Generic Casodex is a high-quality medication which is taken in treatment of prostate cancer. Generic Casodex acts by killing the cancer cells growth.
Other names for this medication:
Also known as: Bicalutamide.
Generic Casodex is a perfect remedy in struggle against prostate cancer.
Generic Casodex acts by killing the cancer cells growth.
Casodex is also known as Bicalutamide, Cosudex, Calutide, Kalumid, Bicalox.
Generic name of Generic Casodex is Bicalutamide.
Brand name of Generic Casodex is Casodex.
Take Generic Casodex tablets orally with or without food.
Take Generic Casodex at the same time every day with water.
Do not crush or chew it.
This medicine is only for men.
If you want to achieve most effective results do not stop taking Generic Casodex suddenly.
If you overdose Generic Casodex and you don't feel good you should visit your doctor or health care provider immediately.
Store between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.
The most common side effects associated with Casodex are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Casodex if you are allergic to Generic Casodex components.
Use contraception and avoid vaccinations.
Try to be careful using Generic Casodex if you take warfarin (Coumadin), aspirin-substitute products, aspirin.
Be very careful with Generic Casodex if you suffer from or have a history of liver disease.
Do not stop taking Generic Casodex suddenly.
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A 58-year-old man, without any personal or familial risk factors for prostate cancer, visited his primary care physician for a first routine prostate cancer screening with a serum PSA test.
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The majority of available antiandrogens have been reported to possess agonist activity to induce prostate-specific antigen, which might result in antiandrogen withdrawal syndrome. Here we report the identification of 3 beta-acetoxyandrost-1,5-diene-17-ethylene ketal (ADEK) from dehydroepiandrosterone metabolites and derivatives as a potent antiandrogen. We found ADEK could interrupt androgen binding to the androgen receptor (AR) and suppress androgen-induced transactivations of WT AR and a mutant AR in prostate cancer cells. ADEK inhibited prostate-specific antigen expression as well as growth in LNCaP prostate cancer cells stimulated by androgen. Importantly, ADEK had only marginal agonist effects, as compared with commonly used antiandrogens such as hydroxyflutamide and bicalutamide, leading to a lower possibility of inducing withdrawal response. Moreover, ADEK could block an adrenal androgen androstenediol-induced AR transactivation that hydroxyflutamide and bicalutamide failed to block. These unique antiandrogenic activities make ADEK a potential therapeutic compound that might be able to inhibit AR-mediated prostate cancer progression. Further in vivo studies might facilitate the development of a better antiandrogen for the treatment of prostate cancer.
Testicular macrophages increase in concentration during postnatal development in rats. This process may be under hormonal control since administration of hCG stimulates a similar increase to occur precociously. The purpose of the present studies was to determine how the macrophage population is regulated during normal postnatal development and in response to exogenous hCG. We first determined that testicular macrophages proliferate in situ during development and that hCG administration results in an increase in proliferation when given to 10-day-old rats. We next evaluated whether hCG might exert its effects through enhanced secretion of testosterone from Leydig cells. We found that testosterone could not induce a precocious increment in the macrophage concentration when it was administered to newborn pups for 10 days. Finally, the normal increase in macrophage concentration that occurs prior to puberty could not be blocked by treatment with the antiandrogen Casodex. The results are consistent with the hypothesis that the macrophage population expands by proliferation, perhaps under gonadotropin control. In addition, neither the precocial expansion that occurs in response to hCG nor the normal expansion that occurs before puberty is mediated by testosterone.
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Combination treatment of carbidopa plus bicalutamide significantly inhibited cell viability in both cell lines and induced apoptosis. The combination treatment also decreased androgen-induced PSA transactivation by 62.6% in LNCaP cells and by 55.6% in C4-2 cells compared to control, while bicalutamide monotherapy reduced PSA levels by 27.5% and 29.1% in LNCaP and C4-2 cells. In vivo, bicalutamide monotherapy delayed LNCaP CRPC tumor growth rate by 72.2%, while combination treatment reduced tumor growth by 84.4% compared to control. Serum PSA was also reduced 70.6% with bicalutamide monotherapy, while combination therapy reduced PSA levels by 76.7% compared to control.
The progression of prostate cancer to castration-resistant prostate cancer (CRPC) is often a result of somatic alterations in the PI3K/Akt/mTOR (mammalian target of rapamycin) pathway, suggesting that therapies targeting this pathway might lead to improved survival and efficacy. Here, we systematically evaluate the results of clinical trials investigating mTOR inhibition in CRPC and utilize preclinical data to predict clinical outcomes.
