WordNet
- not in favor of (an action or proposal etc.)
- a person who is opposed (to an action or policy or practice etc.); "the antis smelled victory after a long battle"
- social insect living in organized colonies; characteristically the males and fertile queen have wings during breeding season; wingless sterile females are the workers (同)emmet, pismire
- male sex hormone that is produced in the testes and responsible for typical male sexual characteristics (同)androgenic_hormone
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- 《話》(特定の慣習・政策・行動などに)反対する人
- 『アリ』
- =ain't
- アンドロゲン(男性ホルモン)
- (次にくる語の発音が母音で始まるときに用いる) / (子音[h]で始まり第1音節に強勢のない語の場合はanを用いることがある.ただし,この場合は[h]を発音しない)
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/03/11 06:58:30」(JST)
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Antiandrogens, or androgen antagonists, first discovered in the 1960s, prevent androgens from expressing their biological effects on responsive tissues.[1] Antiandrogens alter the androgen pathway by blocking the appropriate receptors, competing for binding sites on the cell's surface, or affecting androgen production.[2] Antiandrogens can be prescribed to treat an array of diseases and disorders. In men, antiandrogens are most frequently used to treat prostate cancer.[3] In women, antiandrogens are used to decrease levels of male hormones causing symptoms of hyperandrogenism.[4] Antiandrogens present in the environment have become a topic of concern. Many industrial chemicals, pesticides and insecticides exhibit antiandrogenic effects.[5][6] Certain plant species have also been found to produce antiandrogens. Environmental antiandrogens can have harmful effects on reproductive organ development in fetuses exposed in utero as well as their offspring.[5]
Contents
- 1 Mechanism of action
- 2 Medical applications
- 2.1 Pharmaceuticals for men
- 2.1.1 Prostate cancer
- 2.2 Pharmaceuticals for women
- 2.1 Pharmaceuticals for men
- 3 Environmental exposure
- 3.1 Pesticides and insecticides
- 3.2 Industrial chemicals
- 3.3 Phytochemicals
- 4 Future research
- 5 See also
- 6 References
Mechanism of action[edit]
Antiandrogens are classified as steroidal or nonsteroidal. Steroidal antiandrogens not only counter androgens, but also affect secondary sex characteristics. Steroidal antiandrogens directly affect gene expression due to their fat-soluble nature that allows them to diffuse through the plasma membrane’s phospholipid bilayer and prevent the binding of testosterone and dihydrotestosterone (DHT) to the androgen receptor.[7] Non-steroidal antiandrogens, or "pure" antiandrogens, such as nilutamide and flutamide, counter androgens and have no steroidal effects. Antiandrogens inhibit circulating androgens by blocking androgen receptors, suppressing androgen synthesis, or acting in both those ways.[8] The most common antiandrogens are androgen receptor (AR) antagonists which act on the target cell level and competitively bind to androgen receptors.[2]
Inhibition of androgen production occurs through a unique mechanism for each antiandrogen. For example, ketoconazole not only competes with androgens such as testosterone and DHT for androgen receptor binding, but also suppresses androgen synthesis by inhibiting cytochrome P450 and 17,20-lyase, which partake in synthesizing and degrading steroids, including the precursors of testosterone. The result is a decrease in the overall testosterone production of the adrenal cortex.[9] Gonadotrophins, pituitary hormones capable of altering androgen synthesis, are also affected by antiandrogens. Antiandrogens can have suppressive effects on gonadotropin secretion by down-regulating gonadotropin-releasing hormone receptors (GnRHR) in the pituitary gland. A decreased amount of GnRHRs results in gonadotropin-releasing hormone (GnRH) not being able to bind sufficiently. GnRH is responsible for the release of the gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH stimulates the Leydig cells of the testes and the theca cells of the ovaries to produce testosterone (and indirectly estradiol). Therefore, if GnRH cannot bind, testosterone synthesis is not induced in the testes or ovaries.[10]
Medical applications[edit]
Antiandrogenic pharmaceuticals are used to treat an array of medical conditions that are dependent on the androgen pathway. Antiandrogens are often prescribed for men with prostate cancer, benign prostatic hyperplasia, hypersexuality, male contraception, and for those that are undergoing gender reassignment. For women, antiandrogens are often prescribed for severe cases of acne, amenorrhea, seborrhea, hirsutism, androgenic alopecia, hidradenitis suppurativa, and hyperandrogenism.
