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PubMed1980

Determination of estramustine and its 17-keto metabolite in plasma by high-performance liquid chromatography.

A rapid, sensitive and specific high-performance liquid chromatographic (HPLC) assay was developed for the determination of estramustine and its 17-keto metabolite in plasma. The assay involves extraction of the compounds into hexane from plasma buffered to pH 9.0, the residue obtained by evaporation of the hexane extract is dissolved in the mobile phase hexane-ethanol (92.5:7.5) with HPLC analysis performed on a 5-micrograms silica gel column using a fluorescence detector with excitation at 195 nm and emission at wavelengths greater than 250 nm. The overall recoveries and limits of sensitivity for estramustine and the 17-keto metabolite are 74.7% and 40 ng/ml of plasma and 85.1% and 50 ng/ml of plasma, respectively. The method was used to obtain plasma concentration-time profiles in three subjects with prostatic cancer following oral administration of a single 7 mg/kg dose of estramustine phosphate.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Phase II trial of vinorelbine and estramustine in the treatment of metastatic hormone-resistant prostate cancer.

The purpose of this study was to investigate the efficacy and safety of combination chemotherapy using estramustine and vinorelbine in chemotherapy-naïve patients with hormone-resistant prostate cancer (HRPC). The patients (n = 54) received oral estramustine 840 mg/day on Days 1 to 14 and IV vinorelbine 25 mg/m(2) on Days 1 and 8 of every 3 wk cycle. The median number of cycles per patient was 9 (range, 1 to 27). Fifty-three patients were evaluable for toxicity and survival and 52 for prostate specific antigen (PSA) response. Median age was 68 (range, 46-80). PSA sustained decrease >50% was seen in 52% of patients (95% CI: 38-66%). A complete response was seen in 3 and a partial response in 12 of 25 patients with measurable disease, for an overall objective response of 60% (95% CI: 41-79%). Improvement in performance status was observed in 30 out of 43 evaluable for clinical benefit response. The median duration of response was 7 mo and median time to progression was 6 mo. The median survival time was 15 mo. The most common adverse event was mild gastrointestinal toxicity. In general, toxicity G3-4 was low: granulocytopenia Grade 3-4 (8%), thrombocytopenia Grade 3 (6%), and anemia Grade 3 (13%). Other Grade 3 toxicities included deep vein thrombosis (4%), hepatic (2%), cardiac ischemia (2%), fatigue (6%), and sensory neuropathy (2%). There were 2 treatment-related deaths (4%). We conclude that vinorelbine and estramustine as used in this trial is an efficacious and well-tolerated therapeutic regimen in the management of HRPC.

Antineoplastic Agents↗
PubMed1998

Induction of aneuploidy by the antineoplastic drug estramustine in human lymphocytes.

Estramustine (EM) is an antineoplastic drug used in the therapy of human prostatic carcinoma. The aim of our work was to evaluate the potential aneuploidogenic activity of estramustine, by analysing its cytogenetic effects induced in human lymphocytes. To estimate the ability of EM to induce mitotic spindle disturbances, two parameters were used: the presence of c-mitoses (according to the degree of chromatid spreading and contraction) and mitotic index evaluation (increase after exposure indicating the accumulation of mitoses). EM induced c-mitoses and mitotic index increases starting from the 4 microM dose: statistically significant increases were observed up to the highest dose (40 microM). A strong correlation between c-mitoses and mitotic index increase was found. The micronucleus (MN) assay combined with the fluorescence in situ hybridization technique with a pancentromeric DNA probe was also carried out. Compared to the control, EM induced significant MN increases in binucleated lymphocytes at two doses (8-16 microM). Moreover, we found that estramustine induced significant percentages of MN with positive hybridization signal at the same doses, confirming the presence of entire chromosomes in micronuclei. Additional experiments included induction of numerical and structural chromosome aberrations, and evaluation of sister chromatid exchanges (SCE) and satellited (D- and G-group chromosomes) chromosome associations. The results of numerical chromosome aberration analysis indicated that EM was positive in inducing a statistically significant increase in aneuploid cells and/or polyploid cells at all doses tested. On the basis of these observations, EM may be defined as a typical aneuploidy inducer, whereas it was not found to increase the frequency of structural chromosome aberrations and SCE frequency.

