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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Androgen receptors (ARs) mediate the physiological effects of androgens in vertebrates. In fishes, AR-mediated pathways can be modulated by aquatic contaminants, resulting in the masculinisation of female fish or diminished secondary sex characteristics in males. The Murray-Darling rainbowfish (Melanotaenia fluviatilis) is a small-bodied freshwater teleost used in Australia as a test species for environmental toxicology research. We determined concentration-response profiles for selected agonists and antagonists of rainbowfish ARα and ARβ using transient transactivation assays. For both ARα and ARβ, the order of potency of natural agonists was 11-ketotestosterone (11-KT)>5α-dihydrotestosterone>testosterone>androstenedione. Methyltestosterone was a highly potent agonist of both receptors relative to 11-KT. The relative potency of the veterinary growth-promoting androgen, 17β-trenbolone, varied by more than a factor of 5 between ARα and ARβ. The non-steroidal anti-androgen bicalutamide exhibited high inhibitory potency relative to the structurally related model anti-androgen, flutamide. The inhibitory potency of the agricultural fungicide, vinclozolin, was approximately 1.7-fold relative to flutamide for ARα, but over 20-fold in the case of ARβ. Fluorescent protein tagging of ARs showed that the rainbowfish ARα subtype is constitutively localised to the nucleus, while ARβ is cytoplasmic in the absence of ligand, an observation which agrees with the reported subcellular localisation of AR subtypes from other teleost species. Collectively, these data suggest that M. fluviatilis ARα and ARβ respond differently to environmental AR modulators and that in vivo sensitivity to contaminants may depend on the tissue distribution of the AR subtypes at the time of exposure.
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The pretreatment serum HER2 level may be a useful independent prognostic factor that is associated with a high risk of biochemical recurrence in metastatic prostate cancer patients about to undergo endocrine therapy.
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In summary, we demonstrated that NCOR1 function declines with prostate cancer progression. Reduction in NCOR1 levels causes bicalutamide resistance in LNCaP cells and compromises response to bicalutamide in mouse prostate in vivo Clin Cancer Res; 22(15); 3937-49. ©2016 AACR.
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Low-dose DES and 50 mg of bicalutamide per day are equally effective in hormone refractory prostate carcinoma with respect to biochemical response, although DES has more severe adverse effects. This is a small sample and larger multicentre trials are needed to give us a definite conclusion.
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Using this criteria for the histological effects of anti-cancer treatment, the histological effect of endocrine therapy was most frequently observed in class G3b with 61.0%, and correlations with PSA nadir and initial biopsy positive number before endocrine therapy were observed. After biopsy, radical prostatectomy was performed on 9 patients (endocrine therapy was concurrently performed on 4), endocrine therapy on 67 (intermittent administration on 21), and radiation therapy on 1 (MAB was concurrently performed). Outcomes included PSA failure in 14, of whom 2 died of cancer. Three-year and 5-year PSA-failure free survival rates were 91.1% and 76.3%, respectively. Pathological disease stage in radical prostatectomy specimens was examined by dividing it into class G0-2 and class G0-3. This revealed a significant correlation between histological effect and pathological disease stage (pT2-3). PSA-failure free survival was analyzed in 67 of the 77 patients who underwent endocrine therapy. A significantly large number of PSA-failures occurred in class G0-2. Multivariate analysis revealed that the histological effect alone was the influencing factor in PSA-failure.
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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.
