Aromatase Inhibitors
Nitriles
Fadrozole
Aromatase
Androstatrienes
Antineoplastic Agents, Hormonal
Tamoxifen
Androstenedione
Postmenopause
Neoplasms, Hormone-Dependent
Estrogens
Estrogen Antagonists
Androstadienes
Estradiol
Receptors, Estrogen
Estrogen Receptor Modulators
Testolactone
Chemotherapy, Adjuvant
Selective Estrogen Receptor Modulators
Testosterone
Estrone
Gynecomastia
Enzyme Inhibitors
Receptors, Progesterone
Megestrol Acetate
Estrogen Receptor alpha
Ovary
Clinical Trials as Topic
Androgens
Drug Resistance, Neoplasm
Puberty, Precocious
Papio anubis
Hot Flashes
Dihydrotestosterone
Endometriosis
Sex Differentiation
Follicle Stimulating Hormone
Clomiphene
Bone Density Conservation Agents
Treatment Outcome
Neoadjuvant Therapy
Estrogen Receptor beta
Gonadotropins
Luteinizing Hormone
Receptor, erbB-2
Randomized Controlled Trials as Topic
Mammary Neoplasms, Experimental
Ovulation Induction
Placenta
Puberty, Delayed
Fibrous Dysplasia, Polyostotic
Steroids
Diphosphonates
Double-Blind Method
Drug Administration Schedule
Bone Density
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.
Prostaglandin-endoperoxide synthase 2
Papillary carcinomas of the breast
Cushing's syndrome
Acacetin
Steroidal aromatase inhibitor
Triphenylethylene
Tropoflavin
Obesity and fertility
Effects of hormones on sexual motivation
Triadimefon
Brassaiopsis glomerulata
Estrogen receptor beta
Breast cancer classification
Pharmacology of bicalutamide
Obesogen
Miconazole
Valproate
Melatonin
Estrogen-dependent condition
Melatonin as a medication and supplement
Ketoconazole
Dronabinol
List of OMIM disorder codes
Breast International Group
Hesperetin
Leptin
Anovulation
Amenorrhea
Ellagitannin
Temperature-dependent sex determination
Aromatase Inhibitors Increase Risk of Heart Problems
DailyMed - Search Results for Aromatase Inhibitors
Aromatase Inhibitors - PubMed
Aromatase inhibitors
Adaptation of an Evidence-Based Arthritis Program for Breast Cancer Survivors on Aromatase Inhibitor Therapy Who Experience...
Grant Abstract: Vitamin D3 Effects on Musculoskeletal Symptoms with Use of Aromatase Inhibitors
Aromatase-Inhibitor-Induced Musculoskeletal Inflammation Is Observed Independent of Oophorectomy in a Novel Mouse Model - PubMed
Aromatase Inhibitors
DailyMed - Search Results for Aromatase Inhibitors
Frontiers | Gynecomastia: A systematic review of pharmacological treatments
Aromatase Inhibitors for Sale - Buy Aromatase Inhibitors for Men
Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated
Analgesic - Side Effects & Precautions | Everyday Health
Palbociclib in combination with endocrine therapy versus capecitabine in hormonal receptor-positive, human epidermal growth...
Extending aromatase-inhibitor adjuvant therapy to 10 years<...
A Phase 1b Study of T-DXd Combinations in HER2-low Advanced or Metastatic Breast Cancer - Full Text View - ClinicalTrials.gov
First crystal structures of human carbonic anhydrase II in complex with dual aromatase-steroid sulfatase inhibitors. -...
Morphometric vertebral fractures in breast cancer patients treated with adjuvant aromatase inhibitor therapy: A cross-sectional...
Breast Cancer: Symptoms, Risk Factors, Diagnosis, Treatment & Prevention
Induction Press Page | National Inventors Hall of Fame®
Category:Breast cancer - Wikimedia Commons
Wine | GreenMedInfo | Substance | Natural Medicine | Alternative
ESR1 Mutated Metastatic Breast Cancer Diagnostics Market is expected to accumulate a value of US$ 185 Million by 2033 at a CAGR...
PA-19-200: Mechanisms Underlying the Contribution of Sleep Disturbances to Pain (R01 Clinical Trial Optional)
Efficacy of a combined alendronate and calcitriol agent (Maxmarvil®) in Korean postmenopausal women with early breast cancer...
