Antineoplastic Agents, Hormonal
Estrogen Receptor alpha
Gene Expression Regulation, Enzymologic
Estrogen Receptor beta
Estrogen Receptor Modulators
Follicle Stimulating Hormone
Steroidogenic Factor 1
Cholestenone 5 alpha-Reductase
Selective Estrogen Receptor Modulators
Cholesterol Side-Chain Cleavage Enzyme
Reverse Transcriptase Polymerase Chain Reaction
Promoter Regions, Genetic
Gonadal Steroid Hormones
Leydig Cell Tumor
Gene Expression Regulation, Neoplastic
Fushi Tarazu Transcription Factors
Cytochrome P-450 Enzyme System
Ovotesticular Disorders of Sex Development
Molecular Sequence Data
Drug Resistance, Neoplasm
Dose-Response Relationship, Drug
Clinical Trials as Topic
In Situ Hybridization
Follicle Stimulating Hormone, Human
Granulosa Cell Tumor
Tumor Cells, Cultured
Mammary Neoplasms, Experimental
Constitutional genetic variation at the human aromatase gene (Cyp19) and breast cancer risk. (1/1297)The activity of the aromatase enzyme, which converts androgens into oestrogens and has a major role in regulating oestrogen levels in the breast, is thought to be a contributing factor in the development of breast cancer. We undertook this study to assess the role of constitutional genetic variation in the human aromatase gene (Cyp19) in the development of this disease. Our genotyping of 348 cases with breast cancer and 145 controls (all Caucasian women) for a published tetranucleotide repeat polymorphism at intron 4 of the Cyp19 gene revealed the presence of six common and two rare alleles. Contingency table analysis revealed a significant difference in allelic distribution between cases and controls (chi2 5df = 13.52, P = 0.019). The allele measuring 171 bp was over-represented in cases; of 14 individuals homozygous for this allele, 13 were cases. These individuals had a higher incidence of cancer in family members and an earlier age at diagnosis than other cases. In sequencing Cyp19's coding exons and regulatory regions, we discovered a perfect association between a silent polymorphism (G-->A at Val80) and the high-risk genotype. Our conclusion is that constitutional genetic variation at the Cyp19 locus is associated with the risk of developing breast cancer, with the 171-bp allele serving as the high-risk allele. (+info)
Endometriosis: a dysfunction and disease of the archimetra. (2/1297)Endometriosis is considered primarily a disease of the endometrial-subendometrial unit or archimetra. The clinical picture of endometriosis characterises this disease as a hyperactivation of genuine archimetrial functions such as proliferation, inflammatory defence and peristalsis. While the aetiology of the disease remains to be elucidated, a key event appears to consist in the local production of extraovarian oestrogen by a pathological expression of the P450 aromatase. The starting event may consist in a hyperactivity of the endometrial inflammatory defence, a hyperactivity of the endometrial oxytocin/oxytocin receptor system or in the pathological expression of the P450 aromatase system itself. Regardless of which of these levels the starting event is localized in, they influence each other on both the level of the archimetra and the endometriotic lesions. Locally elevated oestrogen levels inevitably up-regulate the endometrial oxytocin mRNA and increased levels of oxytocin result in uterine hyperperistalsis, increased transtubal seeding of endometrial tissue fragments and finally subfertility and infertility by impairment of the uterine mechanism of rapid and sustained sperm transport. Locally increased levels of oestrogen lead, on both the level of the endometrial-subendometrial unit and the endometriotic lesion, to processes of hyperproliferation. These processes result, on the level of the uterus, in an infiltrative growth of elements of the archimetra into the neometra and, on the level of the endometriotic lesion, in infiltrative endometriosis. There is circumstantial evidence that trauma might be an important initial event that induces the specific biochemical and cellular responses of the archimetra. This model is able to explain both the pleiomorphic appearance of endometriosis and the, up until now, enigmatic infertility associated with mild and moderate endometriosis. (+info)
The aromatase inactivator 4-hydroxyandrostenedione (4-OH-A) inhibits tamoxifen metabolism by rat hepatic cytochrome P-450 3A: potential for drug-drug interaction of tamoxifen and 4-OH-A in combined anti-breast cancer therapy. (3/1297)Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 microM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA. (+info)
The mechanism of action of epidermal growth factor and transforming growth factor alpha on aromatase activity in granulosa cells from polycystic ovaries. (4/1297)We investigated aromatization and the mechanism of action of epidermal growth factor (EGF) and transforming growth factor alpha (TGFalpha) on oestradiol biosynthesis in freshly prepared granulosa cells from polycystic ovaries. Freshly prepared granulosa cells from polycystic ovaries incubated for only 3 h under basal conditions secreted significantly (P< 0.001) greater amounts of oestradiol-17beta than that of granulosa cells from normal ovaries. 8-Bromo-cyclic adenosine monophosphate (8-Br-cAMP), but not follicle stimulating hormone (FSH) or luteinizing hormone (LH), further enhanced this activity. Both EGF and TGFalpha inhibited gonadotrophinor 8-Br-cAMP-stimulated, but not basal, oestradiol production. LH receptor (LHR) binding, estimated by immunolabelling the bound LH, was significantly (P< 0.001) reduced in granulosa cells from polycystic ovaries when compared with cells from normal ovaries. EGF or TGFalpha significantly reduced the binding in cultured cells from all patient groups (P< 0.05). More interestingly, a further increase of the inhibitory effect was seen in granulosa cells from polycystic ovaries (P < 0.001). In conclusion, granulosa cells from polycystic ovaries contain high levels of basal aromatase activity in vitro, which is probably inherited from the in-vivo condition. EGF and TGFalpha suppress oestradiol synthesis at a step beyond the production of cAMP and also LHR binding with more effect in granulosa cells from polycystic ovaries. (+info)
Effect of labor induction on the expression of oxytocin receptor, cytochrome P450 aromatase, and estradiol receptor in the reproductive tract of the late-pregnant ewe. (5/1297)In this study, we investigated the timing of changes in aromatase, estradiol receptor, and oxytocin receptor expression in ovine uterine and placental tissues before parturition. Labor was induced by betamethasone injection into the fetus on Days 130-132 of pregnancy. Tissue samples were collected at injection and then every 14 h until labor (56 h) from four ewes at each time point. Samples were analyzed for aromatase, estradiol receptor, and oxytocin receptor expression by in situ hybridization; for oxytocin binding to its receptor using a specific antagonist; and for estradiol receptor quantitation by immunocytochemistry. Aromatase mRNA expression increased by 14 h postinjection (p < 0.02) in the fetal villi and remained high until labor. Expression of estradiol and oxytocin receptor mRNAs was unchanged in myometrium but increased in the endometrial luminal epithelium by 28 h (p < 0.05) and remained high until labor. Estradiol receptor protein concentration increased modestly at labor while oxytocin receptor binding in the luminal epithelium changed in parallel to the mRNA concentration. IN CONCLUSION: 1) induction of aromatase may facilitate the expression of endometrial estradiol and oxytocin receptors in the placentome, 2) changes in endometrial rather than myometrial oxytocin receptor may be important in inducing parturition, and 3) the transcription of estradiol receptor and oxytocin receptor in the uterine epithelium are positively correlated during parturition. (+info)
