatase, a third generation drug. Anastrozole belongs to the group of steroids, but ...
SEARCH RESULTS for: Aromatase Inhibitors [Drug Class] (92 results) *Share : JavaScript needed for Sharing tools. Bookmark & ...
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. ... taking aromatase inhibitors.. Aromatase Inhibitors And Estradiol. Aromatase inhibitors - drugs that reduce activity of the ... Aromatase Inhibitors. In the lives of most serious athletes, sooner or later there comes a time when the reception of exogenous ... To deal with increased levels of estradiol, aromatase inhibitors are used.. How To Raise Estradiol Levels In Men. All of us at ...
Clinical trial for Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated Musculoskeletal Pain in Breast ... Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated Musculoskeletal Pain in Breast Cancer Survivors - AIMSS ... Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated Musculoskeletal Pain in Breast Cancer Survivors: a ... pain secondary to aromatase inhibitor (AI) treatment of hormone receptor-positive breast cancer. Many breast cancer survivors ...
What Are Aromatase Inhibitors?. Aromatase inhibitors are a class of drugs that reduce the production of estrogen in the body. ... What Are COX-2 Inhibitors?. COX-2 Inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAIDs) that treat inflammatory ...
PEARL is a multicentre, phase III randomised study in which patients with aromatase inhibitor (AI)-resistant MBC were included ... aromatase inhibitor-resistant metastatic breast cancer: a phase III randomised controlled trial-PEARL. ... Inibidores da Aromatase; Neoplasias da Mama; Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico; Inibidores ... Inibidores da Aromatase Tipo de estudo: Ensaio clínico controlado Aspecto: Preferência do paciente Limite: Humanos Idioma: ...
"Extending aromatase-inhibitor adjuvant therapy to 10 years",. abstract = "BACKGROUND: Treatment with an aromatase inhibitor for ... 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. ...
Part 2: Only 1 prior treatment line of ET with or without a targeted therapy (such as CDK4/6, mTOR or PI3-K inhibitors) for MBC ... Part 1: At least 1 prior treatment line of ET with or without a targeted therapy (such as CDK4/6, mTOR or PI3-K inhibitors), ... Prior treatment with ADC that comprises of an exatecan derivative that is a topoisomerase I inhibitor. ...
... novel dual aromatase-steroid sulfatase inhibitors (DASIs) containing a sulfamate group are now being developed. In this study, ... Both inhibitors ligate to the active site zinc(II) atom via their sulfamate nitrogen, while the rest of the molecule is ... Small changes in inhibitor structure can cause large changes in binding to CA II, and this underlines the importance of ... we show that CA II is potently inhibited by several members of this class of inhibitor. The structures of CA II complexed with ...
BACKGROUND: The impact of long-term adjuvant therapy with aromatase inhibitors (AIs) on vertebral fracture (VF) risk is still ... BACKGROUND: The impact of long-term adjuvant therapy with aromatase inhibitors (AIs) on vertebral fracture (VF) risk is still ... Morphometric vertebral fractures in breast cancer patients treated with adjuvant aromatase inhibitor therapy: A cross-sectional ...
Medicines such as raloxifene, tamoxifen, and aromatase inhibitors. *Surgery to remove your breasts or ovaries ... Medications such as pembrolizumab (Keytruda) a PD-1 Inhibitor, help your immune system fight cancer. Find out the pros and cons ...
Aromatase Inhibitors (Posthumous). Angela Hartley Brodie discovered and developed a class of drugs called aromatase inhibitors ... Aromatase inhibitors are among the leading therapies against breast cancer.. *Marjorie Stewart Joyner: Permanent Wave Machine ( ... 6, 2023 - Sixteen innovation pioneers whose inventions range from wheelchair technology to aromatase inhibitors will be honored ...
Aromatase Inhibitor.svg 512 × 384; 604 KB. *. Bc-classification.png 1,000 × 1,500; 1.29 MB. ...
Pharmacological Actions : Aromatase Inhibitors. [+] Red wine extract inhibits VEGF secretion and its signalling pathway in ... Pharmacological Actions : Antioxidants, NF-kappaB Inhibitor, Vascular Cell Adhesion Molecule-1 Inhibitor ... Red wine extract has anti-aromatase activity which abrogates hyperpasia in mammary tissue. May 01, 2001. ...