Adult↗
PubMed1988

Estramustine phosphate inhibits germinal vesicle breakdown and induces depolymerization of microtubules in mouse oocyte.

The first meiotic cell division (meiotic maturation) of the dictyate stage of mouse oocytes, removed from the follicle, resumes spontaneously in vitro. This study indicates that estramustine phosphate reversibly blocks meiotic maturation by inhibiting germinal vesicle breakdown. Oocyte cryostat sections were stained with anti-tubulin and two antibodies (anti-MAP1: JA2 and 5051) which decorated the metaphase spindle during meiotic maturation. It was found that (1) estramustine phosphate depolymerized microtubules in ovo and dispersed non-tubulin antigens associated with microtubules of the metaphase spindle at various stages of maturation, and (2) estramustine phosphate decreased the ability of taxol to induce cytoplasmic asters. These results suggest that germinal vesicle breakdown and microtubule polymerization may be linked.

Alkaloids↗
PubMed1996

Symptomatic improvement associated with combined estramustine and vinblastine chemotherapy for metastatic prostate cancer.

We evaluated the effectiveness of combination chemotherapy using estramustine and velban for metastatic prostate cancer. Patients with progressive metasatatic prostate cancer and rising prostate-specific antigen (PSA) values were evaluated between 1992 and 1994. All treatment was given on an outpatient basis. Vinblastine, 4 mg/m2 i.v., was given weekly for 6 weeks with a 2-week rest period. Estramustine, 10 mg/kg orally, was given in three divided doses for 6 weeks with a 2-week rest period between cycles. Of 15 patients, six (40%) had a response, in which a 25% decrease in PSA was associated with subjective improvement. There were no complete responses. Five partial responders had less pain. Median duration of response or time to progression was 9 months. Survival was 11.7 months for responders, 13.2 months for nonresponders. The combination of estramustine and velban is an effective therapy in progressive metastatic prostate cancer as measured by a decrease in PSA and improvement of symptoms.

Aged↗
PubMed1998

Evaluation of estramustine phosphate combined with weekly doxorubicin in patients with androgen-independent prostate cancer.

Thirty-one patients with progressive metastatic prostate cancer refractory to first- or second-line hormonal therapy were treated with a combination of daily oral estramustine phosphate (600 mg) and weekly intravenous doxorubicin (20 mg/m2). Eighteen (58%) patients demonstrated a biologic response with a 50% or more serum prostate-specific antigen decline. The median duration of biologic response was three months. Five (45%) of the 11 patients with measurable lesions achieved a partial response in liver or retroperitoneal lymph nodes. The median duration of these objective responses was four months. Of 22 patients who required analgesics at the onset of the study, six (27%) achieved a significant reduction of pain. The combination of doxorubicin and estramustine phosphate was tolerated on an outpatient schedule. The occurrence of severe toxicities required suspension of therapy in six patients. At the end of the observation time, all patients but one had died, 29 of progressive prostatic cancer and one of toxicity. The median survival time from the onset of chemotherapy was 12 months. The administration of weekly doxorubicin with phosphate estramustine appears to be a safe combination for those patients with hormone-resistant prostate cancer who require chemotherapy. The benefit of chemotherapy should be investigated using relevant quality-of-life criteria in future trials.

Adult↗
PubMed2005

Matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine: tumor-reducing effects on hormone-sensitive prostate cancer in rats.

Therapeutic efficacy of the novel matrix metalloproteinase (MMP) inhibitor, Ro 28-2653 (5-biphenyl-4-yl-5-[4-(-nitro-phenyl)-piperazin-1-yl]-pyrimidine-2,4,6-trione), has been shown in various models of different tumor entities. The tumor growth-reducing effect has been demonstrated in the orthotopic rat prostate Dunning model (subline MatLyLu). Based on these results we investigated Ro 28-2653 in combination with estramustine on the G subline of the Dunning tumor. This subline is characterized by a low metastatic ability and androgen sensitivity. Efficacy was determined by recording tumor growth in vivo by magnetic resonance imaging (MRI). Tumor cells were injected into the prostates of 81 Copenhagen rats. MRI was performed at day 100 and at day 126 after tumor cell injection. The duration of therapy was 17 days with daily oral application of Ro 28-2653 (100 mg/kg) and four i.p. injections of estramustine (7.5 mg/kg). Histological evaluations were conducted to provide further information about the effects on tumor morphology. Orthotopic tumor induction was successful in 100% of the animals. Tumor volume calculations with MRI showed a significant difference between the control groups, the animals treated with Ro 28-2653, and the animals treated with the combination of Ro 28-2653 and estramustine. The new MMP inhibitor Ro 28-2653 reduces tumor growth and provides a compatible therapeutic alternative for patients with prostate cancer.