A 500-bp region, approximately 40 kb upstream of the human CYP19 (aromatase) gene, mediates placenta-specific expression in transgenic mice. (6/1297)In humans, aromatase P450 (product of CYP19 gene), which catalyzes conversion of C19 steroids to estrogens, is expressed in a number of tissues, including ovary, adipose, and syncytiotrophoblast of the placenta. The 5' untranslated regions of CYP19 mRNA transcripts in these tissues are encoded by different tissue-specific first exons, which are spliced onto a common site just upstream of the translation initiation site in exon II. In placenta, the 5' untranslated region of CYP19 mRNA transcripts is encoded by exon I.1, which lies approximately 40 kb upstream of exon II. To map genomic sequences required for placenta-specific CYP19 expression, fusion genes containing 2,400 and 501 bp of placenta-specific exon I.1 5' flanking DNA linked to the human growth hormone gene (hGH), as reporter, were introduced into transgenic mice. Expression of CYP19(I.1):hGH fusion genes containing as little as 501 bp of 5' flanking DNA was placenta-specific and developmentally regulated. Furthermore, transgene expression occurred specifically in the labyrinthine trophoblast of the mouse placenta, which contains syncytial cells that may be analogous to the human syncytiotrophoblast. We show that a relatively small segment of DNA (approximately 500 bp) >40 kb upstream of the protein coding region of a human gene is able to direct expression in an appropriate tissue- and cell-specific manner in transgenic mice. These findings suggest that 5' flanking DNA within 501 bp of exon I.1 of the human CYP19 gene contains cis-acting elements that bind placenta-specific transcription factors that are conserved between humans and mice. (+info)
Intrafollicular content of luteinizing hormone receptor, alpha-inhibin, and aromatase in relation to follicular growth, estrous cycle stage, and oocyte competence for in vitro maturation in the mare. (7/1297)The intrafollicular content of LH receptor, alpha-inhibin, and aromatase are known good indicators of follicular status. We investigated the amounts of these proteins in granulosa and cumulus cells in relation to oocyte competence for in vitro maturation, follicular growth, and estrous cycle stage in the mare. Follicular punctures were performed 34 h after an injection of crude equine gonadotropins, either during the follicular phase, at the end of the follicular phase, or during the luteal phase. The cumulus-oocyte complex, granulosa cells, and follicular fluid of follicles larger than 5 mm were collected. The nuclear stage of the oocytes after in vitro culture was determined microscopically. Granulosa and cumulus cell amounts of LH receptor, alpha-inhibin, and aromatase were assessed by the semiquantitative Western blot method and image analysis. Follicular fluids were assayed for progesterone (P4) and estradiol-17beta (E2). The three factors were expressed in mural granulosa and cumulus cells from all follicles from the gonadotropin-independent growth period until the preovulatory stage. Considering all the follicles punctured, the amounts of LH receptor and alpha-inhibin in granulosa cells were not different for the three physiological stages studied. The amounts of aromatase in granulosa cells, as well as the E2:P4 ratios, were higher for follicles punctured during the follicular phase than for the two other groups (p < 0.05). Considering the data from the three groups, the E2:P4 ratio and the LH receptor and aromatase contents, but not alpha-inhibin, in granulosa cells increased with an increase in follicular diameter (p < 0.01). The E2:P4 ratios and the amounts of LH receptor, alpha-inhibin, and aromatase in granulosa cells were lower in follicles 5-9 mm in diameter than in larger ones (p < 0.05). In cumulus cells, the amounts of the three factors were different neither between the three groups nor between the follicular diameters. Although we could not establish any obvious relationship to oocyte competence for in vitro maturation, the influence of the follicle diameter on the content of LH receptors, alpha-inhibin, and aromatase in granulosa cells was similar to the influence of follicle diameter on oocyte competence. Therefore, one can hypothesize that, in the mare, there is a link between the acquisition of oocyte competence and the expression of these factors in the follicular cells. (+info)
Dynamics of periovulatory steroidogenesis in the rhesus monkey follicle after ovarian stimulation. (8/1297)The temporal relationships and regulation of events in the primate follicle during the periovulatory interval are poorly understood. This study was designed to elucidate the dynamics of steroid synthesis in the macaque follicle during ovarian stimulation cycles in which serum/follicular fluid aspirates were collected at precise intervals before (0 h) and after (up to 36 h) administration of the ovulatory human chorionic gonadotrophin (HCG) bolus. Serum concentrations of progesterone increased (P < 0.05) within 30 min, and follicular fluid progesterone concentrations were elevated 180-fold within 12 h, of HCG injection, and remained elevated until the time of ovulation. In contrast, 17beta-oestradiol concentrations increased initially, but then declined (P < 0.05) by 36 h post-HCG. Acute incubation of granulosa cells with and without steroidogenic substrates demonstrated that: (i) 3beta-hydroxysteroid dehydrogenase and aromatase activities were present in equivalent amounts before and after HCG; whereas (ii) P450 side-chain cleavage activity increased (P < 0.05) within 12 h of HCG; and (iii) exogenous low-density lipoprotein and cholesterol were not utilized for steroidogenesis. This model should be useful for further studies on ovulation and luteinization in primates, and enable elucidation of the local actions of progesterone and other steroids at specific time points during the periovulatory interval. (+info)
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Examples of hormone-dependent neoplasms include:
1. Breast cancer: Many breast cancers are estrogen receptor-positive (ER+), meaning that they grow in response to estrogen. These cancers can be treated with selective estrogen receptor modulators (SERMs) or aromatase inhibitors, which block the effects of estrogen on cancer growth.
2. Prostate cancer: Some prostate cancers are androgen-dependent, meaning that they grow in response to androgens such as testosterone. These cancers can be treated with androgen deprivation therapy (ADT), which reduces the levels of androgens in the body to slow or stop cancer growth.
3. Uterine cancer: Some uterine cancers are estrogen-dependent, meaning that they grow in response to estrogen. These cancers can be treated with hormone therapy to reduce estrogen levels.
Hormone-dependent neoplasms are often characterized by the presence of hormone receptors on the surface of the cancer cells. These receptors can bind to specific hormones and trigger signals that promote cancer growth and progression. Targeting these hormone receptors with hormone therapy can be an effective way to slow or stop the growth of these cancers.
The term "gynecomastia" comes from the Greek words "gyneco," meaning "womanlike," and "mastos," meaning "breast." The condition can occur at any age, but it is most common in infants, teenagers, and older men.