Aromatase inhibitors. *Ovarian suppression. *Fulvestrant. *Elacestrant. For more Report Customization, connect with us at@ ...
Aromatase inhibitor arthralgias. *Metastatic bone pain. *Radiation-induced pain syndromes. In addition, NCI is interested in ...
... in Korean postmenopausal women with early breast cancer receiving aromatase inhibitor: A double-blind, randomized, placebo- ... in Korean postmenopausal women with early breast cancer receiving aromatase inhibitor: A double-blind, randomized, placebo- ...
Aromatase inhibitors. Used as hormone therapy for some women with certain types of breast cancer. ...
... and an aromatase inhibitor. Others took Tykerb with an aromatase inhibitor. A third group took trastuzumab and an aromatase ... their cancer getting worse than people who only took Herceptin and an aromatase inhibitor or Tykerb and an aromatase inhibitor ... The aromatase inhibitors used included anastrozole (Arimidex), exemestane (Aromasin), and letrozole (Femara). ... No one who took trastuzumab with an aromatase inhibitor had paronychia. And paronychia wasnt reported in clinical trials of ...
Perioperative Aromatase Inhibitors: No Effect on Recurrence, but Ki67 Level Important. Updated analysis from the United ... However, the study did show that tumor Ki67 levels after 2 weeks of perioperative aromatase inhibitor therapy are... ... Kingdoms POETIC trial found no evidence that perioperative aromatase inhibitor therapy slows or prevents time to recurrence of ...
  • 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). (
  • 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. (
  • 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). (
  • Standard treatments for ER+ breast cancer are endocrine therapies such as tamoxifen and aromatase inhibitors. (
  • These women were assigned to receive standard hormone therapy such as tamoxifen or aromatase inhibitors, but didn't undergo chemotherapy. (
  • The aromatase inhibitors include anastrozole, letrozole and exemestane, some of which have been implicated in causing rare instances of clinically apparent liver injury. (
  • For this reason, letrozole belongs to a larger group of drugs known as aromatase inhibitors, many of which are potent agents used primarily for the treatment of cancers that depend on estrogens to stimulate their growth. (
  • In the 1980s scientists at the Swiss company Ciba-Geigy AG (now Novartis AG ) discovered letrozole while screening compounds for their ability to inhibit aromatase. (
  • Letrozole was far more potent than any other aromatase inhibitor discovered. (
  • Anastrozole is by far the most popular aromatase inhibitor, due to its accessibility. (
  • All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive breast cancer. (
  • 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. (
  • Adding aromatase inhibitors (AIs) to adjuvant treatment of postmenopausal women with hormone-receptor-positive breast cancer significantly reduces cancer recurrence. (
  • Background: Adjuvant hormone treatment of postmenopausal breast cancer is mainly based on aromatase inhibitors. (
  • 5. Inhibition of aromatase with CGS 16949A in postmenopausal women. (
  • 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. (
  • These symptoms, referred to as aromatase inhibitor-associated musculoskeletal symptoms (AIMSS), decrease quality of life and medication adherence. (
  • 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. (
  • The primary objective of this trial is to assess the efficacy of targeted individualised physiotherapeutic treatment on aromatase inhibitor-associated musculoskeletal pain. (
  • 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. (
  • 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. (
  • 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. (
  • The enzyme aromatase converts that hormone into estrogen. (
  • Aromatase inhibitors interfere with the enzyme aromatase to decrease the female hormones in your body. (
  • The two most important of them is the activity of aromatase enzyme and body fat. (
  • Aromatase - an enzyme that is responsible, not just for flavoring, in someone it is more active, in someone less active. (
  • Aromatase inhibitors - drugs that reduce activity of the enzyme aromatase. (
  • Small changes in inhibitor structure can cause large changes in binding to CA II, and this underlines the importance of structure-based drug design with this enzyme and other isoforms relevant to potential anticancer therapy. (
  • The drug specifically targets an enzyme called aromatase , which catalyzes the formation of estrogens from androgens , such as testosterone. (