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Androgen receptor (AR) signaling is crucial for the genesis and progression of prostate cancer (PCa). We compared the growth responses of AR(+) LNCaP and LNCaP C4-2 vs. AR(-) DU145 and PC-3 PCa cell lines to galbanic acid (GBA) isolated from the resin of medicinal herb Ferula assafoetida and assessed their connection to AR signaling and cell cycle regulatory pathways. Our results showed that GBA preferentially suppressed AR(+) PCa cell growth than AR(-) PCa cells. GBA induced a caspase-mediated apoptosis that was attenuated by a general caspase inhibitor. Subapoptotic GBA downregulated AR protein in LNCaP cells primarily through promoting its proteasomal degradation, and inhibited AR-dependent transcription without affecting AR nuclear translocation. Whereas docking simulations predicted binding of GBA to the AR ligand binding domain with similarities and differences with the AR antagonist drug bicalutamide (Bic), LNCaP cell culture assays did not detect agonist activity of GBA. GBA and Bic exerted greater than additive inhibitory effect on cell growth when used together. Subapoptotic GBA induced G(1) arrest associated with an inhibition of cyclin/CDK4/6 pathway, especially cyclin D(1) without the causal involvement of cyclin-dependent kinase (CDK) inhibitory proteins P21(Cip1) and P27(Kip1) . In summary, the novelty of GBA as an anti-AR compound resides in the distinction between GBA and Bic with respect to AR protein turnover and a lack of agonist effect. Our observations of anti-AR and cell cycle arrest actions plus the anti-angiogenesis effect reported elsewhere suggest GBA as a multitargeting drug candidate for the prevention and therapy of PCa.
Radiotherapy combined with hormones improved local tumor control in comparison with endocrine therapy alone. Residual prostate cancer was significantly associated with serum prostate-specific antigen recurrence, local tumor progression, clinical recurrence, and cancer-specific death in univariable analysis. Residual cancer was predictive of prostate-specific antigen recurrence in multivariable analysis.
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A 69-year-old male with tinnitus, vertigo, and progressive hearing loss of left ear was admitted to our hospital. Head magnetic resonance imaging and computed tomography (CT) revealed swelling of multiple neck lymph nodes (LNs) invading the skull base, which involved left mastoid sinus/the eighth cranial nerve. Biopsy of the cervical LN demonstrated small-cell carcinoma (SCC). Whole body CT showed systemic lymphadenopathies (subclavian, para-aortic, and bilateral iliac LNs) and prostatic swelling with multiple pelvic masses. Needle biopsy of the prostate revealed SCC (Gleason score: 5+ 5). Immunohistochemically, neuron-specific enolase (NSE) and NCAM were detected in <10% and -100% of cancer cells, respectively. Despite SCC histology, prostate-specific antigen (PSA) and androgen receptor (AR) were also expressed in -20% and -70% of tumor cells, respectively. Serum PSA and NSE were 464 ng/ml and 12 ng/ml, respectively. After maximum androgen blockade (MAB) with leuprorelin/bicalutamide, the patient showed recovery of hearing loss, regression of cervical LNs (partial response), and decline of serum markers (PSA 7.38 ng/ml and NSE 3.7 ng/ml, respectively). As re-increase of PSA was observed after ten months, MAB menu was changed to leuprorelin/fultamide. Another four months later, the treatment was changed to docetaxel/ estramustine due to the appearance of systemic bone pain and recurrence of LN metastases. He is alive (39 months after diagnosis) with cancer. Widespread metastases at the time of diagnosis were compatible with SCC. However, this case was AR-positive and responded to androgen ablation, at least temporarily. Even though the initial symptoms are atypical for a prostatic carcinoma, SCC of prostate needs to be included as a rare differential diagnosis.
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Sexual disruption in wild fish has been linked to the contamination of river systems with steroid oestrogens, including the pharmaceutical 17α-ethinylestradiol, originating from domestic wastewaters. As analytical chemistry has advanced, more compounds derived from the human use of pharmaceuticals have been identified in the environment and questions have arisen as to whether these additional pharmaceuticals may also impact sexual disruption in fish. Indeed, pharmaceutical anti-androgens have been shown to induce such effects under laboratory conditions. These are of particular interest since anti-androgenic biological activity has been identified in the aquatic environment and is potentially implicated in sexual disruption alone and in combination with steroid oestrogens. Consequently, predictive modelling was employed to determine the concentrations of two anti-androgenic human pharmaceuticals, bicalutamide and cyproterone acetate, in UK sewage effluents and river catchments and their combined impacts on sexual disruption were then assessed in two fish models. Crucially, fish were also exposed to the anti-androgens in combination with steroid oestrogens to determine whether they had any additional impact on oestrogen induced feminisation. Modelling predicted that the anti-androgenic pharmaceuticals were likely to be widespread in UK river catchments. However, their concentrations were not sufficient to induce significant responses in plasma vitellogenin concentrations, secondary sexual characteristics or gross indices in male fathead minnow or intersex in Japanese medaka alone or in combination with steroid oestrogens. However, environmentally relevant mixtures of oestrone, 17β-oestradiol and 17α-ethinylestradiol did induce vitellogenin and intersex, supporting their role in sexual disruption in wild fish populations. Unexpectedly, a male dominated sex ratio (100% in controls) was induced in medaka and the potential cause and implications are briefly discussed, highlighting the potential of non-chemical modes of action on this endpoint.
