Androgens
Receptors, Androgen
Cyproterone Acetate
Dihydrotestosterone
Androgen Receptor Antagonists
Testosterone
Testosterone Congeners
Metribolone
Hormone Antagonists
Androgen-Insensitivity Syndrome
Dopamine Antagonists
Excitatory Amino Acid Antagonists
Neurokinin-1 Receptor Antagonists
Histamine H2 Antagonists
Dose-Response Relationship, Drug
Prostate
Interleukin 1 Receptor Antagonist Protein
Rats, Sprague-Dawley
Muscarinic Antagonists
GABA Antagonists
Histamine H1 Antagonists
Purinergic P1 Receptor Antagonists
Androstenedione
Histamine Antagonists
Nicotinic Antagonists
Neoplasms, Hormone-Dependent
Adenosine A2 Receptor Antagonists
Adrenergic alpha-1 Receptor Antagonists
Purinergic P2 Receptor Antagonists
Nandrolone
Androstane-3,17-diol
Dehydroepiandrosterone
Serotonin 5-HT3 Receptor Antagonists
Serotonin 5-HT2 Receptor Antagonists
3-Oxo-5-alpha-Steroid 4-Dehydrogenase
Rats, Wistar
Adenosine A1 Receptor Antagonists
Leukotriene Antagonists
Angiotensin Receptor Antagonists
Estradiol
Signal Transduction
RNA, Messenger
Binding, Competitive
Adrenergic alpha-2 Receptor Antagonists
Gonadotropin-Releasing Hormone
Adrenergic Antagonists
GABA-A Receptor Antagonists
Nitriles
Testis
Adrenergic alpha-Antagonists
Cells, Cultured
Estrogen Antagonists
Radioligand Assay
Histamine H3 Antagonists
Ligands
Steroid 17-alpha-Hydroxylase
Dehydroepiandrosterone Sulfate
Aromatase
Receptors, Serotonin
Estrogens
Receptors, Endothelin
Cholestenone 5 alpha-Reductase
Adrenergic beta-2 Receptor Antagonists
Receptors, N-Methyl-D-Aspartate
The effects of androgens and antiandrogens on hormone-responsive human breast cancer in long-term tissue culture. (1/1203)
We have examined five human breast cancer cell lines in continuous tissue culture for androgen responsiveness. One of these cell lines shows a 2- to 4-fold stimulation of thymidine incorporation into DNA, apparent as early as 10 hr following androgen addition to cells incubated in serum-free medium. This stimulation is accompanied by an acceleration in cell replication. Antiandrogens [cyproterone acetate (6-chloro-17alpha-acetate-1,2alpha-methylene-4,6-pregnadiene-3,20-dione) and R2956 (17beta-hydroxy-2,2,17alpha-trimethoxyestra-4,9,11-triene-1-one)] inhibit both protein and DNA synthesis below control levels and block androgen-mediated stimulation. Prolonged incubation (greater than 72 hr) in antiandrogen is lethal. The MCF- cell line contains high-affinity receptors for androgenic steroids demonstrable by sucrose density gradients and competitive protein binding analysis. By cross-competition studies, androgen receptors are distinguishable from estrogen receptors also found in this cell line. Concentrations of steroid that saturate androgen receptor sites in vitro are about 1000 times lower than concentrations that maximally stimulate the cells. Changes in quantity and affinity of androgen binding to intact cells at 37 degrees as compared with usual binding techniques using cytosol preparation at 0 degrees do not explain this difference between dissociation of binding and effect. However, this difference can be explained by conversion of [3H]-5alpha-dihydrotestosterone to 5alpha-androstanediol and more polar metabolites at 37 degrees. An examination of incubation media, cytoplasmic extracts and crude nuclear pellets reveals probable conversion of [3H]testosterone to [3H]-5alpha-dihydrotestosterone. Our data provide compelling evidence that some human breast cancer, at least in vitro, may be androgen dependent. (+info)Pharmacokinetics of flutamide in patients with renal insufficiency. (2/1203)
AIMS: The aim of this study was to determine the pharmacokinetic parameters of flutamide, a nonsteroidal antiandrogenic compound, and its pharmacologically active metabolite, hydroxyflutamide, in renal insufficiency. Haemodialysis (HD) clearance of flutamide and hydroxyflutamide was also determined. METHODS: Pharmacokinetic parameters were assessed for flutamide and hydroxyflutamide in 26 male subjects with normal renal function (creatinine clearance by 24 h urine collection, CLcr, greater than 80 ml min(-1) 1.73 m(-2); n=6) or reduced renal function; CLcr=50-80 (n=7), 30-49 (n=3), 5-29 (n=4), and <5 ml min(-1) 1.73 m(-2)-HD (n=6), following a single, oral 250 mg flutamide dose. Subjects undergoing HD received a second 250 mg dose of flutamide 4 h prior to HD; blood and dialysate were collected during HD to determine dialysability of flutamide and hydroxyflutamide. RESULTS: Cmax, tmax, AUC, t1/2, and renal clearance of flutamide and hydroxyflutamide did not differ between groups. Less than 1% of the dose appeared in dialysate as hydroxyflutamide. No serious adverse events were observed. CONCLUSIONS: Renal function did not affect flutamide nor hydroxyflutamide disposition. HD did not alter hydroxyflutamide pharmacokinetics. Dosing adjustments for renal impairment or HD are not indicated for flutamide. (+info)Androgen-independent induction of prostate-specific antigen gene expression via cross-talk between the androgen receptor and protein kinase A signal transduction pathways. (3/1203)
