High Dose Bicalutamide for Androgen Independent Prostate Cancer: Effect of Prior Hormonal Therapy

Joyce, Robin; Fenton, Mary Anne; Rode, Paola; Constantine, Michael; Gaynes, Lisa; Kolvenbag, Geert J.C.M.; DeWolf, William C.; Balk, Steve; Taplin, Mary Ellen; Bubley, Glenn J.

doi:10.1016/s0022-5347(01)64039-4

Cited by 183 publications

(103 citation statements)

References 16 publications

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“…27 BCL alone has been shown to be safe and have some activity against CRPC. [28][29][30] When combined with tri-weekly DTX, BCL has a synergistic effect, as confirmed by a phase III trial in androgen-dependent prostate cancer. 31 In addition, a recent study reported that deferred BCL therapy could be at least partially useful after DTX failure for patients with CRPC.…”

Section: Introductionmentioning

confidence: 82%

“…Pre-clinical and clinical data have demonstrated that BCL exerts some anti-tumour activity in patients with CRPC, particularly for those previously treated long-term or who failed flutamide. [27][28][29] Our study included patients who had previously failed flutamide. Suzuki et al 34 reported that 35.8% (83 of 232) of patients had a .50% decline in PSA, which was observed after administering an alternative drug (flutamide was replaced by BCL) to patients with CRPC, and the decline lasted .6 months.…”

Section: Intermittent Docetaxel For Prostate Cancer Yf LI Et Al 776mentioning

confidence: 99%

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Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

Zhang²,

Tao-tao³

et al. 2013

Asian J Androl

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Whether continuous docetaxel (DTX) chemotherapy offers an advantage over intermittent therapy for castration-resistant prostate cancer (CRPC) is unknown. In this study, we evaluated the efficacy, toxicity and quality of life (QoL) of intermittent tri-weekly DTX with bicalutamide in CRPC. Forty-two patients (group A) with CRPC were enrolled. The patients received intravenous DTX (75 mg m 22 ) once tri-weekly with oral bicalutamide (50 mg) once daily. Patients had a DTX holiday when the prostate-specific antigen (PSA) level declined o50%. DTX was restarted in patients with a PSA increase o25%. Sixty patients (group B) who had matching characteristics and had continuously received DTX without bicalutamide for 10-12 cycles were also enrolled. There were no statistically significant differences in progression-free survival (8 months vs. 9 months, P50.866) or overall survival (19 months vs. 21 months, P50.753) between groups A and B; however, the proportions of patients in group A with all grades of neutropenia (33% vs. 58%, P50.013) and nausea/vomiting (11% vs. 29%, P50.024) were significantly less compared to group B. A significant improvement in the global health and fatigue scores was recorded for group A post-chemotherapy compared to pre-chemotherapy (P,0.05). The fatigue, nausea/ vomiting and appetite loss scores in group B were increased post-chemotherapy compared to pre-chemotherapy (P,0.05). In conclusion, intermittent tri-weekly DTX plus bicalutamide is well tolerated and has the potential to achieve comparable disease control with an improvement in QoL for patients with CRPC.

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Section: Introductionmentioning

confidence: 82%

Section: Intermittent Docetaxel For Prostate Cancer Yf LI Et Al 776mentioning

confidence: 99%

Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

Zhang²,

Tao-tao³

et al. 2013

Asian J Androl

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“…However, it is well documented that some antiandrogens can lead to the selection of tumors expressing AR mutants that can be activated by the therapeutic agent. Some of those tumors can still be sensitive to a second-line antiandrogen (22,23).…”

Section: Introductionmentioning

confidence: 99%

Castration-Resistant Prostate Cancer: Locking Up the Molecular Escape Routes

Attar¹,

Takimoto²,

Gottardis

2009

Clinical Cancer Research

187

159

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The understanding of the key role that androgens play on the normal and pathological physiology of the prostate guided the development of different therapies for the treatment of locally advanced or metastatic prostate cancer (PCa). These so-called androgen deprivation therapies include surgical or chemical castration, achieved by the administration of gonadotropin-releasing hormone analogs; inhibition of steroidogenic enzymes; and finally, blocking of the binding of androgens to their receptor (AR) by the use of antiandrogens. Despite an excellent initial response, in approximately 2 to 3 years, most of these patients will succumb to the castration resistant form of the disease. Remarkably, even in the presence of castration levels of circulating androgens, these tumors are still dependent on a functional AR, and several molecular mechanisms have been proposed to explain this phenomenon. These include: (1) gene amplification and increased expression of the AR mRNA and protein, (2) selection of mutations in the AR that confer broader ligand specificity, (3) changes in the ratios or expression between the AR and its coregulators, (4) increased expression of steroidogenic enzymes, and (5) up-regulation of cross-talk signal transduction pathways that can activate the AR in a ligand-independent manner. We will summarize how these molecular hypotheses are being tested in the clinic by the latest therapeutic modalities.

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“…The percentage of men with a greater than 50% decline in PSA was 35.8%; the response duration was a little over 6 months (Suzuki H, et al 2008). In another small trial of 31 men with CRPC treated with high dose bicalutamide 150 mg/day, only 22.5% of men had a PSA decline of > 50% for more than 2 months, almost all in men without prior treatment with flutamide (Joyce R, et al 1998). The modest efficacy and limited duration of response of first generation anti-androgens may in part be due to the fact that these molecules can act as partial agonists of the AR, especially AR which develop point mutations as a mechanism of resistance to these anti-androgens.…”

Section: First Generation Antiandrogensmentioning

confidence: 97%

Development of Novel Secondary Hormonal Therapies for Castrate-Resistant Prostate Cancer

Aggarwal¹,

Ryan²

2011

Drug Development - A Case Study Based Insight Into Modern Strategies

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High Dose Bicalutamide for Androgen Independent Prostate Cancer: Effect of Prior Hormonal Therapy

Abstract: Bicalutamide at this dose is modestly effective for some patients with androgen independent prostate cancer, particularly for those previously treated with long-term flutamide. This study indicates that previous antiandrogen therapy alters the response to subsequent hormonal agents.

Cited by 183 publications

References 16 publications

Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

Castration-Resistant Prostate Cancer: Locking Up the Molecular Escape Routes

Development of Novel Secondary Hormonal Therapies for Castrate-Resistant Prostate Cancer

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