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Triple negative breast cancer (TNBC) is a heterogeneous collection of biologically diverse cancers, which contributes to variable clinical outcomes. Previously, we identified a TNBC subtype that has a luminal phenotype and expresses the androgen receptor (AR+). TNBC cells derived from these luminal AR + tumors have high frequency phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutations. The purpose of this study was to determine if targeting phosphoinositide 3-kinase (PI3K) alone or in combination with an AR antagonist is effective in AR + TNBC.
A patient affected by metastatic prostatic carcinoma and hypogonadotropic hypogonadism (HH) was treated with flutamide 750 mg/day plus an LH-RH analog. After confirmation of basal castration during treatment, he continued with antiandrogens alone. Following the normalization of gonadic function and subjective mild bone flare-up, the patient resumed the initial treatment and obtained a partial response. When flutamide was interrupted because of liver toxicity, the patient showed progressive disease in the bone, which was unresponsive to both flutamide resumption and salvage hormone therapy (bicalutamide). The patient is currently receiving chemotherapy with VP16 and estramustine phosphate and is showing both serologic (PSA) and symptomatic response. The interest of this case lies in the incidental detection of HH during therapy and in the responsiveness to treatment.
Androgen receptor (AR) plays a critical role in bladder cancer (BCa) development. Our early studies found AR knock-out mice (with few androgens and deleted AR) failed to develop BCa, yet 50% of castrated mice (with few androgens and existing AR) still developed BCa in an N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) carcinogen-induced BCa mouse model, suggesting the existing AR in BCa of castrated mice may still play important roles in promoting BCa development at the castration level of androgens. The mechanism underlying this and/or which factors potentiate AR function at the castration level of androgen remains unclear. Epidermal growth factor (EGF), a key player in BCa progression, has been demonstrated to be able to potentiate AR transactivation in prostate cancer. In the present study, we found that EGF could increase BCa cell growth, migration and invasion in the presence of AR under the low amount of androgen and EGF was able to potentiate AR transactivation through EGFR by activating PI3K/AKT and MAPK pathway at castration androgen level. The increased suppression effects by EGFR inhibitor of PD168393 on AR function after addition of anti-androgen, Casodex, further suggested AR might play a key role in the effects of EGF on BCa progression and metastasis. Collectively, our results indicate that EGF may be able to potentiate AR transactivation that leads to enhancing BCa progression, which may help us to develop a better therapeutic approach to treat BCa via targeting both EGF and AR signaling.
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The study included 187 patients with T1c-T3a prostate cancer unsuitable for local definitive treatment and treated with primary CAB. Clinical outcomes, predictive factors of PSA relapse and adverse events were investigated.
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This open-label, non-comparative, multicentre study included 51 patients receiving bicalutamide 150 mg for the treatment of non-metastatic prostate cancer (T1b-T4, Nx, M0). Patients who developed symptomatic gynaecomastia and/or breast pain received two 6-Gy fractions of external-beam radiation to the breasts and were then assessed at two 3-monthly follow-up visits.
Antiandrogens are defined as substances which prevent androgens from expressing their activity at target sites. Based on their chemical structures, antiandrogens are divided into steroidal and nonsteroidal antiandrogens. In addition to antiandrogenic action, steroidal antiandrogens simulate the negative feedback inhibition of the hypothalamus, resulting in lowering the concentration of plasma testosterone. On the other hand, in nonsteroidal antiandrogens, the androgenic actions are blocked in both hypothalamus and target tissues. Therefore, negative feedback signals are inhibited and production of testosterone is increased in the testis. For the endocrine therapy of prostate cancer, chlormadinone acetate, flutamide and bicalutamide are or will be available in Japan. Antiandrogen is generally used by the combination with surgical or medical castration, namely as total androgen blockade.