Animals↗
PubMed2004

Phase II trial of estramustine and etoposide in androgen-sensitive metastatic prostate carcinoma.

BACKGROUND: Early chemohormonal therapy in metastatic prostate cancer may offer an advantage by simultaneously targeting androgen-dependent and -independent clones. Hence, a phase II trial was conducted to evaluate the efficacy and toxicity of estramustine and etoposide in hormone-sensitive metastatic prostate cancer. PATIENT AND METHODS: Eligibility consisted of untreated metastatic prostate cancer, adequate organ function, and a performance status of 0 to 2 by Zubrod criteria. A 21-day schedule of oral estramustine (10 mg/kg/day) and etoposide (50 mg/m2/day) was administered every 28 days. Hormonal therapy was allowed at the end of the protocol therapy. Toxicity was assessed weekly, PSA levels were assessed with each cycle, and objective response was evaluated every 3 cycles. RESULTS: Twenty-one patients were enrolled (10 white, 11 black) with a median age of 59.5 years (range, 42-79 years), a median PSA of 338 ng/mL (range, 0.9-20,000 ng/mL), and a median Gleason score of 8 points. Ten patients had bone-only metastases, 11 had measurable disease, of whom 4 had visceral metastases. A total of 128 cycles were administered (median, 6 cycles). No dose reductions were required. Nineteen patients were able to be evaluated for response. Severe toxicities included thromboembolic events and anemia in 2 patients each and fatigue in 1 patient. There were no episodes of febrile neutropenia. Response was observed in 8 of 11 patients (73%) with measurable disease. Median PSA nadir after therapy was 0.45 ng/mL, and undetectable PSA (<0.1 ng/mL) was achieved in 4 patients. Median time to PSA progression was 16.65 months. At a median follow-up of 34 months, 18 patients were alive. The 1-, 2-, and 3-year overall survival rates were 90%, 82%, and 72% respectively. Median survival has not yet been reached. CONCLUSION: The combination of estramustine and etoposide is well tolerated, and has promising activity in newly diagnosed metastatic prostate cancer.

Adult↗
PubMed2005

High dose pulse calcitriol, docetaxel and estramustine for androgen independent prostate cancer: a phase I/II study.

PURPOSE: We determined the safety and preliminary efficacy of the combination of high dose pulse calcitriol (1,25-dihydroxycholecalciferol) with a standard regimen of docetaxel plus estramustine in patients with metastatic androgen independent prostate cancer. MATERIALS AND METHODS: Patients were treated with 60 microg calcitriol orally on day 1, 280 mg estramustine orally 3 times daily on days 1 to 5 and 60 mg/m docetaxel on day 2 (70 mg/m after cycle 1) every 21 days for up to 12 cycles. Patients also received 325 mg aspirin and 1 or 2 mg warfarin orally daily. Regimen safety was assessed in the first 6 patients and a dose de-escalation scheme for calcitriol was planned if dose limiting toxicities were noted during treatment cycle 1 in greater than a third of patients. RESULTS: A total of 24 patients, including 11 who were chemotherapy naïve and 13 who had previously been treated with docetaxel, were evaluable for toxicity and 22 for prostate specific antigen decrease data. The regimen was generally well tolerated. Treatment related grades 3 or greater toxicity seen in more than 1 patient included hypophosphatemia in 16.7% and neutropenia in 12.5%. Four patients had thromboembolic complications. Asymptomatic hypercalcemia was seen in 4 patients, including grades 2 and 1 in 1 and 3, respectively. Six of 11 evaluable, chemotherapy naïve patients (55%) met prostate specific antigen response criteria. One of 11 patients (9%) treated with prior docetaxel met these criteria. CONCLUSIONS: High dose calcitriol may be safely added to docetaxel and estramustine administered on a 21-day schedule.

Administration, Oral↗
PubMed1977

Treatment of advanced carcinoma of the prostate with estramustine phosphate.