Gynecomastia can be caused by a variety of factors, including:
1. Hormonal imbalance: An imbalance of testosterone and estrogen hormones can lead to breast tissue growth.
2. Medications: Certain medications, such as antidepressants, anti-anxiety drugs, and heart medications, can cause gynecomastia as a side effect.
3. Medical conditions: Conditions such as hypogonadism (low testosterone levels), hyperthyroidism (high thyroid hormone levels), and liver or kidney disease can contribute to gynecomastia.
4. Genetic factors: Some men may inherit a tendency to develop gynecomastia due to genetic mutations.
5. Other factors: Gynecomastia can also be caused by other factors such as obesity, alcohol consumption, and certain types of foods or supplements.
Symptoms of gynecomastia may include:
* Enlarged breasts
* Breast tenderness
* Nipple sensitivity
* Pain in the breasts
* Swelling in the armpits
Gynecomastia is usually diagnosed through a physical examination and medical history. Imaging tests such as mammography or ultrasound may also be used to help rule out other conditions.
Treatment for gynecomastia depends on the underlying cause of the condition. In some cases, medications may be prescribed to address hormonal imbalances or other medical conditions that are contributing to the development of gynecomastia. Surgery may also be an option to remove excess breast tissue and improve the appearance of the chest.
In conclusion, gynecomastia is a relatively common condition in men that can have a significant impact on their self-esteem and quality of life. Understanding the causes and symptoms of gynecomastia is essential for proper diagnosis and effective treatment.
In the medical field, the term is often used to describe various conditions that affect gender development or sexual differentiation in individuals with variations in sex chromosomes, hormones, or genitalia. Feminization can occur in individuals assigned male at birth but who exhibit female physical characteristics, such as those with congenital adrenal hyperplasia (CAH) or other intersex traits.
The term is also used to describe the effects of estrogen on the male body, particularly during puberty. For example, boys taking estrogen medication for hormone therapy may experience feminization of their physical features, such as breast tissue growth and a softer voice.
It's important to note that the term feminization is sometimes used in medical contexts to describe a process or outcome that is perceived as negative or undesirable, particularly when it comes to gender identity or expression. However, it's essential to recognize that all individuals, regardless of their gender identity or expression, deserve respect and support in their healthcare needs.
In summary, feminization within the medical field refers to a process or condition whereby male characteristics are acquired by an individual or group, often as a result of hormonal or genetic factors. The term is used to describe various conditions affecting gender development or sexual differentiation and the effects of estrogen on the male body. However, it's important to recognize that the term can be perceived as negative, and healthcare providers should approach patients with respect and sensitivity regardless of their gender identity or expression.
Endometriosis can cause a range of symptoms, including:
* Painful periods (dysmenorrhea)
* Heavy menstrual bleeding
* Pelvic pain or cramping
* Infertility or difficulty getting pregnant
* Abnormal bleeding or spotting
* Bowel or urinary symptoms such as constipation, diarrhea, or painful urination during menstruation
The exact cause of endometriosis is not known, but it is thought to involve a combination of genetic, hormonal, and environmental factors. Some possible causes include:
* Retrograde menstruation: The backflow of endometrial tissue through the fallopian tubes into the pelvic cavity during menstruation
* Coelomic metaplasia: The transformation of cells that line the abdominal cavity (coelom) into endometrial cells
* Immunological factors: Abnormal immune responses that lead to the growth and accumulation of endometrial cells outside of the uterus
* Hormonal factors: Fluctuations in estrogen levels, which can stimulate the growth of endometrial cells
* Genetic factors: Inherited traits that increase the risk of developing endometriosis
There are several risk factors for developing endometriosis, including:
* Family history: A woman's risk increases if she has a mother, sister, or daughter with endometriosis
* Early onset of menstruation: Women who start menstruating at a younger age may be more likely to develop endometriosis
* Frequent or heavy menstrual bleeding: Women who experience heavy or prolonged menstrual bleeding may be more likely to develop endometriosis
* Polycystic ovary syndrome (PCOS): Women with PCOS are at higher risk for developing endometriosis
* Obesity: Being overweight or obese may increase the risk of developing endometriosis
There is no cure for endometriosis, but there are several treatment options available to manage symptoms and improve quality of life. These may include:
* Hormonal therapies: Medications that reduce estrogen levels or block the effects of estrogen on the endometrium can help manage symptoms such as pain and heavy bleeding
* Surgery: Laparoscopic surgery can be used to remove endometrial tissue and scar tissue, and improve fertility
* Alternative therapies: Acupuncture, herbal remedies, and other alternative therapies may help manage symptoms and improve quality of life
It's important for women with endometriosis to work closely with their healthcare provider to find the best treatment plan for their individual needs. With proper diagnosis and treatment, many women with endometriosis can go on to lead fulfilling lives.
The symptoms of choriocarcinoma can vary depending on the location and size of the tumor, but they may include:
* Abnormal vaginal bleeding
* Pelvic pain
* Abdominal pain
* Weakness and fatigue
* Shortness of breath
* Nausea and vomiting
If choriocarcinoma is suspected, a variety of tests may be performed to confirm the diagnosis. These may include:
* Ultrasound: This imaging test uses high-frequency sound waves to create pictures of the uterus and ovaries. It can help doctors identify any abnormal growths or tumors in the area.
* Hysteroscopy: This procedure involves inserting a thin, lighted tube through the cervix to visualize the inside of the uterus. Doctors may use hysteroscopy to collect samples of tissue for testing.
* Laparoscopy: This procedure involves making small incisions in the abdomen and using a thin, lighted tube to visualize the inside of the pelvis. Doctors may use laparoscopy to collect samples of tissue for testing or to remove any tumors that are found.
* Biopsy: In this test, doctors take a small sample of tissue from the uterus and examine it under a microscope for cancer cells.
If choriocarcinoma is confirmed, treatment may involve a combination of surgery, chemotherapy, and radiation therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as the patient's overall health.
Prognosis for choriocarcinoma varies depending on the stage of the cancer when it is diagnosed. In general, the prognosis is good if the cancer is caught early and treated promptly. However, if the cancer has spread to other parts of the body (metastasized), the prognosis may be poorer.
It's important for women who have had a molar pregnancy or choriocarcinoma to follow up with their healthcare provider regularly to ensure that any remaining tissue is removed and to monitor for any signs of recurrence.
These tumors typically affect adult men and are relatively slow-growing. They can cause symptoms such as painless testicular swelling, difficulty urinating, or abdominal discomfort due to pressure on surrounding organs.
Leydig cell tumors are relatively rare, accounting for less than 1% of all testicular tumors. They are usually benign (non-cancerous), but in some cases can be malignant (cancerous). Treatment typically involves surgical removal of the affected testicle (orchiectomy) and may also involve hormone therapy to reduce levels of male hormones, such as testosterone.
Leydig cell tumors are classified into two main types: Leydig cell adenoma and Leydig cell carcinoma. Leydig cell adenoma is the more common type and typically grows slowly, while Leydig cell carcinoma is less common but can grow faster and be more aggressive.