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Although androgen ablation therapy is the foundation of current prostate cancer treatment, most patients ultimately develop castration-resistant disease. One proposed mechanism to account for androgen receptor (AR) activity in the castrate environment is via crosstalk with other signaling pathways. Specifically, reciprocal interactions between the AKT/mTOR and AR pathways have been implicated in prostate cancer progression. Here, we used the potent inhibitor ridaforolimus to target mTOR signaling alone and in combination with AR blockade by bicalutamide to examine the effect of abrogating these signaling pathways. Ridaforolimus treatment inhibited the proliferation of all six prostate cancer cell lines examined with the greatest sensitivity associated with loss of PTEN and elevated AKT/mTOR pathway activity. Dual inhibition of the AR and mTOR signaling pathways provided further benefit with the ridaforolimus-bicalutamide combination producing synergistic antiproliferative effects in prostate cancer cells in vitro when compared with each agent alone. Pharmacodynamic analysis confirmed that combination treatment resulted in full inhibition of each of the respective pathways. Importantly, the ridaforolimus-bicalutamide combination exhibited potent antitumor activity with parallel reductions in plasma PSA levels in vivo. Taken together, ridaforolimus exhibited potent antiproliferative and antitumor activity in prostate cancer models and the addition of bicalutamide represents a potentially effective combination strategy for patient therapy.
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Androgen deprivation is the only effective systemic therapy available for patients with prostatic carcinoma, but is associated with a gradual transition to a hormone-refractory prostate cancer (HRCAP) in which ligand-independent activation of the androgen receptor has been implicated. The beta(2)-adrenergic receptor (beta(2)-AR) is a well-known activator of the androgen receptor.
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Many men who show evidence of a progression of prostate cancer by rising prostate-specific antigen (PSA) or other symptoms are treated with anti-androgens. Anti-androgen withdrawal represents the first line of treatment after failure of hormonal manipulation. Flutamide is an approved anti-androgen that has been incorporated in many of the combined androgen blockade studies. Bicalutamide is also a nonsteroidal anti-androgen that offers the advantages of reduced dosage amounts and reduction in side effects. Additionally, there are a variety of therapeutic agents that can suppress adrenal secretion of androgens. The most promising of these agents include aminoglutethamide, ketoconazole, and corticosteroids, with an expected response rate of 10% to 15%. Studies have shown that some patients may respond to an anti-estrogen such as tamoxifen. There are a variety of therapeutic treatment options available for patients with hormone refractory prostate cancer. However, quality-of-life issues are becoming increasingly important and should be incorporated into clinical trial endpoints.
Cell apoptosis was assessed by both annexin V/propidium iodide labeling and poly (ADP-ribose) polymerase cleavage assays. Gene and protein expression changes were determined by quantitative real-time PCR and western blot assays. The effect of cyproterone acetate on gene promoter activity was determined by luciferase reporter assay.
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Taxane based chemotherapy is the standard of care treatment in castration resistant prostate cancer (CRPC). There is convincing evidence that taxane therapy affects androgen receptor (AR) but the exact mechanisms have to be further elucidated. Our studies identified c-jun as a crucial key player which interacts with AR and thus determines the outcome of the taxane therapy given. Docetaxel (Doc) and paclitaxel (Pac) agents showed different effects on LNCaP and LNb4 evidenced by alteration in the protein and mRNA levels of c-jun, AR and PSA. Docetaxel-induced phophorylation of c-jun occurred before JNK phosphorylation which suggests that c-jun phosphorylation is independent of JNK pathways in prostate cancer cells. A xenograft study showed that mice treated with Pac and bicalutamide showed worse outcome supporting our hypothesis that upregulation of c-jun might act as a potent antiapoptotic factor. We observed in our in vitro studies an inverse regulation of PSA- and AR-mRNA levels in Doc treated LNb4 cells. This was also seen for kallikrein 2 (KLK 2) which followed the same pattern. Given the fact that response to taxane therapy is measured by PSA decrease we have to consider that this might not reflect the true activity of AR in CRPC patients.