40 patients with inoperable, histologically proved carcinoma of the prostate were treated with estramustine phosphate. 35 patients had progressive, symptomatic, metastatic disease unresponsive to conventional oestrogens and/or castration Estramustine phosphate was given intravenously initially at a dose of 150 mg/day increasing to 300 mg/day. After 3 weeks or more oral therapy was substituted in 23 patients at a dose of 560 mg/day. Of 23 evaluable patients given the drug by both routes, 17 died after a mean treatment period of 12.5 months and 6 are alive and well after a mean treatment period of 27.7 months. The cause of death in 2 patients was probably, and in a third certainly, due to myocardial infarction. The other 31 deaths were due to carcinoma of the prostate. 18 patients showed transient toxic side-effects. No haematological abnormalities were found during treatment. An attempt at active treatment with estramustine phosphate in patients with prostatic cancer is justified when the disease is resistant to treatment with conventional oestrogens.

Aged↗
PubMed1985

Plasma hormone levels in patients with prostatic carcinoma treated with diethylstilboestrol and estramustine.

Plasma testosterone, oestradiol, luteinising hormone (LH) growth hormone and prolactin were measured serially in 140 patients with advanced prostatic carcinoma (T3, T4, MI and MO) randomised in a trial of diethylstilboestrol 3 mg/day against estramustine 560 mg/day. Both drugs suppressed plasma testosterone and LH and increased plasma growth hormone and prolactin, though estramustine induced a greater rise in prolactin. Oestradiol levels fell on stilboestrol but were considerably elevated on estramustine. Initial hormone levels reflected neither the extent of disease nor the response to treatment. The data also showed that close attention should be given to plasma LH in identifying patients who are unreliable, since intermittent hormone dosage caused an exaggerated rise even when plasma testosterone remained at castrate levels.

Aged↗
PubMed1987

Effects of estramustine, a new anti-microtubule drug, on the induction of casein gene expression by prolactin.

Estramustine, a new anti-microtubule drug, was added to the culture medium of rabbit mammary explants with lactogenic hormones. In the absence of the drug, prolactin with insulin and cortisol stimulated DNA synthesis and it induced beta-casein and beta-casein mRNA accumulation in the tissue. As opposed to other anti-microtubule agents such as colchicine, estramustine was unable to prevent prolactin actions. An examination of the mammary cells by immunofluorescence revealed that the microtubule network was significantly altered under the influence of estramustine. These data indicate that the integrity of microtubules is not required for prolactin to deliver its message to the mammary cell. These data also suggest that other anti-microtubule drugs such as colchicine which prevent prolactin action act through their binding to tubulin molecule unrelated to microtubule structures.

Animals↗
PubMed2001

Oral combination of cyclophosphamide, uracil plus tegafur and estramustine for hormone-refractory prostate cancer.

OBJECTIVE: To evaluate the clinical usefulness of an oral combination of cyclophosphamide, uracil plus tegafur (UFT) and estramustine in the treatment of patients with hormone-refractory prostate cancer (HRPC). METHODS: Twenty-one patients were treated with oral administration of cyclophosphamide (100 mg/day), UFT (400 mg/day) and estramustine phosphate (560 mg/day). The median age of the patients was 70 years. Twelve patients had symptomatic bone metastasis, 6 had asymptomatic bone metastasis, 5 had lymph node metastasis, while 2 had only biochemical progression evaluated by prostate-specific antigen (PSA). RESULTS: Twelve (57%) out of 21 patients showed a PSA decline of 50% or greater. The median response duration was 7 months (range 2-15 months). Among the 20 patients assessable for bone pain, 2 (10%) improved, 12 (60%) remained stable and 6 (30%) progressed. Among the 10 patients assessable for bone metastasis, 1 (10%) improved, 5 (50%) were stable and 4 (40%) progressed on bone scan. Among 3 patients assessable for measurable disease (lymph node metastasis), 2 (67%) showed partial response and 1 (33%) progression. Most toxicities were mild. CONCLUSIONS: The combination of cyclophosphamide, UFT and estramustine is an active and well-tolerated regimen for HRPC. To evaluate the survival benefit, further randomized studies are required.

Administration, Oral↗
PubMed2005

Characterization of prognostic factors and efficacy in a phase-II study with docetaxel and estramustine for advanced hormone refractory prostate cancer.