Overall, Leydig cell tumors are rare and often slow-growing, but they can cause significant symptoms and may require surgical intervention to treat.
The word "arthralgia" comes from the Greek words "arthron," meaning joint, and "algos," meaning pain. It is often used interchangeably with the term "joint pain," but arthralgia specifically refers to a type of pain that is not caused by inflammation or injury.
Arthralgia can manifest in different ways, including:
1. Aching or dull pain in one or more joints
2. Sharp or stabbing pain in one or more joints
3. Pain that worsens with movement or weight-bearing activity
4. Pain that improves with rest
5. Pain that is localized to one joint or multiple joints
6. Pain that is accompanied by stiffness or limited range of motion
7. Pain that is worse in the morning or after periods of rest
8. Pain that is triggered by certain activities or movements
The diagnosis of arthralgia typically involves a comprehensive medical history and physical examination, as well as diagnostic tests such as X-rays, blood tests, or imaging studies. Treatment for arthralgia depends on the underlying cause and may include medications, lifestyle modifications, or other interventions.
The causes of virilism can be due to various factors including:
1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive levels of androgens such as testosterone.
2. Androgen insensitivity syndrome (AIS): A condition where the body is unable to respond to androgens, leading to virilization.
3. 5-alpha-reductase deficiency: A rare genetic disorder that affects the production of the enzyme 5-alpha-reductase, which is important for the development of male characteristics.
4. Genetic mutations: Some individuals may have genetic mutations that lead to the overproduction of androgens or the underproduction of anti-androgens.
5. Hormonal imbalances: Imbalances in hormone levels, such as high testosterone and low estrogen, can also cause virilism.
Virilism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as hormone level measurements. Treatment options for virilism depend on the underlying cause and may include hormone replacement therapy, surgery, or psychological counseling.
In summary, virilism is a condition characterized by the excessive development of male characteristics in individuals who are not biologically male, and it can be caused by various genetic or hormonal factors. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can improve outcomes.
Types of Adrenal Cortex Neoplasms:
1. Adrenocortical carcinoma (ACC): A rare and aggressive malignant tumor that originates in the adrenal cortex. It is often associated with virilization (excessive masculinization) in women.
2. Adrenocortical adenoma (ACA): A benign tumor that originates in the adrenal cortex. It is less common than ACC and may not cause any symptoms.
3. Pheochromocytoma: A rare tumor that originates in the adrenal medulla, which is the inner part of the adrenal gland. It can secrete excessive amounts of hormones that regulate blood pressure and heart rate.
4. Paraganglioma: A rare tumor that originates in the paraganglia, which are clusters of cells located near the adrenal glands. These tumors can produce excessive amounts of hormones and cause similar symptoms as pheochromocytoma.
Symptoms of Adrenal Cortex Neoplasms:
1. Virilization (excessive masculinization) in women, such as deepening of the voice, excessive body hair growth, and clitoral enlargement.
2. Headache, fatigue, and weight gain due to excessive production of steroid hormones.
3. High blood pressure and heart rate due to excessive production of catecholamines (hormones that regulate blood pressure and heart rate).
4. Abdominal pain, nausea, and vomiting due to the tumor's size and location.
Diagnosis of Adrenal Cortex Neoplasms:
1. Imaging tests such as CT scans or MRI to visualize the tumor and determine its size and location.
2. Laboratory tests to measure hormone levels in the blood, including cortisol, aldosterone, and catecholamines.
3. Biopsy to obtain a tissue sample for further examination under a microscope.
Treatment of Adrenal Cortex Neoplasms:
1. Surgery to remove the tumor, which is usually curative.
2. Medications to control symptoms such as high blood pressure and hormone levels.
3. Radiation therapy may be used in cases where surgery is not feasible or if there is a risk of recurrence.
Prognosis of Adrenal Cortex Neoplasms:
The prognosis for adrenal cortex neoplasms depends on the type and size of the tumor, as well as the extent of hormone production. In general, the prognosis is good for patients with benign tumors that are removed surgically. However, malignant tumors can have a poorer prognosis and may require additional treatments such as radiation therapy or chemotherapy.
Prevention of Adrenal Cortex Neoplasms:
There is no known prevention for adrenal cortex neoplasms, but early detection and treatment can improve outcomes. Regular monitoring of hormone levels and imaging tests can help detect tumors at an early stage.
1. Reduce stress: High levels of cortisol can be caused by stress, so finding ways to manage stress can help prevent adrenal cortex neoplasms.
2. Maintain a healthy diet: Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains can help support overall health and well-being.
3. Exercise regularly: Regular physical activity can help reduce stress and improve overall health.
4. Get enough sleep: Aim for 7-8 hours of sleep per night to help regulate hormone levels.
5. Limit caffeine and alcohol: Both substances can disrupt hormone levels and contribute to the development of adrenal cortex neoplasms.
Some common types of uterine diseases include:
1. Endometriosis: A condition in which tissue similar to the lining of the uterus grows outside the uterus, causing pain, inflammation, and infertility.
2. Fibroids: Noncancerous growths that develop in the uterus, often causing heavy menstrual bleeding, pelvic pain, and infertility.
3. Adenomyosis: A condition where tissue similar to the lining of the uterus grows into the muscle wall of the uterus, leading to heavy menstrual bleeding, pain, and infertility.
4. Uterine polyps: Growths that develop on the inner lining of the uterus, often causing abnormal bleeding or spots on the uterine lining.
5. Uterine cancer: Cancer that develops in the cells of the uterus, often caused by factors such as obesity, hormonal imbalances, or family history of cancer.
6. Endometrial hyperplasia: A condition where the lining of the uterus becomes thicker than normal, often due to hormonal imbalances or excessive estrogen exposure.
7. Asherman's syndrome: Scar tissue that develops inside the uterus, often after a D&C procedure, leading to infertility and irregular menstrual bleeding.
8. Uterine septum: A congenital condition where a wall of tissue divides the uterus into two compartments, often causing irregular menstrual bleeding and fertility problems.
9. Endometrial cysts: Fluid-filled sacs that develop on the inner lining of the uterus, often causing abnormal bleeding or pelvic pain.
10. Uterine tuberculosis: A rare condition where the uterus becomes infected with tuberculosis bacteria, often caused by poor sanitation and hygiene.
These are just a few of the many conditions that can affect the uterus and cause abnormal bleeding. It's important to consult with a healthcare provider if you experience any unusual or persistent vaginal bleeding to determine the underlying cause and receive proper treatment.
Precocious puberty is a condition wherein children under the age of 8 or 9 experience early onset of pubertal changes, such as breast development, menstruation, or enlargement of the testes and scrotum. It is also known as central precocious puberty (CPP) when it is caused by premature activation of the hypothalamic-pituitary-gonadal axis, resulting in early release of sex hormones.