Pharmaceuticals for men[edit]
Antiandrogens in males can result in hyposexuality (diminished sexual desire or libido), reduced activity or function of the accessory male sex organs, and slowed or halted development or reversal of male secondary sex characteristics.[11]
Antiandrogenic drugs are often indicated to treat severe male sexual disorders, such as hypersexuality (excessive sexual desire) and sexual deviation such as paraphilia (a disorder involving intense recurrent sexual urges), since lowering male hormone levels decreases libido.[12] As a part of a program for registered sex offenders recently released from prisons, the offender is sometimes administered antiandrogen drugs to reduce the likelihood of repeat offenses by reducing sexual drive.[12] On occasion, antiandrogens are used as a male contraceptive agent.
Prostate cancer[edit]
Decreasing the body’s response to androgen can have beneficial effects in treating prostate cancer. Prostate cancer is the most commonly diagnosed form of cancer found in men.[3] Some prostate cancer cells require androgens for growth. To counteract cancer cell proliferation, antiandrogenic drugs are used for hormone therapy called androgen deprivation therapy (ADT). Some antiandrogenic drugs suppress androgen production while others inhibit androgens from binding to the cancer cells’ androgen receptors. These two classes of drugs can be prescribed separately or can be used together for a complete/combined androgen blockade (CAB). When the body is deprived of androgens, the therapy is termed castration-based therapy as the lack of androgens mimics castration. By competing with circulating androgens for binding sites on prostate cell receptors, antiandrogens promote apoptosis and inhibit prostate cancer growth.[3] Hormone therapy antiandrogen drugs can be prescribed as monotherapy or in addition to radical radiotherapy or prostatectomy.[3] Antiandrogen monotherapy generally causes fewer side effects in males although it may block androgen less effectively than combined therapies. Monotherapy is often preferred by men as it is less likely than combined therapies to diminish libido or cause tenderness of the breasts, diarrhea, and nausea.[13]
Androgen-deprivation therapy (ADT) has been shown to cause initial reduction of prostate tumors.[14] However, antiandrogenic drugs can cause prostate cancer tumors to become androgen independent. Androgen independence occurs when cells that are not reliant on androgen proliferate and spread while cells that require androgen for survival undergo apoptosis. The cells that do not require androgen become the basis of the tumors, causing reoccurring tumors a few years after the initial disappearance of the prostate cancer. Once prostate cancer becomes androgen independent, hormone therapy will most likely no longer benefit the individual and a new treatment approach will be needed.[14]
In one study, the efficacy of reducing prostate cancer cells by castration was compared to combined androgen blockade (CAB) in which castration is combined with an antiandrogenic drug. Flutamide (brand name Eulexin), nilutamide (brand names Anandron and Nilandron) and bicalutamide (brand name Casodex) are nonsteroidal, "pure" antiandrogens. Flutamide has several side effects that the newer bicalutamide does not. Used in combination with castration, nilutamide and flutamide were found to have a minimal effect on prolonging survival while bicalutamide significantly prolonged life in prostate cancer patients.[15] As a result of these conclusions, since 2007 combined androgen blockade with bicalutamide has been used as an effective, safe, and cost-efficient treatment of prostate cancer.[15]
5-alpha-reductase inhibitors such as finasteride (brand names Proscar and Propecia), dutasteride (brand name Avodart), bexlosteride, izonsteride, turosteride, and epristeride are antiandrogenic as they prevent the conversion of testosterone to dihydrotestosterone (DHT).[16] DHT is 3-5 times more potent than testosterone or other androgens (except in skeletal muscle tissue, where testosterone is the main androgen). They are unique because they do not counteract the effects or production of other androgens other than DHT. Dihydrotestosterone is necessary for development of both external male sex organs and the prostate. 5α-reductase inhibitors are most often used to treat benign prostatic hyperplasia since the resulting decrease in dihydrotestosterone inhibits proliferation of prostate cells.[16]
Pharmaceuticals for women[edit]
Hyperandrogenism is a condition found in women where ovaries overproduce androgens, which are typically considered male hormones as they are important for the development of male reproductive organs and secondary male characteristics.[4] Antiandrogenic drugs can help to counteract male hormones that cause skin and hair problems in women. Gonadotrophin, a pituitary hormone, is involved in ovarial androgen production and its suppression can result in reduced testosterone production. Antiandrogens can inhibit the release of the gonadotropic hormone, luteinizing hormone (LH), suppressing testosterone synthesis in the ovaries.[10] Androgenic alopecia (a type of hair loss and pattern baldness), acne vulgaris, seborrhea, amenorrhea (absence of menstrual periods), hirsutism (excessive facial and bodily hair in women), and hidradenitis suppurativa can all be caused by an excess of male hormones.[17]