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Hormones and growth factors influence the proliferation and invasiveness of human mesenchymal tumors. The highly aggressive human fibrosarcoma HT1080 cell line harbors classical androgen receptor (AR) that responds to androgens triggering cell migration in the absence of significant mitogenesis. As occurs in many human cancer cells, HT1080 cells also express epidermal growth factor receptor (EGFR).
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MRP4/ABCC4 mRNA/protein levels were higher in localized PC compared to non-cancer (P = 0.006). MRP4/ABCC4 levels were significantly decreased in PCs treated with AA compared to cancers exposed to normal testosterone levels (P < 0.0001). MRP4/ABCC4 expression in normal human tissues was limited to the prostate and the renal tubules. MRP4/ABCC4 protein levels increased in LNCaP cells after DHT which was partially blocked by bicalutamide. However, DHT did not alter the activation of the MRP4/ABCC4 promotor in luciferase reporter assays and testosterone, DHT, flutamide and hydroxy-flutamide were not substrates for MRP4/ABCC4.
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Bicalutamide is an anti-androgen that is used worldwide to treat prostate cancer (CaP). However, there are no data on blood bicalutamide concentrations in hemodialysis (HD) patients with CaP. Therefore, we investigated the plasma levels of bicalutamide during the peridialysis period in this population. The study group included 5 HD patients with CaP who had been treated with bicalutamide (80 mg/day) for at least 3 months. Blood samples were taken during and between HD sessions and the plasma concentrations of the active R enantiomer (R-bicalutamide) were assessed using an HPLC assay. The plasma R-bicalutamide levels on the non-dialysis day were measured in 2 patients (patients 1 and 2) immediately before dosing and 8 and 24 h after dosing. These levels were 18,730, 19,090 and 19,420 ng/ml (patient 1), and 4,522, 4,581, and 5,296 ng/ml (patient 2), respectively. The mean plasma levels of R-bicalutamide in all 5 subjects just before HD, and 2 and 4 h after the start of HD were 8,726, 9,354 and 10,068 ng/ml, respectively. These results show that bicalutamide does not accumulate and is not diluted in the blood circulation of HD patients when given at the normal dosage used in the general population.
Continue androgen deprivation (pharmaceutical or surgical) indefinitely. Abiraterone acetate/prednisone, enzalutamide, or (223)Ra should be offered; docetaxel/prednisone should also be offered, accompanied by discussion of toxicity risk. Sipuleucel-T may be offered to asymptomatic/minimally symptomatic men. For men who have experienced progression with docetaxel, cabazitaxel may be offered, accompanied by discussion of toxicity risk. Mitoxantrone may be offered, accompanied by discussion of limited clinical benefit and toxicity risk. Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, accompanied by discussion of limited known clinical benefit. Bevacizumab, estramustine, and sunitinib should not be offered. There is insufficient evidence to evaluate optimal sequences or combinations of therapies. Palliative care should be offered to all patients.
• 29 Romanian men participated in this study: 17 heterosexual and 12 homosexual. Patients were undergoing treatment for prostate cancer consisting of a standard daily dose of 50 mg bicalutamide, a fast acting non-steroidal anti-androgen with action comparable to other anti-androgen drugs but with reportedly fewer sexual side effects. • Patients retrospectively provided information regarding their sexual functioning measured by the IIEF prior to commencing bicalutamide treatment. • Then, about five weeks later, patients were asked to prospectively provide information regarding their current sexual functioning while undergoing bicalutamide treatment.
We previously developed carborane-containing potent AR antagonists, BA321 and BA341, on the basis of our hypothesis that the carborane cage would be an excellent hydrophobic pharmacophore in place of steroidal C and D rings. As an extension of that work, we designed and synthesized carborane-containing AR antagonist candidates with a pyridine ring. Compound 6b, which has a pyridine ring directly bound to the p-carborane cage at the 3-position, exhibited potent AR-antagonistic activity in transcriptional activation assay using NIH3T3 cells transfected with a hAR-expression plasmid. In addition, it showed more potent antiandrogenic activity than that of the well-known antiandrogen flutamide and comparable activity to that of (R)-bicalutamide in SC-3 cell proliferation assay.
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