Precocious Puberty: Causes
The exact cause of precocious puberty is not known; however, several factors have been implicated, including:
1. Genetics: In some cases, precocious puberty may be inherited, with a family history of early puberty or other hormonal disorders.
2. Brain tumors: Tumors in the hypothalamus or pituitary gland can cause early activation of the HPG axis and result in precocious puberty.
3. Congenital anomalies: Some children may be born with abnormalities in the HPG axis, leading to early puberty.
4. Trauma: Traumatic brain injury or stroke may trigger premature activation of the HPG axis and result in precocious puberty.
5. Infections: Certain infections, such as meningitis or encephalitis, can cause inflammation in the hypothalamus or pituitary gland, leading to early puberty.
6. Nutritional factors: Malnutrition or rapid weight gain may contribute to early puberty.
7. Hormonal imbalance: Some children may have an imbalance of sex hormones, such as estrogen or testosterone, which can lead to early puberty.
8. Thyroid disorders: Hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid) can cause early puberty.
9. Chronic diseases: Certain chronic diseases, such as type 1 diabetes mellitus or inflammatory bowel disease, may increase the risk of early puberty.
It is important to note that in many cases, the exact cause of precocious puberty cannot be determined. If you suspect that your child is experiencing early puberty, it is essential to consult with a healthcare professional for proper evaluation and treatment.
The term "ovotesticular" refers to the presence of both ovarian and testicular tissue, while "disorders of sex development" (DSD) is a broader category that encompasses a wide range of conditions that affect the development of sex characteristics. OSDS are considered to be a subset of DSDs.
Examples of OSDS include:
1. Androgen insensitivity syndrome (AIS): A condition in which individuals with XY chromosomes do not respond to androgens, leading to the development of female physical characteristics.
2. Complete and partial ovary-testis duplication: Conditions in which there is an extra ovary and/or testis present in addition to the normal ovary and testis.
3. Mixed gonadal dysgenesis (MGD): A condition in which there is a combination of ovarian and testicular tissue, but the exact combination can vary.
4. Swyer syndrome: A condition in which individuals with XY chromosomes have a normal appearing ovary and uterus, but do not produce sperm.
The management of OSDS is complex and requires a multidisciplinary approach, including endocrinologists, geneticists, gynecologists, and psychologists. Treatment options may include hormone therapy, surgery, and/or gender confirmation surgeries. The goal of treatment is to help individuals with OSDS achieve optimal physical and emotional well-being, as well as to provide support and counseling for families and individuals affected by these conditions.
Adrenocortical carcinoma can be subdivided into three main types based on their histological features:
1. Typical adrenocortical carcinoma: This is the most common type and accounts for about 70% of all cases. It is characterized by a large, irregular tumor that grows in the cortex of the adrenal gland.
2. Adenomatous adrenocortical carcinoma: This type is less aggressive than typical adrenocortical carcinoma and accounts for about 20% of cases. It is characterized by a small, well-circumscribed tumor that grows in the cortex of the adrenal gland.
3. Adrenocortical sarcoma: This is the least common type and accounts for about 10% of cases. It is characterized by a rare, malignant tumor that grows in the cortex of the adrenal gland.
Adrenocortical carcinoma can cause a variety of symptoms, including abdominal pain, weight loss, fatigue, and skin changes. The diagnosis is typically made through a combination of imaging studies, such as CT scans and MRI, and tissue biopsy. Treatment options include surgery, chemotherapy, and radiation therapy, and the prognosis depends on the stage and aggressiveness of the tumor.
Overall, adrenocortical carcinoma is a rare and aggressive cancer that requires prompt diagnosis and treatment to improve patient outcomes.
The tumor usually grows slowly and may not cause any symptoms in its early stages. However, as it progresses, it can cause abdominal pain, bloating, and irregular vaginal bleeding. GCTs are generally diagnosed through a combination of pelvic examination, imaging studies such as ultrasound or computed tomography (CT), and biopsy.
There are several subtypes of GCT, including:
1. Granulosa cell tumor with stromal element (GCT-SE): This is the most common type of GCT and accounts for about 70% of all cases. It is characterized by the presence of stromal cells, which are connective tissue cells that provide support and structure to the tumor.
2. Granulosa cell tumor without stromal element (GCT-wSE): This type of GCT lacks stromal cells and accounts for about 30% of all cases. It tends to be more aggressive than GCT-SE and is more likely to spread to other parts of the body.
3. Mucinous granulosa cell tumor (MGCT): This is a rare subtype of GCT that produces mucin, a type of protein that is found in the ovary. MGCTs tend to be slower-growing than other types of GCT and have a better prognosis.
Treatment for GCT typically involves surgery to remove the tumor, followed by radiation therapy and/or chemotherapy to destroy any remaining cancer cells. The prognosis for GCT is generally good, with a 5-year survival rate of about 80% for women with early-stage disease. However, the prognosis can be poorer for women with more advanced stages of the disease.
In summary, granulosa cell tumor is a rare type of ovarian cancer that originates from the granulosa cells of the ovary. It can present in different forms and has a good prognosis if treated early. Treatment typically involves surgery, radiation therapy, and/or chemotherapy.
Examples of 'Mammary Neoplasms, Experimental' in a sentence:
1. The researchers studied the effects of hormone therapy on mammary neoplasms in experimental animals to better understand its potential role in human breast cancer.
2. The lab used mice with genetic mutations that predispose them to developing mammary neoplasms to test the efficacy of new cancer drugs.
3. In order to investigate the link between obesity and breast cancer, the researchers conducted experiments on mammary neoplasms in rats with diet-induced obesity.
There are several theories about the causes of hot flashes, including hormonal changes, neurotransmitter imbalances, and blood vessel dilation. Some risk factors for hot flashes include age, family history, and certain medical conditions such as hypertension and diabetes.
Treatment options for hot flashes include hormone therapy, selective serotonin reuptake inhibitors (SSRIs), and non-hormonal medications such as clonidine and gabapentin. Lifestyle modifications such as dressing in layers, using a fan, and avoiding triggers like spicy foods and alcohol can also help manage hot flashes.
In conclusion, hot flashes are a common symptom of menopause that can have a significant impact on quality of life. While their exact cause is still not fully understood, there are several effective treatment options available to manage their frequency and severity. By understanding the causes and risk factors for hot flashes, women can work with their healthcare providers to find the best course of treatment for their individual needs.
Steroidal aromatase inhibitor
Aromatase excess syndrome
Non steroidal aromatase inhibitors
List of OMIM disorder codes
Angela Hartley Brodie
Cytochrome p450 family 19 subfamily a member 1
Estrogen insensitivity syndrome
Selective estrogen receptor degrader
Aromatase excess syndrome - About the Disease - Genetic and Rare Diseases Information Center
Aromatase excess syndrome: MedlinePlus Genetics
DailyMed - Search Results for Aromatase Inhibitors
Aromatase Inhibitors Increase Risk of Heart Problems
Aromatase Inhibitors - PubMed
Aromatase Inhibitors - PubMed
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
Anne Hudson Blaes, MD, on Aromatase Inhibitors and Cardiovascular Disease - The ASCO Post
Aromatase expression predicts survival in women with early-stage non small cell lung cancer.