Cancer treatment: dealing with hot flashes and night sweats: MedlinePlus Medical Encyclopedia
Tykerb: Side effects, dosage, use with other drugs, and more
February 25, 2018 - The ASCO Post
Tamoxifen5
- 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)
- 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)
- Standard treatments for ER+ breast cancer are endocrine therapies such as tamoxifen and aromatase inhibitors. (eurekalert.org)
- These women were assigned to receive standard hormone therapy such as tamoxifen or aromatase inhibitors, but didn't undergo chemotherapy. (nih.gov)
Letrozole4
- 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)
- 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. (britannica.com)
- 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. (britannica.com)
- Letrozole was far more potent than any other aromatase inhibitor discovered. (britannica.com)
Anastrozole1
- Anastrozole is by far the most popular aromatase inhibitor, due to its accessibility. (steroidsforsale.biz)
Postmenopausal5
- All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive breast cancer. (lbbc.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)
- Adding aromatase inhibitors (AIs) to adjuvant treatment of postmenopausal women with hormone-receptor-positive breast cancer significantly reduces cancer recurrence. (cdc.gov)
- Background: Adjuvant hormone treatment of postmenopausal breast cancer is mainly based on aromatase inhibitors. (who.int)
- 5. Inhibition of aromatase with CGS 16949A in postmenopausal women. (nih.gov)
Adjuvant treatment1
- 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)
Musculoskeletal6
- These symptoms, referred to as aromatase inhibitor-associated musculoskeletal symptoms (AIMSS), decrease quality of life and medication adherence. (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)
- The primary objective of this trial is to assess the efficacy of targeted individualised physiotherapeutic treatment on aromatase inhibitor-associated musculoskeletal pain. (inclinicaltrials.com)
- 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)
- 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)
Enzyme7
- 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)
- The two most important of them is the activity of aromatase enzyme and body fat. (steroidsforsale.biz)
- Aromatase - an enzyme that is responsible, not just for flavoring, in someone it is more active, in someone less active. (steroidsforsale.biz)
- Aromatase inhibitors - drugs that reduce activity of the enzyme aromatase. (steroidsforsale.biz)
- 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. (ox.ac.uk)
- The drug specifically targets an enzyme called aromatase , which catalyzes the formation of estrogens from androgens , such as testosterone. (britannica.com)
Hormonal1
- 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. (bvsalud.org)
Therapies1
- Aromatase inhibitors are among the leading therapies against breast cancer. (invent.org)
Chemotherapy1
- 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)
Arimidex1
- Arimidex is a powerful drug suppressing aromatase, a third generation drug. (dragonpharmaceuticals.com)
Abstract1
- 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)
Estradiol1
- To deal with increased levels of estradiol, aromatase inhibitors are used. (steroidsforsale.biz)
Metastatic2
- 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)
- 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)
Placebo1
- 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)
Estrogen production2
- 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)
- 13. The potent and selective inhibition of estrogen production by non-steroidal aromatase inhibitor, YM511. (nih.gov)
Adrenal3
- 8. The new aromatase inhibitor CGS-16949A suppresses aldosterone and cortisol production by human adrenal cells in vitro. (nih.gov)
- 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. (nih.gov)
- 18. The effects of CGS 16949A, an aromatase inhibitor on adrenal mineralocorticoid biosynthesis. (nih.gov)
Hormone-dependent2
- 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. (ox.ac.uk)
- 19. CGS 16949A, a new nonsteroidal aromatase inhibitor: effects on hormone-dependent and -independent tumors in vivo. (nih.gov)
Breast4
- 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)
- Extending treatment with an aromatase inhibitor to 10 years may further reduce the risk of breast-cancer recurrence. (arizona.edu)
- 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. (ascopost.com)
- It may also help relieve joint pain associated with the use of aromatase inhibitors, which are drugs used in people with breast cancer. (nih.gov)
Potent1
- 1. In vitro and in vivo studies demonstrating potent and selective estrogen inhibition with the nonsteroidal aromatase inhibitor CGS 16949A. (nih.gov)
Treatment2
- 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)
- Aromatase inhibitor treatment of menorrhagia and subsequent pregnancy in a patient with familial hyperparathyroidism-jaw tumor syndrome. (nih.gov)
Drugs1
- 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. (invent.org)
Women1
- Evaluation of the safety of vitamin D3 supplements in women treated with aromatase inhibitors is crucial. (nih.gov)
Androgens1
- 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)
Therapy2
- BACKGROUND: The impact of long-term adjuvant therapy with aromatase inhibitors (AIs) on vertebral fracture (VF) risk is still unclear. (unibs.it)
- However, the study did show that tumor Ki67 levels after 2 weeks of perioperative aromatase inhibitor therapy are. (ascopost.com)
Belongs1
- It belongs to a class of medications called tyrosine kinase inhibitors (TKIs). (medicalnewstoday.com)
Compounds1
- 17. Reversible inhibition of human placental microsomal aromatase by CGS 18320B and other non-steroidal compounds. (nih.gov)
Effect1
- 3. Effect of aromatase inhibitors on estrogen 2-hydroxylase in rat liver. (nih.gov)
Side effects2
- 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. (lbbc.org)
- Even though the AIs work in similar ways, a different aromatase inhibitor may not cause the same side effects for you. (lbbc.org)
Human2
Determine1
- 6. An in vitro method to determine the selective inhibition of estrogen biosynthesis by aromatase inhibitors. (nih.gov)
Type1
- 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). (nih.gov)
Active1
- 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. (ox.ac.uk)