Transcription of the prostate-specific antigen (PSA) gene escapes regulation by androgens in advanced prostate cancer. To determine the molecular mechanism(s) of androgen-independent regulation of the PSA gene, the possibility that the androgen receptor (AR) is activated in the absence of androgen by stimulation of protein kinase A (PKA) was investigated. Activation of PKA by forskolin resulted in elevated expression of the PSA gene in androgen-depleted LNCaP cells, an effect that was blocked by the antiandrogen, bicalutamide. Further evidence that induction of PSA gene expression was dependent on AR was obtained from experiments using PC3 cells devoid of AR. Neither PSA, PB, nor ARR3 androgen-responsive reporters could be induced by activation of PKA in the absence of transfected AR. In addition, when nuclear AR from forskolin-treated LNCaP cells was incubated with oligonucleotides encoding an androgen response element of the PSA promoter and examined by electromobility shift assay, an increase in AR-androgen response element complex formation was observed. Lastly, cotransfection of an expression vector for a chimeric protein encoding the amino-terminal domain of the human AR linked to Gal4 and a 5xGal4UAS reporter gene construct resulted in activation of the amino-terminal domain of the AR by stimulation of PKA activity. These results demonstrate androgen-independent induction of PSA gene expression in prostate cancer cells by an AR-dependent pathway. (+info)Does androgen insufficiency cause lacrimal gland inflammation and aqueous tear deficiency? (4/1203)
PURPOSE: The current investigators have shown that androgen treatment suppresses inflammation and stimulates the function of lacrimal glands in mouse models of Sjogren's syndrome. Recently, others have hypothesized that androgen insufficiency induces an autoimmune process in lacrimal tissue, leading to inflammation, a Sjogren's syndrome-like pathology, and aqueous tear deficiency. The purpose of the present study was to test this hypothesis. METHODS: Lacrimal glands were obtained from adult testicular feminized (Tfm) and control mice; castrated rats, guinea pigs, and rabbits; and castrated rats without anterior or whole pituitary glands and were processed for histology and image analysis. Tear volumes were measured in mice, in patients taking antiandrogen medications, and in age-matched human control subjects. RESULTS: Tfm mice, which are completely resistant to classical androgen action, did not have increased lymphocyte infiltration in their lacrimal glands or decreased tear volumes. No inflammation was evident in lacrimal tissues of male or female rats, guinea pigs, or rabbits 12 to 31 days after castration, no inflammation existed in rat lacrimal glands 15 to 31 days after orchiectomy and pituitary removal, and no aqueous tear deficiency was apparent in patients receiving antiandrogen therapy. CONCLUSIONS: Androgen deficiency may promote the progression of Sjogren's syndrome and its associated lacrimal gland inflammation, meibomian gland dysfunction, and severe dry eye. However, androgen insufficiency alone does not cause lacrimal gland inflammation, a Sjogren's syndrome-like pathology in lacrimal tissue, or aqueous tear deficiency in nonautoimmune animals and humans. (+info)From HER2/Neu signal cascade to androgen receptor and its coactivators: a novel pathway by induction of androgen target genes through MAP kinase in prostate cancer cells. (5/1203)
Overexpression of the HER2/Neu protooncogene has been linked to the progression of breast cancer. Here we demonstrate that the growth of prostate cancer LNCaP cells can also be increased by the stable transfection of HER2/Neu. Using AG879, a HER2/Neu inhibitor, and PD98059, a MAP kinase inhibitor, as well as MAP kinase phosphatase-1 (MPK-1), in the transfection assay, we found that HER2/Neu could induce prostate-specific antigen (PSA), a marker for the progression of prostate cancer, through the MAP kinase pathway at a low androgen level. Reporter assays and mammalian two-hybrid assays further suggest this HER2/Neu-induced androgen receptor (AR) transactivation may function through the promotion of interaction between AR and AR coactivators, such as ARA70. Furthermore, we found this HER2/Neu --> MAP kinase --> AR-ARAs --> PSA pathway could not be blocked completely by hydroxyflutamide, an antiandrogen used in the treatment of prostate cancer. Together, these data provide a novel pathway from HER2/Neu to AR transactivation, and they may represent one of the reasons for the PSA re-elevation and hormone resistance during androgen ablation therapy in prostate cancer patients. (+info)Differentially expressed genes in hormone refractory prostate cancer: association with chromosomal regions involved with genetic aberrations. (6/1203)