WT1 and DAX-1 inhibit aromatase P450 expression in human endometrial and endometriotic stromal cells<...
DailyMed - Search Results for Aromatase Inhibitors
Resveratrol Has Aromatase Inhibiting Activity
APExBIO - Aromatase - Endocrinology and Hormones - Signaling Pathways
Aromatase | Order Aromatase Online | Buy Aromatase Online
Targeted Physiotherapeutic Treatment for Aromatase Inhibitor-associated
Frontiers | Gynecomastia: A systematic review of pharmacological treatments
Aromatase Inhibitors for Sale - Buy Aromatase Inhibitors for Men
Overexpression of aromatase associated with loss of heterozygosity of the STK11 gene accounts for prepubertal gynecomastia in...
AROMATASE ACTIVITY OF BRAIN AND OVARY IN RELATION TO ANNUAL REPRODUCTIVE CYCLE OF THE INDIAN CATFISH, HETEROPNEUSTES FOSSILIS
Extending aromatase-inhibitor adjuvant therapy to 10 years<...
375 A MULTICENTER STUDY OF THE ASSOCIATION OF AROMATASE AND ESTROGEN RECEPTOR GENES WITH HIP AND KNEE OSTEOARTHRITIS - Nuffield...
MEDLINE Data Changes - 2005. NLM Technical Bulletin. 2004 Nov-Dec
Aromatase Expression in Health and Disease<...
Analgesic - Side Effects & Precautions | Everyday Health
Placental aromatase is deficient in placental ischemia and preeclampsia<...
- The aromatase inhibitors include anastrozole, letrozole and exemestane, some of which have been implicated in causing rare instances of clinically apparent liver injury. (nih.gov)
- Arimidex 1mg ( buy Anastrozole ) Arimidex 1mg ( buy Anastrozole ) buy AstraZeneca Pharmaceuticals LP is a non-steroidal aromatase inhibitor, which reduces the amount of oestrogen (female sex hormone) made by the body. (gradepharma.com)
- Anastrozole is by far the most popular aromatase inhibitor, due to its accessibility. (steroidsforsale.biz)
- 11. Formestane, a steroidal aromatase inhibitor after failure of non-steroidal aromatase inhibitors (anastrozole and letrozole): is a clinical benefit still achievable? (nih.gov)
- The enzyme aromatase converts that hormone into estrogen. (lbbc.org)
- Aromatase inhibitors interfere with the enzyme aromatase to decrease the female hormones in your body. (lbbc.org)
- Aromatase inhibitors block the enzyme aromatase, which converts androgen hormone into small quantities of estrogen in the body. (newhealthguide.org)
- instead they work by inhibiting a key enzyme aromatase, which converts other hormones into estrogen. (newhealthguide.org)
- Aromatase inhibitors work by blocking the enzyme aromatase, which turns the hormone androgen into small amounts of estrogen in the body. (gradepharma.com)
- Aromatase inhibitors - drugs that reduce activity of the enzyme aromatase. (steroidsforsale.biz)
Benefits of aromatase inhibitors2
Treated with aromatase inhibitors1
- Evaluation of the safety of vitamin D3 supplements in women treated with aromatase inhibitors is crucial. (nih.gov)
- These symptoms, referred to as aromatase inhibitor-associated musculoskeletal symptoms (AIMSS), decrease quality of life and medication adherence. (nih.gov)
- The primary objective of this trial is to assess the efficacy of targeted individualised physiotherapeutic treatment on aromatase inhibitor-associated musculoskeletal pain. (inclinicaltrials.com)
- The aim is to compare targeted individualized physiotherapeutic treatment and medical care with medical care alone on aromatase inhibitor associated musculoskeletal pain in female breast cancer survivors. (inclinicaltrials.com)
- It is hypothesized that targeted physiotherapeutic treatment and medical care reduces musculoskeletal pain significantly in women with aromatase inhibitor associated musculoskeletal pain when compared to medical care alone. (inclinicaltrials.com)
Postmenopausal breast cancer2
- Background: Adjuvant hormone treatment of postmenopausal breast cancer is mainly based on aromatase inhibitors. (who.int)
- 4. The effect of second-line antiestrogen therapy on breast tumor growth after first-line treatment with the aromatase inhibitor letrozole: long-term studies using the intratumoral aromatase postmenopausal breast cancer model. (nih.gov)
- In affected males, the increased aromatase and subsequent conversion of androgens to estrogen are responsible for the gynecomastia and limited bone growth characteristic of aromatase excess syndrome. (medlineplus.gov)
- Aromatase cytochrome P450, the key enzyme of estrogen biosynthesis from androgens, is encoded by CYP19. (archives-ouvertes.fr)
- Aromatase is the enzyme that changes androgens (testosterone) into estrogen. (invitehealth.com)
- MEDLINE, Embase, and Cochrane CENTRAL were searched for the terms "gynecomastia", "pubertal", and "adolescent" in conjunction with medications from the Selective Estrogen Receptor Modulator (SERM), aromatase inhibitors (AI), and androgens groups in different combinations to optimize the search results. (frontiersin.org)
- In human placenta androgens derived from the maternal and fetal adrenal glands are converted into estrogens by the enzymatic action of placental aromatase. (uandes.cl)
- Aromatase content and estrogens and androgens concentrations were measured. (uandes.cl)
- We used a human lung cancer xenograph model system to analyze the effect of aromatase or estradiol on tumor growth. (nih.gov)
- In the present study, we used RT-PCR to characterize aromatase transcripts and real-time PCR to quantify the expression of the total aromatase mRNA at the different stages of the estrous cycle and from an ovariectomy and estradiol replacement model. (archives-ouvertes.fr)
- After ovariectomy, we observed an increase of aromatase mRNA levels, and this effect was completely prevented by estradiol administration. (archives-ouvertes.fr)
- To deal with increased levels of estradiol, aromatase inhibitors are used. (steroidsforsale.biz)
- Recent studies have shown that sex steroidogenesis-related mRNA and protein expressions, such as for 17β-hydroxysteroid dehydrogenase (HSD), 3β-HSD, 5α-reductase and aromatase cytochrome P-450 (P450arom) enzymes, are detected in the skeletal muscle, while testosterone, estradiol, and 5α-dihydrotestosterone (DHT) were locally synthesized in skeletal muscle from dehydroepiandrosterone (DHEA). (nih.gov)
- After menopause the ovaries no longer produce estrogen and at this point it is much more effective to block aromatase (since an aromatase inhibiting drug doesn't work well on the ovaries but efficiently blocks estrogen production by other tissues). (invitehealth.com)
- Aromatase is an enzyme which belongs to the cytochrome p450 superfamily. (apexbt.com)
- The aromatase inhibitors block estrogen synthesis and are used as therapy of estrogen receptor positive breast cancer, usually after resection and as a first line treatment or after failure of tamoxifen (another antiestrogen that acts by blocking the estrogen receptor). (nih.gov)
- That's why aromatase inhibitors work well in women after menopause. (invitehealth.com)
- Aromatase inhibitors are substances that inhibit the production of estrogen in women who have undergone menopause. (newhealthguide.org)