BACKGROUND: Docetaxel based chemotherapy not only reduces pain and improves quality of life in advanced hormone refractory prostate cancer (HRPC), but it also improves survival. We investigated the combination of docetaxel and estramustine in patients with HRPC regarding efficacy and prognostic parameters. PATIENTS AND METHODS: We conducted a phase-II trial, administering docetaxel (70 mg/m(2) i.v., day 2, every 3 weeks) and estramustine (280 mg 3 times daily p.o., 1 day prior to docetaxel, on 5 consecutive days) to patients with HRPC. Patients were monitored for PSA (prostate-specific antigen) response and toxicity. RESULTS: 62 patients were treated. The median age was 67.5 years, the median PSA was 177.9 ng/ml. The median number of cycles was 6. The median time to progression (TTP) and median survival time were 14 (+/-2) and 24 (+/-5) months, respectively. A = 50% decrease in PSA levels from baseline occurred in 38 (61.3%) patients of whom 25 (40.3%) had a = 75% PSA decrease. The main grade 3-4 hematologic toxicities were neutropenia 34% and anemia 18%. CONCLUSIONS: The combination of docetaxel and estramustine exerts substantial activity in HRPC suggesting an overall survival benefit with manageable toxicity. This trial also demonstrated a survival advantage for patients with early chemotherapeutic intervention. We identified PSA relapse, baseline PSA and hemoglobin as valuable prognostic factors in this setting.

Adult↗
PubMedDate not supplied

Dose-finding study of weekly docetaxel plus estramustine in patients with hormone-refractory metastatic prostate cancer.

OBJECTIVE: The aim of this phase I study was to find the maximum tolerated dose of weekly docetaxel in association with estramustine in hormone-refractory prostate cancer. METHODS: Eleven patients with hormone-refractory prostate cancer were treated with escalating weekly doses of docetaxel (level I, 3 patients, 30 mg/m2; level II, 3 patients, 35 mg/m2, level III, 3 patients, 40 mg/mz; level IV, 2 patients, 45 mg/m2) associated with fixed dosage of estramustine (840 mg/day). RESULTS: In level I, there was only one episode of grade 3 neutropenia; grade 1 nausea and vomiting were registered in 1 patient; in 1 patient mild edema of the lower limbs was noted. In level II, grade 2 stomatitis and grade 1 sensory symptoms occurred in 1 patient, and grade 1 edema in 1 case. In level Ill, grade 2 edema was noted in 2 patients, damage to nails in 1 patient, asthenia in 1 patient, grade 1 neuropathy in 2 patients, and grade 1 nausea in 1 patient. In level IV, grade 2 edema was present in 1 patient, grade 3 edema in 1 patient, changes with fall of nails and grade 2 erythema of face in 2 patients, asthenia in 2 patients, grade 1 neuropathy in both patients. Nine patients had a more than a 50% decrease in PSA after 2 cycles of therapy. CONCLUSIONS: The results of the study suggest a good tolerability of weekly 35 Mg/m2 docetaxel in hormone-refractory prostate cancer in association with estramustine.

Aged↗
PubMed1994

Phase II evaluation of oral estramustine and oral etoposide in hormone-refractory adenocarcinoma of the prostate.

PURPOSE: Estramustine and etoposide (VP-16) have been demonstrated to inhibit the growth of prostate cancer cells in experimental models. This led us to evaluate the effectiveness of this combination in the treatment of patients with metastatic prostate carcinoma refractory to hormone therapy. PATIENTS AND METHODS: Estramustine 15 mg/kg/d and VP-16 50 mg/m2/d, were administered orally in divided doses for 21 days. Patients were then taken off therapy for 7 days and the cycle then repeated. Therapy continued until evidence of disease progression. RESULTS: Forty-two patients have been enrolled onto this trial with a minimum of 40 weeks follow-up. Of 18 patients with measurable soft tissue disease, three demonstrated a complete response (CR) and six a partial response (PR) for longer than 2 months. Of these 18 patients, pretreatment prostate-specific antigen (PSA) levels decreased by at least 75% in five men (28%) and by at least 50% in nine (50%). The median survival duration has not been reached in those patients who demonstrated a response either by soft tissue or PSA criteria. Of 24 patients with disease limited to bone, six (25%) demonstrated improvement and nine (38%) demonstrated stability in their bone scans. Five men (21%) demonstrated a decrease of at least 75% in pretreatment PSA levels and 14 (58%) demonstrated at least a 50% decrease; the median survival duration has not been reached in these patients. Pretreatment performance status is an important predictor of survival. CONCLUSION: We conclude that the combination of estramustine and VP-16 is an active oral regimen in hormone-refractory prostate cancer.