Differential gene expression between the androgen sensitive human prostate cancer cell line LNCaP and an insensitive clonal variant, LNCaP-r, was demonstrated by suppression subtractive hybridization. Twenty-one sequences were identified of which 9 are homologous to known genes, 11 are represented by expressed sequence tags (ESTs), and 1 is novel. We present data for 5 of 7 sequences confirmed to be differentially expressed by Northern blot analysis and semiquantitative RT-PCR. Only one gene, fibronectin (FN), was highly overexpressed (>60-fold) in LNCaP-r cells, consistent with previously reported overexpression of FN in prostate cancer. Four sequences were down-regulated in LNCaP-r cells, including an inactive variant of the E2 ubiquitin conjugating enzyme (UEV-1), a novel metalloproteinase-related collagenase (PM5), and a potential tumor suppressor gene (breast basic conserved gene, BBC1). UEV-1 is multifunctional, regulates the cell cycle via cdk1, has homology to MMS2 and likewise functions as a DNA protection protein, and also has homology to TSG101. Aberrant splice variants of TSG101 occur frequently in both breast and prostate cancer, but its mechanism of action is unknown. FN, BBC1, and UEV-1 localize to regions of chromosomal aberration (2q3.4, 16q24.3, and 20q13.2, respectively) associated with advanced prostate cancer and thus may be highly relevant to disease progression. (+info)Overexpression of the cyclin-dependent kinase inhibitor p16 is associated with tumor recurrence in human prostate cancer. (7/1203)
The INK4A gene maps to the 9p21 region and was initially described [M. Serrano et al., Nature (Lond.), 366: 704-707, 1993; A. Kamb et al., Science (Washington DC), 264: 436-440, 1994] as encoding a 148-amino-acid protein termed p16. The p16 protein associates exclusively with Cdk4 and Cdk6, inhibiting their complexation with D-type cyclins and the consequent phosphorylation of pRb. This contributes to cell cycle arrest. The purpose of the present study was to evaluate patterns of p16 expression in a well-characterized cohort of prostatic adenocarcinomas while exploring potential associations between alterations of p16 and clinicopathological variables. Normal and malignant tissues from 88 patients with prostate carcinoma were examined. In situ hybridization and immunohistochemistry assays were used to determine the status of the INK4A exon 1alpha transcripts and levels of p16 protein, respectively. Associations between altered patterns of expression and clinicopathological variables, including pretreatment prostate-specific antigen (PSA) level, Gleason grade, pathological stage, and hormonal status, were evaluated using the Mantel-Haenszel chi2 test. Biochemical (PSA) relapse after surgery was evaluated using the Kaplan-Meier method and the log-rank test. Levels of p16 expression and INK4A exon 1alpha transcripts in normal prostate and benign hyperplastic tissues were undetectable. However, p16 nuclear overexpression was observed in 38 (43%) prostate carcinomas, whereas the remaining 50 (57%) cases showed undetectable p16 levels. Overexpression of p16 protein was found to correlate with increased INK4A exon 1alpha transcripts. Moreover, p16 overexpression was associated with a higher pretreatment PSA level (P = 0.018), the use of neoadjuvant androgen ablation (P = 0.001), and a sooner time to PSA relapse after radical prostatectomy (P = 0.002). These data suggest that p16 overexpression is associated with tumor recurrence and a poor clinical course in patients with prostate cancer. (+info)Selection for androgen receptor mutations in prostate cancers treated with androgen antagonist. (8/1203)
The role of androgen receptor (AR) mutations in androgen-independent prostate cancer (PCa) was determined by examining AR transcripts and genes from a large series of bone marrow metastases. Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide. In contrast, the single mutant AR found among 17 patients treated with androgen ablation monotherapy was not flutamide stimulated. Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs. These findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment. (+info)Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.
Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.
In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.
People with AIS typically have female physical characteristics, such as a lack of facial and body hair, a narrow pelvis, and underdeveloped genitalia. They may also experience infertility and heightened risk of certain medical conditions, such as gonadal dysgenesis and cardiovascular disease.
AIS is diagnosed through a combination of clinical evaluation, hormone level testing, and genetic analysis. Treatment options for the condition include hormone replacement therapy to promote masculinization and address any associated medical issues, as well as psychological support and counseling to address any gender identity or expression concerns.
It is important to note that AIS is a rare condition, and its prevalence is estimated to be around 1 in 10,000 to 1 in 20,000 male births. However, the condition is often misdiagnosed or undiagnosed, and some individuals may not receive an accurate diagnosis until later in life.
Overall, Androgen Insensitivity Syndrome is a complex and rare genetic disorder that can have significant implications for the physical and psychological well-being of affected individuals. It is important to provide appropriate medical care and support to those with AIS to help them live healthy and fulfilling lives.
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.
Clascoterone
11α-Hydroxyprogesterone
Side effects of cyproterone acetate
Benorterone
RU-22930
RU-59063
Nonsteroidal antiandrogen
Steroidal antiandrogen
RU-57073
Flutamide
Azasteroid
AA560
Pharmacology of cyproterone acetate
Feminizing hormone therapy
Metribolone
Dienogest
Nilutamide
RU-56187
Comparison of bicalutamide with other antiandrogens
Hydroxyflutamide
Bicalutamide
Cyproterone acetate
Delanterone
Seborrhoeic dermatitis
Ethyltestosterone
Rosterolone
Enzalutamide
BOMT
Apalutamide
EM-5854
7α-Thioprogesterone
Benperidol
Cushing's syndrome
Glucocorticoid receptor
Prostate cancer
Progesterone synthesis inhibitor
Index of biochemistry articles
Nuclear receptor
Effects of hormones on sexual motivation
Drugs and sexual desire
LG-120907
Estrogen receptor beta
Ozarelix
Agonistic behaviour
Cruciferous vegetables
Benzhydrocodone
Mexrenone
Gonadotropin-releasing hormone agonist
Metformin
Pharmacology of bicalutamide
Eplerenone
Fossa (animal)
Estrone
Steroid hormone
Valproate
Dichlorodiphenyldichloroethylene
Estrogen-dependent condition
Δ4-Abiraterone
Androgen Receptor Antagonists
Integrative epigenetic taxonomy of primary prostate cancer | Nature Communications
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DeCS
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Receptor11
- The Androgen Receptor (AR) is the key-driving transcription factor in prostate cancer, tightly controlled by epigenetic regulation. (nature.com)
- Darolutamide is a structurally unique androgen-receptor antagonist that is under development for the treatment of prostate cancer. (urotoday.com)
- The FDA recently announced approval of the novel nonsteroidal androgen receptor (AR) antagonist for the treatment of this patient population. (urologytimes.com)
- The UCLA team of chemists and biologists then used preclinical models to identify novel androgen receptor antagonists that blocked the growth of tumors, and it was these studies led to the clinical development of enzalutamide. (uclahealth.org)
- Vinclozolin (Vin CAS 50471-44-8), a dicarboximide fungicide, has been reported be an antagonist of androgen receptor binding in rats, effects that could result in decreased fertility, defects in reproductive organs or cancer. (cdc.gov)
- Darolutamide is a nonsteroidal androgen receptor antagonist for the treatment of nonmetastatic castrate-resistant prostate cancer (nmCRPC). (affygility.com)
- This condition occurs in the majority of patients with advanced prostate cancer who have been treated with androgen receptor antagonists. (affygility.com)
- Furthermore, NPM1 binds to androgen receptor (AR) and modulate its activity. (oncotarget.com)
- We showed that phosphorylated forms of NPM1 interact with androgen receptor (AR) in nucleoplasm. (oncotarget.com)
- Propecia is not approved for use as an androgen-receptor antagonist or as a 5-a reductase inhibitor. (bountybooks.net)