- In human bone cells, intracrine mechanism through aromatase activity, together with a positive regulation of aromatase activity by glucocorticoid and VD 3 , may contribute to the local production of estrogens, thus leading to protective effect against osteoporosis especially after menopause. (elsevier.com)
- Common questions at our breast cancer support group are about endocrine aromatase inhibitors, menopause, and estrogen hormone treatment. (ironwoodcrc.com)
- The orphan nuclear receptor steroidogenic factor-1 (SF-1) induces the expression of Müllerian inhibiting substance (MIS) and many steroidogenic genes, including aromatase P450 (P450arom). (northwestern.edu)
- Interestingly, DEX and 1α,25- dihydroxyvitamin D 3 (VD 3 ) synergistically enhanced aromatase activity as well as P450arom mRNA expression. (elsevier.com)
- When Do Symptoms of Aromatase excess syndrome Begin? (nih.gov)
- Aromatase excess syndrome is a genetic disease, which means that it is caused by one or more genes not working correctly. (nih.gov)
- Aromatase excess syndrome is a condition characterized by elevated levels of the female sex hormone estrogen in both males and females. (medlineplus.gov)
- Males with aromatase excess syndrome experience breast enlargement (gynecomastia) in late childhood or adolescence. (medlineplus.gov)
- The ability to have children (fertility) is usually normal in both males and females with aromatase excess syndrome. (medlineplus.gov)
- Rearrangements of genetic material involving the CYP19A1 gene cause aromatase excess syndrome. (medlineplus.gov)
- Fukami M, Shozu M, Ogata T. Molecular bases and phenotypic determinants of aromatase excess syndrome. (medlineplus.gov)
- Adding aromatase inhibitors (AIs) to adjuvant treatment of postmenopausal women with hormone-receptor-positive breast cancer significantly reduces cancer recurrence. (cdc.gov)
- Conclusion: The VES-13 and the G-8 tools could be valuable predictors of the onset of toxicity associated with aromatase inhibitors in the adjuvant treatment of breast cancer in elderly patients aged ?70. (who.int)
- Immunohistochemistry studies in the rat have shown that pituitary aromatase expression is sex-dependent and varies across the estrous cycle, suggesting that estrogens might be involved in the regulation of aromatase activity and might act locally as a paracrine or autocrine factor in the pituitary. (archives-ouvertes.fr)
- The Resveratrol competed with the aromatase and also inhibited the genes that create aromatase so it affected aromatase in two ways. (invitehealth.com)
- The gene encoding human aromatase has been cloned and characterized and shown to be unusual compared to genes encoding other P450 enzymes, since there are a number of untranslated first exons that occur in aromatase transcripts in a tissue-specific fashion, due to differential splicing as a consequence of the use of tissue-specific promoters. (elsevierpure.com)
- The aromatase activity in cultured human osteoblast cells was significantly increased by dexamethasone (DEX). (elsevier.com)
- CONCLUSIONS: The extension of treatment with an adjuvant aromatase inhibitor to 10 years resulted in significantly higher rates of disease-free survival and a lower incidence of contralateral breast cancer than those with placebo, but the rate of overall survival was not higher with the aromatase inhibitor than with placebo. (arizona.edu)
- Results The protein and mRNA content of placental aromatase significantly diminished in placentae obtained from preeclamptic patients compared to controls. (uandes.cl)
- 3. Biology of aromatase inhibitors: pharmacology/endocrinology within the breast. (nih.gov)
- Abstract: DESCRIPTION (provided by applicant): This project will determine the efficacy and safety of vitamin D3 supplements for reducing side effects of treatment with aromatase inhibitors in women with breast cancer. (nih.gov)
- Anne Hudson Blaes, MD , of the University of Minnesota, discusses the association between aromatase inhibitors, endothelial function, and early heart disease (Abstract S5-07). (ascopost.com)
- Ruth O'Regan, MD , of the University of Wisconsin, discusses study findings on buparlisib plus fulvestrant in postmenopausal women with HR-positive, HER2-positive, aromatase inhibitor-treated, locally advanced or metastatic breast cancer, who progressed on or after mTOR inhibitor-based treatment (Abstract S4-07). (ascopost.com)
- The working of aromatase inhibitors is different from the working of tamoxifen and raloxifene. (newhealthguide.org)
- Numerous studies have been done to compare the effects of aromatase inhibitors and tamoxifen in the treatment of early-stage HR+ breast cancer in postmenopausal females. (newhealthguide.org)
- Aromatase inhibitors are the best form of hormonal therapy to treat early-stage, HR+ breast cancer as they have more benefits and lesser side effects in comparison to tamoxifen therapy. (newhealthguide.org)
- Giving aromatase inhibitors after 2-3 years of tamoxifen therapy is more beneficial than taking tamoxifen for 5 years. (newhealthguide.org)
- Taking aromatase inhibitors for a period of 5 years after the completion of 5 years of tamoxifen therapy reduces the risk of recurrence in comparison to taking no treatment after tamoxifen therapy. (newhealthguide.org)
- Fewer side effects are produced from taking aromatase inhibitors in comparison to taking tamoxifen, which increases the risk of stroke, blood clots and endometrial cancer. (newhealthguide.org)
- Aromatase inhibitors are also associated with causing increased heart problems, increased bone loss leading to osteoporosis and more incidences of fractures in comparison to tamoxifen. (newhealthguide.org)
- BACKGROUND: Treatment with an aromatase inhibitor for 5 years as up-front monotherapy or after tamoxifen therapy is the treatment of choice for hormone-receptor-positive early breast cancer in postmenopausal women. (arizona.edu)
- P = 0.01 by a two-sided log-rank test stratified according to nodal status, prior adjuvant chemotherapy, the interval from the last dose of aromatase-inhibitor therapy, and the duration of treatment with tamoxifen). (arizona.edu)
- Being a drug to regulate your hormones, side effects of aromatase inhibitors come along with benefits. (newhealthguide.org)
- Any of the AIs may be the first or primary hormonal therapy your doctor prescribes if you have early- stage disease because aromatase inhibitors are the standard hormonal therapy for postmenopausal women. (lbbc.org)
Production of estrogen1
- Aromatase inhibitors stop the production of estrogen in postmenopausal women. (gradepharma.com)
- Aromatase expression predicts survival in women with early-stage non small cell lung cancer. (nih.gov)
- We further examined the level of protein expression of aromatase in 422 patients with NSCLC using a high-density tissue microarray. (nih.gov)