Adenocarcinoma↗
PubMed1999

Vinblastine versus vinblastine plus oral estramustine phosphate for patients with hormone-refractory prostate cancer: A Hoosier Oncology Group and Fox Chase Network phase III trial.

PURPOSE: To compare vinblastine versus the combination of vinblastine plus estramustine as treatment for patients with hormone-refractory prostate cancer (HRPC). PATIENTS AND METHODS: A total of 201 patients with metastatic prostate cancer, progressive after hormonal therapy and antiandrogen withdrawal (if prior antiandrogen treatment), were randomized to receive vinblastine (V) 4 mg/m(2) by intravenous bolus weekly for 6 weeks followed by 2 weeks off, either alone or together with estramustine phosphate (EM-V) 600 mg/m(2) PO days 1 through 42, repeated every 8 weeks. Of 193 eligible patients, 98 received V, and 95 received EM-V. RESULTS: Overall survival trended in favor of EM-V but was not significantly different as determined by Kaplan-Meier analysis (P =.08). Median survival was 11.9 months for EM-V and 9.2 months for V. EM-V was superior to V for secondary end points of time to progression (P <. 001, stratified log rank test; median 3.7 v 2.2 months, respectively) and for proportion of patients with >/= 50% prostate-specific antigen (PSA) decline sustained for at least 3 monthly measurements (25.2% v 3.2%, respectively; P <.0001). Granulocytopenia was significantly less for EM-V compared with V (grade 2, 3, and 4 = 7%, 7%, and 1% v 27%, 18% and 9%, respectively; P <.0001); however, grade 2 or worse nausea (26% v 7%, respectively; P =.0002) and extremity edema (22% v 8%, respectively; P =.005) were more frequent for EM-V. CONCLUSION: Although overall survival was not significantly greater for the combination, EM-V was superior to V for time to progression and PSA improvement. These results encourage further study of estramustine-based antimicrotubule drug combinations in HRPC.

Administration, Oral↗
PubMed1999

Phase I trial of docetaxel with estramustine in androgen-independent prostate cancer.

PURPOSE: To evaluate the toxicity, efficacy, and pharmacokinetics of docetaxel when combined with oral estramustine and dexamethasone in a phase I study in patients with progressive metastatic androgen-independent prostate cancer. PATIENTS AND METHODS: Thirty-four men were stratified into minimally pretreated (MPT) and extensively pretreated (EPT) groups. Estramustine 280 mg PO tid was administered 1 hour before or 2 hours after meals on days 1 through 5, with escalated doses of docetaxel from 40 to 80 mg/m2 on day 2. Treatment was repeated every 21 days. RESULTS: Thirty-four patients were assessable for toxicity and 33 for response. In the MPT patients, dose-limiting myelosuppression was reached at 80 mg/m2, with six patients experiencing grade 3/4 granulocytopenia. In EPT patients, escalation above 70 mg/m2 was not attempted. Fourteen MPT (70%) and six EPT (50%) patients had a > or = 50% decline in serum PSA on two consecutive measurements taken at least 2 weeks apart. The overall 50% PSA response rate was 63% (95% confidence interval [CI], 28% to 81%). Of the 18 patients with bidimensionally measurable disease, five (28%; 95% CI, 11% to 54%) achieved a partial response. At the time of entry onto the study, 15 patients required narcotic analgesics for bone pain; after treatment, eight (53%) discontinued their pain medications. The area under the curve for docetaxel increased linearly from 40 to 70 mg/m2. At 80 mg/m2, the measured area under the curve was 8.37 (standard deviation, 0.724), which was significantly higher than the previously reported values. CONCLUSION: The recommended phase II dose of docetaxel combined with estramustine is 70 mg/m2 in MPT patients and 60 mg/m2 in EPT patients. This combination is active in men with androgen-independent prostate cancer.

Aged↗