- Today we'll be discussing mineralocorticoid receptor antagonists (MRAs) for diabetic kidney disease. (medscape.com)
RECEPTORS2
- Compounds that bind to and inhibit the activation of ANDROGEN RECEPTORS. (lookfordiagnosis.com)
- Anti-androgens preferentially block the appropriate receptors, competing for binding sites on the cell's surface, effectively inhibiting the androgens' pathway. (susans.org)
Deprivation3
- All patients continued on androgen deprivation therapy. (urologytimes.com)
- Androgen deprivation therapy can increase the risks for diabetes and heart disease. (medlineplus.gov)
- abstract = "Purpose: We determined the testosterone castration level with clinical relevance in patients with prostate cancer on continuous androgen deprivation therapy. (uab.cat)
Insensitivity Syndrome1
- When the tissues do not respond normally to androgens, this is known as Androgen Insensitivity Syndrome . (susans.org)
Enzalutamide2
- Recently, two AR antagonists, namely apalutamide [Erleada] and enzalutamide [XTANDI], demonstrated improvements in metastasis-free survival (MFS) in men with nmCRPC. (urologytimes.com)
- Jung and Drs. Charles Sawyers and Howard Scher of the Memorial Sloan Kettering Cancer Center are being recognized for their groundbreaking work in the discovery and development of the anti-androgen drug enzalutamide (Xtandi). (uclahealth.org)
Prostate cancer8
- Androgens cause prostate cancer cells to grow. (medlineplus.gov)
- Hormone therapy for prostate cancer lowers the effect level of androgens in the body. (medlineplus.gov)
- Some drugs that work by blocking the effect of androgen on prostate cancer cells. (medlineplus.gov)
- Some prostate cancer cells can also make androgens. (medlineplus.gov)
- Anti-androgens are often indicated to treat severe male sexual disorders, such as hypersexuality, (excessive sexual desire) "sexual deviation", and in hormonal therapy in prostate cancer, where there is a direct link between testosterone and the spread of cancer. (susans.org)
- Materials and Methods: Serum testosterone was determined 3 times (in 6 months) in 73 patients with nonmetastatic prostate cancer treated with medical castration, 28 (38.4%) of whom also received bicalutamide (maximal androgen blockade). (uab.cat)
- Maximal androgen blockade might benefit medically castrated cases of prostate cancer with breakthrough increases of more than 50 ng/dl. (uab.cat)
- A clinical trial is being conducted to see the benefit of a known lipid-lowering drug such as pitavastatin in patients with advanced prostate cancer who are being treated with the new anti-androgens. (who.int)
Luteinizing hormone1
- They are called luteinizing hormone-releasing hormone (LH-RH) analogs (injections) and anti-androgens (oral tablets). (medlineplus.gov)
Castration3
- In the initial studies, Sawyers determined that androgen overexpression was responsible for fueling the growth and survival of castration-resistant prostate cancers. (uclahealth.org)
- Surgery to remove the testicles (castration) stops the production of most androgens in the body. (medlineplus.gov)
- During a mean followup of 51 months (range 12 to 240) 41 (67.1%) events of androgen independent progression were identified, and correlated with breakthrough testosterone increases of 50 ng/dl (classic level) and 20 ng/dl (surgical castration level). (uab.cat)
Compounds2
- Compounds which inhibit or antagonize the biosynthesis or actions of androgens. (bvsalud.org)
- An anti-androgen , (or androgen antagonist ) is any of a group of hormone antagonist compounds that are capable of preventing or inhibiting the biological effects of androgens , ( male sex hormones ) on normally responsive tissues in the body, which maintain male secondary sex characteristics . (susans.org)
Testosterone7
- Testosterone is one main type of androgen. (medlineplus.gov)
- Secondary objectives were to analyze the role of associated bicalutamide in breakthrough increases of serum testosterone in these patients and the possible benefit of maximal androgen blockade. (uab.cat)
- The lowest testosterone level with a significant impact on survival free of androgen independent progression was 32 ng/dl. (uab.cat)
- Patients on maximal androgen blockade had an incidence of testosterone increase similar to those receiving monotherapy. (uab.cat)