  • Palbociclib in combination with endocrine therapy versus capecitabine in hormonal receptor-positive, human epidermal growth factor 2-negative, aromatase inhibitor-resistant metastatic breast cancer: a phase III randomised controlled trial-PEARL. (
  • Aromatase inhibitors are among the leading therapies against breast cancer. (
  • 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). (
  • 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. (
  • To deal with increased levels of estradiol, aromatase inhibitors are used. (
  • If you have metastatic breast cancer, you may receive any of the three aromatase inhibitors as a first treatment after your stage IV diagnosis . (
  • 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). (
  • 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. (
  • 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. (
  • 13. The potent and selective inhibition of estrogen production by non-steroidal aromatase inhibitor, YM511. (
  • 8. The new aromatase inhibitor CGS-16949A suppresses aldosterone and cortisol production by human adrenal cells in vitro. (
  • 10. The effect of the aromatase inhibitor, rogletimide (pyridoglutethimide), on guinea pig adrenal cell steroidogenesis and placental microsomal aromatase activity: comparison with aminoglutethimide and CGS 16949A. (
  • 18. The effects of CGS 16949A, an aromatase inhibitor on adrenal mineralocorticoid biosynthesis. (
  • With the acceptance of steroid sulfatase as a target for hormone-dependent cancer, novel dual aromatase-steroid sulfatase inhibitors (DASIs) containing a sulfamate group are now being developed. (
  • 19. CGS 16949A, a new nonsteroidal aromatase inhibitor: effects on hormone-dependent and -independent tumors in vivo. (
  • 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. (
  • Extending treatment with an aromatase inhibitor to 10 years may further reduce the risk of breast-cancer recurrence. (
  • Updated analysis from the United Kingdom's POETIC trial found no evidence that perioperative aromatase inhibitor therapy slows or prevents time to recurrence of breast cancer. (
  • It may also help relieve joint pain associated with the use of aromatase inhibitors, which are drugs used in people with breast cancer. (
  • 1. In vitro and in vivo studies demonstrating potent and selective estrogen inhibition with the nonsteroidal aromatase inhibitor CGS 16949A. (
  • 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. (
  • Aromatase inhibitor treatment of menorrhagia and subsequent pregnancy in a patient with familial hyperparathyroidism-jaw tumor syndrome. (
  • Angela Hartley Brodie discovered and developed a class of drugs called aromatase inhibitors, which can stop the production of hormones that fuel the growth of cancer cells. (
  • Evaluation of the safety of vitamin D3 supplements in women treated with aromatase inhibitors is crucial. (
  • 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. (
  • BACKGROUND: The impact of long-term adjuvant therapy with aromatase inhibitors (AIs) on vertebral fracture (VF) risk is still unclear. (
  • However, the study did show that tumor Ki67 levels after 2 weeks of perioperative aromatase inhibitor therapy are. (
  • It belongs to a class of medications called tyrosine kinase inhibitors (TKIs). (
  • 17. Reversible inhibition of human placental microsomal aromatase by CGS 18320B and other non-steroidal compounds. (
  • 3. Effect of aromatase inhibitors on estrogen 2-hydroxylase in rat liver. (
  • If side effects from a certain aromatase inhibitor become too difficult or interfere with your ability to function, your doctor might suggest another AI for you. (
  • Even though the AIs work in similar ways, a different aromatase inhibitor may not cause the same side effects for you. (
  • First crystal structures of human carbonic anhydrase II in complex with dual aromatase-steroid sulfatase inhibitors. (
  • 7. A comparison of methods measuring aromatase activity in human placenta and rat ovary. (
  • 6. An in vitro method to determine the selective inhibition of estrogen biosynthesis by aromatase inhibitors. (
  • The results highlight that at high concentrations, acetaminophen reduced the gene expression of aromatase (CYP19A1) and type 1 3β-hydroxysteroid dehydrogenase (HSD3B1), and increased the expression of 17β-hydroxysteroid dehydrogenase (HSD17B1). (
  • Both inhibitors ligate to the active site zinc(II) atom via their sulfamate nitrogen, while the rest of the molecule is contained within the hydrophobic binding pocket. (