Hormonal antiandrogen treatment is given to female patients that suffer from multiple symptoms of hyperandrogenism.[8] Acne is the most common of all the skin disorders that result from male hormones overproduction. Fewer androgens present in a female’s tissues results in a reduction of oil (sebum) production and bumps (comedone).[17] Also, antiandrogenic drugs are often combined with topical and oral pharmaceuticals to treat acne. In women that suffer from overproduction of hair due to high testosterone levels (hirsutism), antiandrogenic drugs are used to slow hair growth, lighten hair color, and thin the hair. For females with pattern hair loss (androgenic alopecia), antiandrogens can assist in reducing hair shedding and thinning.[17]
The most common antiandrogenic drugs used to treat women with hyperandrogenism are spironolactone and cyproterone acetate. Spironolactone (brand names Aldactone and Spirotone), a synthetic 17-spirolactone corticosteroid is used primarily to treat low-renin hypertension, hypokalemia, and Conn's syndrome. Cyproterone acetate (brand names Androcur, Climen, Diane 35, and Ginette 35) is a synthetic steroid, a potent antiandrogen that also possesses progestational properties. Oral contraceptives that mediate progesterone have no effect on androgens but may be combined with spironolactone and cyproterone acetate for the purpose of correcting menstrual irregularities.[17]
Also used to purposefully prevent or counteract masculinisation in the case of transsexual women undergoing sex reassignment therapy, and to prevent the symptoms associated with reduced testosterone, such as hot flashes, following castration.[11]
Environmental exposure[edit]
Exposure to antiandrogens can occur unintentionally due to natural or anthropogenic compounds in the environment. Environmental compounds affecting the endocrine system, termed endocrine disruptors, that antagonistically affect androgen receptors and androgen production can negatively affect individuals that come in contact with the compounds as well as their future generations.[5] Certain pesticides and insecticides as well as in industrial chemicals contain antiandrogenic chemicals. Some species of plants produce phytochemicals with antiandrogenic effects. Exposure to these environmental antiandrogens has resulted in adverse effects on animals that allude to human health risks.
Pesticides and insecticides[edit]
Exposure to pesticides and insecticides with antiandrogenic properties has been found to negatively affect humans and laboratory animals. Androgens are important in fetal development as well as in pubertal development. Exposure during critical periods of development can cause reproductive malformations in males while exposure after birth and before puberty can delay pubertal development.[5]
Animal studies with vinclozolin, procymidone, linuron, and the DDT metabolite dichlorodiphenyldichloroethylene (p.p’-DDE) show irregular reproductive development due to their function as androgen receptor antagonists that inhibit androgen-activated gene expression.[5][18] Even with low doses of antiandrogenic pesticides, developmental effects such as reduced anogenital distance and induction of areolas were seen in male rats.[5]
Animal studies show that deformities result in offspring exposed to antiandrogens.[5] Male mice can display malformations that resemble the reproductive organs of females as in the case of exposure to vinclozolin or proymidone. Exposure to vinclozolin or procymidone in utero feminized male offspring, as seen in abnormalities of anogenital distance, small or absent sex accessory glands, hypospadias, undescended testes, retained nipples, cleft phallus, and presence of a vaginal pouch. Male mice exposed before puberty to vinclozolin experienced delayed pubertal development visualized by delayed onset of androgen-dependent preputial separation.[5]
Ketoconazole's imidazole derivative is used as a broad-spectrum antifungal agent effective against a variety of fungal infections. Although ketoconazole is a relatively weak antiandrogen, side-effects seen as a result of exposure include serious liver damage and reduced levels of androgens from both the testicles and adrenal glands.[5]
Organophostphate insecticides such as fenitrothion can also behave as androgen receptor antagonists. Fenitrothion was found to completely inhibit dihydrotestosterone-dependent human androgen receptor activation, resulting in reduced weights of seminal vesicles and the ventral prostate. Structural similarity of fenitrothion with linuron further supports the findings of antiandrogenic activity.[18]
Industrial chemicals[edit]
Industrial chemicals with antiandrogenic effects are ubiquitous in the environment. Consumer products such as toys and cosmetics may contain phthalates or parabens, which disrupt androgen synthesis.[5][6]
Phthalates are mainly found in plastics. Fetuses that are exposed to a mixture of pthalates in utero may show signs of disrupted reproductive development.[6][19] When Di-n-butyl phthalate (DBP), diisobutyl phthalate (DiBP), benzyl butyl phthalate (BBP), Bis(2-ethylhexyl) phthalate (DEHP) and di-n-pentyl phthalate (DPP) were combined, reductions in both testosterone synthesis and gene expression of steroidogenic pathway proteins were seen. The result in male rats was undescended testes and abnormal development of reproductive tissues.[6]
Parabens are commonly found in cosmetics and pharmaceuticals. Paraben esters, such as butylparaben, have been found to mimic androgen antagonist activity. Antiandrogenic endocrine disruption has been shown in aquatic species but the mechanism is unknown. Researchers believe parabens have the ability to bind to human androgen receptors but it still remains unclear.[19]
Phytochemicals[edit]
Antiandrogenic chemicals can also occur naturally in plants.