- sous la marque Anavar,, https://individuelprox.com/achater-du-sustanon-en-europe-booster-de-testosterone-musculation-avis/ . (mediatimenews.com)
- As you likely already know, testosterone is the primary sex hormone in males, but healthy females also produce only small amounts of this androgen. (atplab.com)
- Believe it or not, in male and females, the main starting materials for estrogen production are androgens (testosterone and adrostenedione). (atplab.com)
Darolutamide1
- The [current] results show that darolutamide significantly improves MFS, has a very favorable safety profile with apparently no side effects associated with other AR antagonists, and delays worsening of pain and disease-related symptoms compared with placebo. (urologytimes.com)
Hormones1
- Androgens are male sex hormones. (medlineplus.gov)
Drugs3
- The most common treatment is to take drugs that lower the amount of androgens made by the testicles. (medlineplus.gov)
- These drugs lower androgen levels just as well as surgery does. (medlineplus.gov)
- Three drugs help to stop the body from making androgens from tissue other than the testicles. (medlineplus.gov)
Survival2
- However, maximal androgen blockade provided a significantly longer survival free of androgen independent progression in those with breakthrough increases greater than 50 ng/dl. (uab.cat)
- Breakthrough increases greater than this threshold predicted a lower survival free of androgen independent progression. (uab.cat)
Pills1
- In women, oral contraception pills for preventing pregnancy can be used to counteract androgen hormone activity to treat female pattern hair loss. (thinninghair.com)
Development1
- In the instance that puberty has either just started or is in progress, a strong anti-androgen will either reduce, or in some cases, stop the further development of secondary sex characteristics. (susans.org)
Effects2
- They reduce androgen levels more quickly and have fewer side effects. (medlineplus.gov)
- Androgens have effects all over the body. (medlineplus.gov)
Lower1
- They are often used when medicines to lower androgen levels are no longer working as well. (medlineplus.gov)
Levels1
- This means that cancer only needs low levels of androgen to grow. (medlineplus.gov)
Activity1
- An anti-androgen will also result in reduced activity or function of the accessory male sex organs , and hyposexuality (diminished sexual desire or libido). (susans.org)
Function1
- Through modification via aromatase enzymes (more on this later), androgens are converted to estrogen, which is an essential healthy step for glucose control, cardiovascular health, immunity, bone health, fertility, sexual health, and neural function in males and females. (atplab.com)
Cancer1
- LH-RH antagonists are used in men with advanced cancer. (medlineplus.gov)
Body1
- Androgens can be produced in other areas of the body, such as the adrenal glands. (medlineplus.gov)
Targeting the androgen signall1
- 18. Enzalutamide: targeting the androgen signalling pathway in metastatic castration-resistant prostate cancer. (nih.gov)
Therapies3
- October 24, 2008 - In a phase 1/2 study of a novel androgen-receptor antagonist in advanced prostate cancer patients who have failed standard hormonal therapies and have very poor prognoses, 42% of patients have remained on treatment 24 weeks or more. (medscape.com)
- 11. Investigational therapies targeting the androgen signaling axis and the androgen receptor and in prostate cancer - recent developments and future directions. (nih.gov)
- 16. Discovery of ODM-201, a new-generation androgen receptor inhibitor targeting resistance mechanisms to androgen signaling-directed prostate cancer therapies. (nih.gov)
Prostate21
- Among the other agents is CB7630 from Cougar Biotechnology, which shuts off the adrenal gland and stimulates the production of androgen, and thus cancer-cell proliferation, in prostate cancer. (medscape.com)
- For patients with advanced/metastatic prostate cancer, hormones are used to block the production of androgen. (medscape.com)
- Liver Disease in Men Undergoing Androgen Deprivation Therapy for Prostate Cancer. (nih.gov)
- 1. New approaches to targeting the androgen receptor pathway in prostate cancer. (nih.gov)
- 2. Moving Towards Precision Urologic Oncology: Targeting Enzalutamide-resistant Prostate Cancer and Mutated Forms of the Androgen Receptor Using the Novel Inhibitor Darolutamide (ODM-201). (nih.gov)