- PGE 2 is also an important regulator of aromatase expression in adipose mesenchymal cells via cAMP and PGE 2 appears to be a major factor produced by breast rumors that stimulates estrogen biosynthesis in local mesenchymal sites. (elsevierpure.com)
- Conclusions Placental aromatase expression and functionality are diminished in pregnancies complicated by preeclampsia in comparison with healthy pregnant controls. (uandes.cl)
- For women with this tumor type, standard adjuvant (postsurgery chemotherapy and/or radiation) treatment generally includes an aromatase inhibitor (AI) to reduce the chances for cancer recurrence (4,5). (cdc.gov)
- All three aromatase inhibitors are given to postmenopausal women with hormone receptor-positive breast cancer. (lbbc.org)
- If you have metastatic breast cancer, you may receive any of the three aromatase inhibitors as a first treatment after your stage IV diagnosis . (lbbc.org)
- The aromatase inhibitors (AI) have become a critical component of adjuvant therapy for breast cancer, but they cause bone pain, joint pain, joint stiffness, and muscle weakness in approximately 40% of patients. (nih.gov)
- Within this population, the prognostic value of aromatase was greatest in earlier stage lung cancer (stage I/II). (nih.gov)
- Adding testosterone to the breast cancer cells increased the cell numbers by 50% because aromatase changed the testosterone to estrogen. (invitehealth.com)
- Aromatase inhibitors are a type of new drugs that are used in the treatment of breast cancer in some cases or to help prevent the recurrence of breast cancer post initial surgery. (newhealthguide.org)
- This trial asks a critical, previously unaddressed, question of clinical importance about management of musculoskeletal (MSK) pain secondary to aromatase inhibitor (AI) treatment of hormone receptor-positive breast cancer. (inclinicaltrials.com)
- Extending treatment with an aromatase inhibitor to 10 years may further reduce the risk of breast-cancer recurrence. (arizona.edu)
- Methods: In light of national and international oncological guidelines recommending the use of screening tests for multidimensional geriatric assessment in elderly patients aged ?70 years and eligible for active cancer treatment, we assessed whether the Vulnerable Elder Survey (VES)-13 and the Geriatric (G)-8 could be predictors of toxicity associated with aromatase inhibitors. (who.int)
- Seventy?seven consecutive patients aged ?70 diagnosed with non?metastatic hormone?responsive breast cancer and therefore eligible for adjuvant hormone therapy with aromatase inhibitors, were screened with the VES-13 and the G-8, and underwent a six-monthly clinical and instrumental follow-up in our medical oncology unit, from September 2016 to March 2019 (30 months). (who.int)
- 5. Aromatase, its inhibitors and their use in breast cancer treatment. (nih.gov)
- 6. Aromatase inhibitors for breast cancer in postmenopausal women. (nih.gov)
- 9. An overview of the use of non-steroidal aromatase inhibitors in the treatment of breast cancer. (nih.gov)
- 10. Aromatase and its inhibitors in breast cancer treatment--overview and perspective. (nih.gov)
- 12. Use of aromatase inhibitors in postmenopausal women with advanced breast cancer. (nih.gov)
- 13. New aromatase inhibitors in the treatment of advanced breast cancer. (nih.gov)
- 17. The evolving role of aromatase inhibitors in breast cancer. (nih.gov)
- 19. Aromatase inhibitors and inactivators in breast cancer. (nih.gov)
- Recent attempts to model the three-dimensional structure of aromatase have permitted a model that accounts for the reaction mechanism and predicts the location of aromatase inhibitors. (elsevierpure.com)
- Its structure shows some peculiarities: exons II to X encode the protein, while multiple alternative exons I encode unique 5'-untranslated regions of the aromatase mRNA transcripts. (archives-ouvertes.fr)
- We identified the two previously described aromatase transcripts with a specific 5'untranslated region of the brain 1f and the gonadal PII transcripts. (archives-ouvertes.fr)
- Lower levels of aromatase predicted a greater chance of survival in women 65 years and older. (nih.gov)
- In addition, for women with no history of smoking, lower aromatase levels were a strong predictor of survival. (nih.gov)
- Our findings implicate aromatase as an early-stage predictor of survival in some women with NSCLC. (nih.gov)
- We predict that women whose lung cancers have higher levels of aromatase might be good candidates for targeted treatment with aromatase inhibitors. (nih.gov)
- A rare, genetic endocrine disease characterized by increased levels of estrogen due to elevated extraglandular aromatase activity. (nih.gov)
- If you are considering therapy with aromatase inhibitors, you can ask your doctor to perform a bone densitometry to determine if you will require a bone strengthening medicine along with the aromatase inhibitor. (newhealthguide.org)
- So, if there is differing amounts of aromatization occurring at different points of this cycle, as well as saturation levels increasing at different rates and heavily aromatizing compounds being swapped in and out of the cycle, does it make sense to be using the exact same dose of Aromatase Inhibitor for the entirety of this cycle? (moreplatesmoredates.com)
- 18. Aromatase inhibitors: a dose-response effect? (nih.gov)
- The Virtual Lunch & Learn " Endocrine Aromatase Inhibitors" was recorded live on Tuesday, March 28, 2023. (ironwoodcrc.com)
- These rearrangements alter the activity of the gene and lead to an increase in aromatase production. (medlineplus.gov)
- The two most important of them is the activity of aromatase enzyme and body fat. (steroidsforsale.biz)
- Actually, in cultured human osteoblast cells, DHEA was found to convert to androstenedione by 3β-hydroxysteroid dehydrogenase (3β-HSD) activity and then androstenedione to estrone through the apparent aromatase activity. (elsevier.com)
- A little stronger induction of aromatase activity by DEX and VD 3 was observed in cultured human fibroblasts. (elsevier.com)
- The increase of the aromatase activity by DEX and VD 3 was accompanied with the increase of luciferase activity of fibroblast cells transfected with Exon 1b-promoter-luciferase construct, but not of osteoblasts transfected with the same construct, suggesting a different regulatory mechanism of aromatase by DEX and 1α,25-dihydroxyvitamin D 3 (VD 3 ) between these two cells despite the same promotor usuage. (elsevier.com)
- Aromatase content was reduced in response to low oxygen tension in the choriocarcinoma JEG-3 cell line and in rabbit placentae in response to partial ligation of uterine spiral arteries, suggesting that reduced placental aromatase activity in preeclamptic patients may be associated with chronic placental ischemia and hypoxia later in gestation. (uandes.cl)
- 14. Steroidal aromatase inhibitors in elderly patients. (nih.gov)
- How can you expect to keep your Estrogen levels in the sweet spot with a predetermined dosage of your Aromatase Inhibitor? (moreplatesmoredates.com)