The best known plant-derived anti-androgen is 3,3'-Diindolylmethane(DIM)[20]
Spearmint tea has antiandrogenic properties in females with hirsutism.[21][22]
Scutellaria baicalensis may also have antiandrogenic properties.[23]
The compound N-butylbenzene-sulfonamide (NBBS) isolated from Pygeum africanum is a specific androgen antagonist.[24][25]
Glycyrrhiza glabra has shown antiandrogenic activity in male rats.[26]
A herbal formula (termed KMKKT) containing Korean Angelica gigas Nakai (AGN) root and nine other oriental herbs has shown in vitro anti-androgen activity.[27]
Pygeum africanum contains an antiandrogenic compound atraric acid.[28]
Duke's database (enter 'antiandrogenic' in search field) lists several more herbs that have antiandrogenic properties.
Future research[edit]
Currently, further research is being conducted on the effects of antiandrogens. In the pharmaceutical industry, researchers continue to experiment with antiandrogenic drugs and other treatments in the hope of finding cures to diseases such as prostate cancer. Greater insight into the mechanisms and pathways of antiandrogens would provide more effective treatment that might decrease the likelihood of recurrent prostatic tumors.
The future of antiandrogenic drugs is believed to be peptide antagonists. Current androgen receptor antagonist drugs bind to the ligand binding domain on the receptors and inhibit receptor function. Androgen receptor peptide antagonists act in an alternative manner. A peptide antagonist interrupts androgen receptor protein interactions from the surface of the receptor.[29] This approach is "mechanism-based" and has greater potential for blocking receptor activity than the traditional ligand-receptor binding approach. Researchers are trying to target the ligand-binding domain and N-terminal domain of androgen receptors.[29]
See also[edit]
- Discovery and development of antiandrogens
- Androgen
- SARM
- 5α-reductase inhibitor
- Antiestrogen
- Antiprogestin
References[edit]
- ^ "Medical Dictionary: Anti-androgen".
- ^ a b Mowszowicz I (1989). "Antiandrogens. Mechanisms and paradoxical effects". Ann Endocrinol (Paris) 50 (3): 50(3):189–99. PMID 2530930.
- ^ a b c d Gillatt D (2006). "Antiandrogen treatments in locally advanced prostate cancer: are they all the same?". J Cancer Res Clin Oncol 1: S17–26. doi:10.1007/s00432-006-0133-5. PMID 16845534.
- ^ a b "Medical Dictionary: Hyperandrogenism".
- ^ a b c d e f g h i j Gray LE, Ostby J, Furr J, Wolf CJ, Lambright C, Parks L, Veeramachaneni DN, Wilson V, Price M, Hotchkiss A, Orlando E, Guillette L (2001). "Effects of environmental antiandrogens on reproductive development in experimental animals". Human Reproduction Update 2 (3): 248–64. doi:10.1093/humupd/7.3.248. PMID 11392371.
- ^ a b c d Rider CV, Furr JR, Wilson VS, Gray LE Jr (Apr 2010). "Cumulative effects of in utero administration of mixtures of reproductive toxicants that disrupt common targe tissues via diverse mechanisms of toxicity". International Journal of Andrology 33 (2): 443–62. doi:10.1111/j.1365-2605.2009.01049.x. PMC 2874988. PMID 20487044.
- ^ "Steroidal Antiandrogens". Health and Prostate. Retrieved 9 December 2011.
- ^ a b Zouboulis CC, Rabe T (March 2010). "Hormonal antiandrogens in acne treatment". Journal of the German Society of Dermatology 8 (Suppl 1): S60–74. doi:10.1111/j.1610-0387.2009.07171.x. PMID 20482693.