- 3. A New Old Target: Androgen Receptor Signaling and Advanced Prostate Cancer. (nih.gov)
- 4. Targeting the androgen receptor signaling pathway in advanced prostate cancer. (nih.gov)
- 5. Androgen receptor antagonists for prostate cancer therapy. (nih.gov)
- 6. Novel drugs targeting the androgen receptor pathway in prostate cancer. (nih.gov)
- 7. Second-Generation Androgen Receptor Antagonists as Hormonal Therapeutics for Three Forms of Prostate Cancer. (nih.gov)
- 8. Androgen receptor variant-driven prostate cancer: clinical implications and therapeutic targeting. (nih.gov)
- 9. Orally Bioavailable Androgen Receptor Degrader, Potential Next-Generation Therapeutic for Enzalutamide-Resistant Prostate Cancer. (nih.gov)
- 10. Androgen receptor-dependent and -independent mechanisms driving prostate cancer progression: Opportunities for therapeutic targeting from multiple angles. (nih.gov)
- 13. Interference with the androgen receptor protein stability in therapy-resistant prostate cancer. (nih.gov)
- 14. An Overview of Next-Generation Androgen Receptor-Targeted Therapeutics in Development for the Treatment of Prostate Cancer. (nih.gov)
- 17. Targeting the androgen receptor and overcoming resistance in prostate cancer. (nih.gov)
- 20. Recent progress in the development of protein-protein interaction inhibitors targeting androgen receptor-coactivator binding in prostate cancer. (nih.gov)
- Androgens cause prostate cancer cells to grow. (medlineplus.gov)
- Hormone therapy for prostate cancer lowers the effect level of androgens in the body. (medlineplus.gov)
- Some drugs that work by blocking the effect of androgen on prostate cancer cells. (medlineplus.gov)
- Some prostate cancer cells can also make androgens. (medlineplus.gov)
Estrogens1
- These experimental findings suggest that atrazine-induced gonadal malformations result from the depletion of androgens and production of estrogens, perhaps subsequent to the induction of aromatase by atrazine, a mechanism established in fish, amphibians, reptiles, and mammals (rodents and humans). (nih.gov)
Receptors2
- Clascoterone cream targets androgen receptors in the skin to reduce cutaneous 5-alpha dihydrotestosterone. (medscape.com)
- Antiandrogens bind to androgen receptors and competitively inhibit their interaction with testosterone and dihydrotestosterone. (medscape.com)
Hormone2
- Patients may not have had therapy modulating testosterone levels (such as luteinizing-hormone, releasing-hormone agonists/antagonists and antiandrogens) within 6 months prior to randomization. (nih.gov)
- They are called luteinizing hormone-releasing hormone (LH-RH) analogs (injections) and anti-androgens (oral tablets). (medlineplus.gov)
Therapy1
- MDV3100 is a once-a-day oral therapy and is a novel small-molecule androgen-receptor antagonist that inhibits androgen-receptor function. (medscape.com)
20201
- A first-in-class topical selective androgen receptor inhibitor, clascoterone 1% topical cream, was approved by the FDA in August 2020. (medscape.com)
Adrenal1
- Androgens can be produced in other areas of the body, such as the adrenal glands. (medlineplus.gov)
Hormones1
- Androgens are male sex hormones. (medlineplus.gov)
Effects3
- They reduce androgen levels more quickly and have fewer side effects. (medlineplus.gov)
- Androgens have effects all over the body. (medlineplus.gov)
- Vinclozolin (Vin CAS 50471-44-8), a dicarboximide fungicide, has been reported be an antagonist of androgen receptor binding in rats, effects that could result in decreased fertility, defects in reproductive organs or cancer. (cdc.gov)
Growth1
- It depletes androgens in adult frogs and reduces androgen-dependent growth of the larynx in developing male larvae. (nih.gov)
Drugs2
- The most common treatment is to take drugs that lower the amount of androgens made by the testicles. (medlineplus.gov)
- Three drugs help to stop the body from making androgens from tissue other than the testicles. (medlineplus.gov)
Class1
- LH-RH antagonists are another class of treatments, including degarelix (Firmagon) and relugolix (Orgovyx). (medlineplus.gov)
Data1
- Performance data from applying the ToxCast/Tox 21 androgen receptor model, based on 11 high throughput assays, to 39 reference chemicals. (nih.gov)