PSA Response (psa + response)

Distribution by Scientific Domains


Selected Abstracts


Effects of flutamide as a second-line agent for maximum androgen blockade of hormone refractory prostate cancer

INTERNATIONAL JOURNAL OF UROLOGY, Issue 3 2007
Kenji Nishimura
Abstract: We analyzed clinical effects of flutamide as a second-line agent for maximum androgen blockade (MAB) in patients with relapsing prostate cancer who received bicalutamide as the first-line MAB agent. This study included 13 patients with progressive prostate cancer who had relapsed after first-line MAB, with bicalutamide at 80 mg/day. After checking for antiandrogen withdrawal syndrome, they were given flutamide at 375 mg/day as second-line MAB. The effectiveness of that therapy was evaluated by changes in prostatic specific antigen (PSA) levels, with response defined as a decrease of greater than 50% from the start of therapy. We also compared several factors between responders and non-responders. Nine (69.2%) of the 13 patients showed a decrease in PSA levels, of whom five (38.5%) had a greater than 50% decrease and were defined as responders. The median duration of PSA response was 11.0 months (range 5,20 months). Patients who had a longer duration of response to first-line MAB had a significantly greater response to second-line MAB. For advanced prostate cancer patients who progressed on first-line MAB with bicalutamide, flutamide administration as a second-line antiandrogen was found to be relatively effective, especially for those who showed a longer duration of response to the first-line MAB. Our results confirm previous findings that MAB using flutamide is an effective second-line hormonal therapy. [source]


PSA surge/flare-up in patients with castration-refractory prostate cancer during the initial phase of chemotherapy

THE PROSTATE, Issue 16 2009
T. Nelius
Abstract BACKGROUND Docetaxel-based chemotherapy has shown great promise for the treatment of CRPC and is considered the current standard of care. PSA is mainly used as marker to monitor the treatment response. Several articles were published reporting an initial PSA surge/flare-up after starting chemotherapy. The cause and the impact of this phenomenon are discussed controversially. The intention of this review is to define the significance of initial PSA surge/flare-up and to increase awareness to this phenomenon in the urological community. MATERIALS AND METHODS A comprehensive literature search was performed in different data bases using various key words. Relevant articles and references between 1999 and 2009 were reviewed and analyzed for data on the association between chemotherapy and initial PSA surge/flare. RESULTS The incidence of a PSA surge/flare-up ranges according to the reported studies between 7.6% and 13.6%. A PSA surge/flare-up was reported up to 404% from baseline PSA level followed by PSA response. The median duration of a PSA surge/flare-up is 2,3 weeks and can last up to 6,8 weeks. However, the occurrence of a PSA surge/flare-up did not impact outcome and survival negatively compared to patients with an immediate PSA response. CONCLUSIONS A considerable portion of CRPC patients experience an initial PSA surge/flare-up under systemic chemotherapy. The definitions used for PSA surge/flare-up differ slightly in the literature. This issue needs to be solved since it might impact defining treatment response. As a PSA surge/flare-up did not impact outcome and survival negatively, chemotherapy should be continued according to the literature addressing specifically the phenomenon of a PSA surge/flare-up for a minimum of 8 weeks or 3 rounds of a 3-weekly cycle chemotherapy regimen before further decisions are made about efficacy. However, Scher et al. recommended a 12-week period drug exposure based on their results on PSA progression-free survival and overall survival. This dilemma needs to be addressed in further data analysis in order to establish a general rule regarding when to stop chemotherapy. Physicians should be aware of this effect to avoid inadequate early discontinuation of chemotherapy. The underlying mechanisms of a PSA surge/flare-up are still elusive and need further clarification. Prostate 69: 1802,1807, 2009. © 2009 Wiley-Liss, Inc. [source]


Efficacy of low-dose dexamethasone in castration-refractory prostate cancer

BJU INTERNATIONAL, Issue 4 2008
Ramachandran Venkitaraman
OBJECTIVE To evaluate the prostate-specific antigen (PSA) response rate and duration of PSA response to dexamethasone in patients with castration-refractory prostate cancer (CRPC), as corticosteroids are frequently used as second-line hormonal treatment of CRPC and there is little published evidence concerning the efficacy of low-dose dexamethasone in this setting. PATIENTS AND METHODS In all, 102 patients with progressive CRPC received oral dexamethasone (0.5 mg daily) between January 2003 and October 2006. The median pretreatment PSA level was 83 ng/mL. The main endpoint was the PSA response rate according to the PSA Working Group criteria. RESULTS In all, 50 patients (49%) had a confirmed PSA response. The median (range) time to PSA progression for the entire cohort was 7.4 (1,28) months. In responders, the median duration of the PSA response was 11.6 (1,24) months. CONCLUSION Low-dose dexamethasone has significant activity in CRPC. Subject to validation with more clinically meaningful endpoints, dexamethasone could become the corticosteroid of choice in the management of CRPC, and its potential for use in combination with novel agents should be explored. [source]


A randomized study of docetaxel and dexamethasone with low- or high-dose estramustine for patients with advanced hormone-refractory prostate cancer

BJU INTERNATIONAL, Issue 3 2006
THOMAS NELIUS
OBJECTIVE To test the combination of docetaxel with two different doses of estramustine in patients with hormone-refractory prostate cancer (HRPC), to improve response rates and to lower side-effects, as docetaxel-based chemotherapy is an increasing option for men with advanced HRPC, and alone or combined with estramustine, docetaxel improves median survival. PATIENTS AND METHODS In all, 72 patients with metastatic HRPC were randomly assigned to receive docetaxel (70 mg/m2 intravenously, on day 2 every 21 days) and estramustine (3 × 280 mg/day oral starting 1 day before docetaxel, for 5 consecutive days) for arm A, or estramustine (3 × 140 mg/day oral starting 1 day before docetaxel, for 3 consecutive days) for arm B. Premedication with oral dexamethasone at a total daily dose of 16 mg, in divided doses twice a day was administered in arm A on day 1,5 and in arm B on day 1,3. Initially, six cycles were administered. Chemotherapy was restarted after a significant increase in prostate-specific antigen (PSA) level. Patients were monitored for any measurable PSA response and toxicity. RESULTS Between the arms there was no statistically significant difference in time to progression and overall survival. However, treatment B had less treatment-related toxicity than A. Independent prognostic variables were baseline factors like PSA level, haemoglobin level, Eastern Cooperative Oncology Group performance status, and bone pain at presentation. CONCLUSIONS In this randomized phase II study the combination of docetaxel and estramustine had substantial activity in HRPC, with a significant incidence of severe toxicity, both haematological and not. Nevertheless, treatment-related toxicity was predictable and manageable. There was no better effect with a higher dose of estramustine with docetaxel than for a lower dose. There was a slight tendency to higher toxicity for high-dose estramustine but this was not statistically significant. The present results support the assertion that estramustine is not necessary in docetaxel-based treatment regimens. [source]