- ^ Witjes FJ, Debruyne FM, Fernandez del Moral P, Geboers AD (May 1989). "Ketoconazole high dose in management of hormonally pretreated patients with progressive metastatic prostate cancer. Dutch South-Eastern Urological Cooperative Group". Urology 33 (5): 411–5. doi:10.1016/0090-4295(89)90037-X. PMID 2652864.
- ^ a b "Gonadotropin". Retrieved 9 December 2011.
- ^ a b "Antiandrogen Drugs".
- ^ a b "Anti-androgens for sex offenders". Canadian Medical Association Journal 109 (4): 257. 1973. PMC 1946843. PMID 20312137.
- ^ Kolvenbag GJ, Iversen P, Newling DW (August 2001). "Antiandrogen monotherapy: a new form of treatment for patients with prostate cancer". Urology 58 (2 Suppl 1): 16–23. PMID 11502439.
- ^ a b Massard, C (June 2011). "Targeting Continued Androgen Receptor Signaling in Prostate Cancer". Clinical Cancer Research. 17(12): 3876–883.
- ^ a b Akaza H (Jan 2011). "Combined androgen blockade for prostate cancer: review of efficacy, safety, and cost-effectiveness". Cancer Science 102 (1): 51–6. doi:10.1111/j.1349-7006.2010.01774.x. PMID 21091846.
- ^ a b Flores E, Bratoeff E, Cabeza M, Ramirez E, Quiroz A, Heuze I. (May 2003). "Steroid 5alpha-reductase inhibitors". Mini-Reviews in Medicinal Chemistry 3 (3): 225–37. PMID 12570838.
- ^ a b c d Dr. Amanda Oakley. "Hormonal treatment".
- ^ a b Curtis LR (Mar 2001). "Organophosphate antagonism of the androgen receptor". Toxicological Sciences 60 (1): 1–2. PMID 11222865.
- ^ a b Darbre PD, Harvey PW (Jul 2008). "Paraben esters: review of recent studies of endocrine toxicity, absorption, esterase and human exposure, and discussion of potential human health risks". Journal of Applied Toxicology 28 (5): 561–78. doi:10.1002/jat.1358. PMID 18484575.
- ^ Plant-derived 3,3'-Diindolylmethane is a strong androgen antagonist in human prostate cancer cells.
- ^ Grant P (2010). "Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome. A randomized controlled trial". Phytotherapy Research 24 (2): 186–188.
- ^ Akdogan M. Tamer MN. Cure E. Cure MC. Koroglu BK. Delibas N (May 2007). "Effect of spearmint (Mentha spicata Labiatae) teas on androgen levels in women with hirsutism". Phytotherapy Research 21 (5): 444–7.
- ^ Bonham M, Posakony J, Coleman I, Montgomery B, Simon J, Nelson PS (2005). "Characterization of chemical constituents in Scutellaria baicalensis with antiandrogenic and growth-inhibitory activities toward prostate carcinoma". Clinical Cancer Research 11 (10): 3905–3914.
- ^ Papaioannou M, Schleich S, Roell D, Schubert U, Tanner T, Claessens F, Matusch R, Baniahmad A (December 2010). "NBBS isolated from Pygeum africanum bark exhibits androgen antagonistic activity, inhibits AR nuclear translocation and prostate cancer cell growth". Invest New Drugs 28 (6): 729–43. doi:10.1007/s10637-009-9304-y. PMID 19771394.
- ^ Schleich S, Papaioannou M, Baniahmad A, Matusch R (July 2006). "Extracts from Pygeum africanum and other ethnobotanical species with antiandrogenic activity". Planta Med. 72 (9): 807–13. doi:10.1055/s-2006-946638. PMID 16783690.
- ^ Zamansoltani F, Nassiri-Asl M, Sarookhani MR, Jahani-Hashemi H, Zangivand AA (August 2009). "Antiandrogenic activities of Glycyrrhiza glabra in male rats". Int. J. Androl. 32 (4): 417–22. doi:10.1111/j.1365-2605.2009.00944.x. PMID 19515171.
- ^ Jiang C, Lee HJ, Li GX, Guo J, Malewicz B, Zhao Y, Lee EO, Lee HJ, Lee JH, Kim MS, Kim SH, Lu J (January 2006). "Potent antiandrogen and androgen receptor activities of an Angelica gigas-containing herbal formulation: identification of decursin as a novel and active compound with implications for prevention and treatment of prostate cancer". Cancer Res. 66 (1): 453–63. doi:10.1158/0008-5472.CAN-05-1865. PMID 16397261.