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AQP9 mRNA and protein were expressed in the rat prostate. Surgical castration or bicalutamide treatment significantly decreased their expression. In addition, the treatment with testosterone propionate after castration restored the expression to the level of the controls. An RNAi experiment in PNT2 also decreased the expression.
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beta-Catenin is a multifunctional molecule with important roles in intercellular adhesion and signal transduction. We reported previously that beta-catenin is mutated in human prostate cancer. In this study, we investigated the role of beta-catenin mutations on androgen receptor (AR) signaling. beta-Catenin significantly enhanced androgen-stimulated transcriptional activation by the AR. beta-Catenin also increased AR transcriptional activation by androstenedione and estradiol and diminished the antagonism of bicalutamide. Coimmunoprecipitation of beta-catenin with AR from LNCaP prostate cancer cells showed that the two molecules are present in the same complex. The amount of beta-catenin in complex with AR was increased by androgen. These findings implicate beta-catenin in the regulation of AR function and support a role for beta-catenin mutations in the pathogenesis of prostate cancer.
Castration therapy adjuvant to radiotherapy can significantly improve overall survival compared with radiotherapy alone in patients with locally advanced prostate cancer. Although many of the adverse effects of castration therapy are manageable, they can have a detrimental effect on quality of life. Here we evaluate the efficacy and tolerability of the non-castration-based therapy bicalutamide ('Casodex') 150 mg adjuvant to radiotherapy in patients with T1-4, M0, any n prostate cancer.
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Casodex is an orally active non-steroidal antiandrogen that is highly selective for androgen receptors in animals and man. It is indicated for the non-surgical treatment of advanced prostate cancer in man. The present open controlled study in 13 Casodex-treated and 21 orchidectomy-alone (control) patients addressed the hypothesis that chronic administration of antiandrogens will result in Leydig cell hyperplasia as a result of feedback inhibition of the pituitary resulting in increased luteinising hormone (LH) stimulation of Leydig cells. Although Casodex has been shown to produce a moderate rise in circulating plasma testosterone concentration on chronic treatment in prostate cancer patients, a controlled histopathological and morphometric assessment of the testis following orchidectomy in relapsed Casodex patients showed no effect on Leydig cell populations compared with an orchidectomy alone (control) group. No evidence for induction of Leydig cell hypertrophy or hyperplasia as a result of chronic oral administration of 50 mg Casodex daily was obtained in this study.
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We recently demonstrated that glutamate receptor GRM1 was expressed at high levels in castration-resistant prostate cancer (CR-PCa) tissues and cells. Herein, we determined the relationship between GRM1 and AR, PSA, and tumor growth, remission, and recurrence in preclinical PCa models. The effect of alterations in GRM1 expression was also investigated on PCa cell growth, migration and invasion.
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At 1 year, the mean (standard deviation) change from baseline in growth rate was -1.6 (+/- 5.1) cm/year and -0.1 (+/- 1.8) SD units, and in bone maturation was -2.3 (+/- 0.5) years. The bone age/chronological age ratio was reduced from 2.1 (+/- 0.6) at baseline to 1.0 (+/- 0.4) (p = 0.00013). Steady-state trough R-bicalutamide and anastrozole concentrations were attained by Day 21 and 8, respectively. Gynecomastia (42.9%) and breast tenderness (12.5%) were the most common treatment-related adverse events.
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A multi-institutional prospective trial was performed between July 2000 and May 2003 involving high-risk prostate cancer patients without metastasis, including 21 who received 8 months of NHT before radical prostatectomy. High-risk group was defined as clinical stage > or =T2c and/or prostate-specific antigen (PSA) >20 ng/ml and/or Gleason score > or =8. PSA values were considered elevated (biochemical failure) if values of 0.1 ng/ml or greater were obtained.
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A total of 1344 genes showed more than 2-fold change in expression by ADT, including 35 downregulated and 5 upregulated HIF1 targets. Six genes were shared HIF1 and AR targets, and their downregulation was confirmed with quantitative RT-PCR. Significant suppression of the biological processes proliferation, metabolism, and stress response in androgen-deprived xenografts was found, consistent with tumor regression. Nineteen downregulated HIF1 targets were involved in those significant biological processes, most of them in metabolism. Four of these were shared AR and HIF1 targets, including genes encoding the regulatory glycolytic proteins HK2, PFKFB3, and SLC2A1. Most of the downregulated HIF1 targets were induced by hypoxia in androgen-responsive prostate cancer cell lines, confirming their role as hypoxia-responsive HIF1 targets in prostate cancer. Downregulation of HIF1 targets was consistent with the absence of HIF1α protein in xenografts and downregulation in patients by ADT (P<.001).
These studies took place at the Department of Pharmacological Sciences, University of Milan, Milan, Italy.