- ^ Schleich S, Papaioannou M, Baniahmad A, Matusch R (May 2006). "Activity-guided isolation of an antiandrogenic compound of Pygeum africanum". Planta Med. 72 (6): 547–51. doi:10.1055/s-2006-941472. PMID 16773539.
- ^ a b Gao W (2010). "Peptide antagonist of the androgen receptor". Current Pharmaceutical Design 16 (9): 1106–113. PMID 20030610.
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UpToDate Contents
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- 1. 去勢感受性前立腺癌の初期全身療法 initial systemic therapy for castration sensitive prostate cancer
- 2. 男性型多毛症の治療 treatment of hirsutism
- 3. 去勢抵抗性前立腺癌に対する二次内分泌療法 secondary endocrine therapies for castration resistant prostate cancer
- 4. アンドロゲン除去療法による副作用 side effects of androgen deprivation therapy
- 5. 播種性前立腺癌に対する治療の概要 overview of the treatment of disseminated prostate cancer
English Journal
- Androgen Receptor Coactivators in Regulation of Growth and Differentiation in Prostate Cancer.
- Culig Z1.
- Journal of cellular physiology.J Cell Physiol.2016 Feb;231(2):270-4. doi: 10.1002/jcp.25099.
- Androgen receptor (AR) is a key factor in regulation of growth and differentiation in normal and malignant prostate. Endocrine therapies for prostate cancer include inhibition of androgen production either by analogs of luteinizing hormone releasing hormone or abiraterone acetate and/or use of anti-
- PMID 26201947
- Glucocorticoid receptor antagonism reverts docetaxel resistance in human prostate cancer.
- Kroon J1, Puhr M2, Buijs JT2, van der Horst G2, Hemmer DM2, Marijt KA2, Hwang MS2, Masood M2, Grimm S2, Storm G1, Metselaar JM2, Meijer OC2, Culig Z2, van der Pluijm G3.
- Endocrine-related cancer.Endocr Relat Cancer.2016 Jan;23(1):35-45. doi: 10.1530/ERC-15-0343. Epub 2015 Oct 19.
- Resistance to docetaxel is a major clinical problem in advanced prostate cancer (PCa). Although glucocorticoids (GCs) are frequently used in combination with docetaxel, it is unclear to what extent GCs and their receptor, the glucocorticoid receptor (GR), contribute to the chemotherapy resistance. I
- PMID 26483423
- Estrogen Receptor Agonists and Antagonists in the Yeast Estrogen Bioassay.
- Wang S1, Bovee TF2.
- Methods in molecular biology (Clifton, N.J.).Methods Mol Biol.2016;1366:337-42. doi: 10.1007/978-1-4939-3127-9_26.
- Cell-based bioassays can be used to predict the eventual biological activity of a substance on a living organism. In vitro reporter gene bioassays are based on recombinant vertebrate cell lines or yeast strains and especially the latter are easy-to-handle, cheap, and fast. Moreover, yeast cells do n
- PMID 26585147
Japanese Journal
- A Case of Androgen Receptor-positive Triple Negative Breast Cancer with Good Response to Anti-androgen Therapy
- The Showa University Journal of Medical Sciences 27(2), 131-136, 2015
- NAID 130005110365
- プロシミドンの発生毒性の種差に関する研究—薬物動態、代謝、排泄における顕著な種差—
- Journal of Pesticide Science 40(3), 111-123, 2015
- NAID 130005094228
- プロシミドンの発生毒性の種差に関する研究—薬物動態、代謝、排泄における顕著な種差—
- Journal of Pesticide Science advpub(0), 2015
- NAID 130005089411
Related Links
- Anti-androgen definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it up now! Thesaurus Translate Puzzles & Games Reference Word of the Day Blog Slideshows Apps by Log In ...
- Anti-androgen anti-antibody anti-antitoxin anti-basement membrane antibody anti-basement membrane glomerulonephritis anti-basement membrane nephritis anti-blenorrhagic anti-cancer antibiotic anti-cancer diet anti-Cellano ...
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★リンクテーブル★
| リンク元 | 「アンチアンドロゲン」 |
| 拡張検索 | 「anti-androgen therapy」 |
| 関連記事 | 「ant」「anti」 |
「アンチアンドロゲン」
- 英
- anti-androgen
- 関
- アンドロゲン
「anti-androgen therapy」
「ant」
- n.
- 同
- ants, stinging
「anti」
- comb form.