Muir-Torre syndrome is a genetic disease characterised by the association of sebaceous neoplasms with visceral neoplasms, mainly colorectal cancer and secondly urogenital tumours. Metastases from prostate tumours without systemic disease are rare in the brain and exceptional in the brainstem.
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We assessed whether alternative transcripts (using KLK2, KLK3 and KLK4 as models) are differentially regulated by androgens and anti-androgens as an indicator of prostate cancers as they acquire treatment resistance. Using RNAseq of LNCaP cells treated with dihydrotestosterone, bicalutamide and enzalutamide, we show that the expression of variant KLK transcripts is markedly different to other variant transcripts at those loci. We also reveal that KLK variants are also over 2-fold more highly expressed in prostate cancers compared to their corresponding normal prostate. We propose that androgens and anti-androgens can activate specific variant transcripts of critical prostate cancer genes during treatment resistance.
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Recognition of micro-RNA function and their contribution to the biology of disease has given a new insight into disease mechanisms, with these discoveries potentially improving clinical diagnostic and therapeutic options. miR-125b has been identified as an important regulator in various cancers, including prostate cancer, but the mechanism of this regulation remains incompletely understood. In these studies, the effect of castration on miR-125b serum expression was evaluated in mice, simulating androgen deprivation. Furthermore, miR-125b expression was measured by quantitative real-time polymerase chain reaction (qRT-PCR) in LNCaP prostate cancer cells treated with the antiandrogen bicalutamide. Using LNCaP cells, the effect of miR-125b modulation on apoptotic protein and NCOR2, a co-repressor of androgen receptor (AR), was examined by Western blot. A 3'-untranslated region (UTR) luciferase-binding assay was performed to confirm that miR-125b targets NCOR2. We found that surgical castration induced an initial increase in the expression of circulating miR-125b in mice, while sham surgery did not. In addition, AR blockade via bicalutamide was associated with the rapid release of miR-125b into the cell culture medium of prostate cancer cells. A previously studied target of miR-125b, a regulator in the apoptotic pathway, BAK1, could not completely account for the role of miR-125b in prostate cancer. Thus, we looked for additional targets of miR-125b and found that NCOR2, which is a repressor of AR, is a direct target of miR-125b. We found that NCOR2 protein expression was blocked by mimics of miR-125b, and a luciferase-binding assay confirmed that NCOR2 is a direct target of miR-125b. Our data provide novel evidence that miR-125b is an important regulator of the AR with specific ramification for the effectiveness of antiandrogens and other hormonal therapies in prostate cancer.
We showed that uMtCK could be easily detected in CM of LNCaP lineaged AIPC cells. Exogenous uMtCK in LNCaP cells surprisingly contributed to overproduction of ROS, activation of Akt signaling pathway and more aggressive phenotypes including androgen independence development.
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Intermittent androgen deprivation is an acceptable treatment in different stages of PC. Duration of cycle decreased progressively during therapy. Age, Gleason score and PSA are factors predicting mortality.
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Previous gene array data from our laboratory identified the retinoic acid (RA) biosynthesis enzyme aldehyde dehydrogenase 1A3 (ALDH1A3) as a putative androgen-responsive gene in human prostate cancer epithelial (LNCaP) cells. In the present study, we attempted to identify if any of the three ALDH1A/RA synthesis enzymes are androgen responsive and how this may affect retinoid-mediated effects in LNCaP cells. We demonstrated that exposure of LNCaP cells to the androgen dihydrotestosterone (DHT) results in a 4-fold increase in ALDH1A3 mRNA levels compared with the untreated control. The mRNA for two other ALDH1A family members, ALDH1A1 and ALDH1A2, were not detected and not induced by DHT in LNCaP cells. Inhibition of androgen receptor (AR) with both the antiandrogen bicalutamide and small interfering RNA for AR support that ALDH1A3 regulation by DHT is mediated by AR. Furthermore, specific inhibition of the extracellular signal-regulated kinase and Src family of kinases with PD98059 and PP1 supports that AR's regulation of ALDH1A3 occurs by the typical AR nuclear-translocation cascade. Consistent with an increase in ALDH1A3 mRNA, DHT-treated LNCaP cells showed an 8-fold increase in retinaldehyde-dependent NAD(+) reduction compared with control. Lastly, treatment of LNCaP with all-trans retinal (RAL) in the presence of DHT resulted in significant up-regulation of the RA-inducible, RA-metabolizing enzyme CYP26A1 mRNA compared with RAL treatment alone. Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism.
This case supports a previous report of the marked improvement in severity and duration of hot flashes associated with antiandrogen or GnRH analog therapy in prostate cancer. The mechanism by which gabapentin reduces hot flashes is unknown.
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