Docetaxel and Estramustine Compared with Mitoxantrone and Prednisone for Advanced Refractory Prostate Cancer
Daniel P. Petrylak, M.D., Catherine M. Tangen, Dr.P.H., Maha H.A. Hussain, M.D., Primo N. Lara, Jr., M.D., Jeffrey A. Jones, M.D., Mary Ellen Taplin, M.D., Patrick A. Burch, M.D., Donna Berry, Ph.D., R.N., Carol Moinpour, Ph.D., Manish Kohli, M.D., Mitchell C. Benson, M.D., Eric J. Small, M.D., Derek Raghavan, M.D., Ph.D., and E. David Crawford, M.D.
Background Mitoxantrone-based chemotherapy palliates pain withoutextending survival in men with progressive androgen-independentprostate cancer. We compared docetaxel plus estramustine withmitoxantrone plus prednisone in men with metastatic, hormone-independentprostate cancer.
Methods We randomly assigned 770 men to one of two treatments,each given in 21-day cycles: 280 mg of estramustine three timesdaily on days 1 through 5, 60 mg of docetaxel per square meterof body-surface area on day 2, and 60 mg of dexamethasone inthree divided doses before docetaxel, or 12 mg of mitoxantroneper square meter on day 1 plus 5 mg of prednisone twice daily.The primary end point was overall survival; secondary end pointswere progression-free survival, objective response rates, andpost-treatment declines of at least 50 percent in serum prostate-specificantigen (PSA) levels.
Results Of 674 eligible patients, 338 were assigned to receivedocetaxel and estramustine and 336 to receive mitoxantrone andprednisone. In an intention-to-treat analysis, the median overallsurvival was longer in the group given docetaxel and estramustinethan in the group given mitoxantrone and prednisone (17.5 monthsvs. 15.6 months, P=0.02 by the log-rank test), and the correspondinghazard ratio for death was 0.80 (95 percent confidence interval,0.67 to 0.97). The median time to progression was 6.3 monthsin the group given docetaxel and estramustine and 3.2 monthsin the group given mitoxantrone and prednisone (P<0.001 bythe log-rank test). PSA declines of at least 50 percent occurredin 50 percent and 27 percent of patients, respectively (P<0.001),and objective tumor responses were observed in 17 percent and11 percent of patients with bidimensionally measurable disease,respectively (P=0.30). Grade 3 or 4 neutropenic fevers (P=0.01),nausea and vomiting (P<0.001), and cardiovascular events(P=0.001) were more common among patients receiving docetaxeland estramustine than among those receiving mitoxantrone andprednisone. Pain relief was similar in both groups.
Conclusions The improvement in median survival of nearly twomonths with docetaxel and estramustine, as compared with mitoxantroneand prednisone, provides support for this approach in men withmetastatic, androgen-independent prostate cancer.
Men with newly diagnosed metastatic prostate cancer have a rapidresponse to surgical or medical castration, with improvementin bone pain, regression of soft-tissue metastases, and a declinein serum prostate-specific antigen (PSA) levels.1 Nevertheless,in virtually all patients the tumor ultimately becomes androgen-independenta median of 18 to 24 months after castration.1,2 During thisterminal phase in the natural history of prostate cancer, approximately29,900 affected men in the United States will die of the diseasein 2004.3 Patients with metastatic androgen-independent prostatecancer have a progressive and morbid disease with a median survivalof 10 to 12 months; currently, no treatment offers a survivaladvantage. Chemotherapy for androgen-independent prostate canceris ineffective4: mitoxantrone plus prednisone or hydrocortisone,the current standard of care, palliates bone pain in approximately30 percent of patients but does not improve survival.5,6
Immunohistochemical studies have demonstrated that the antiapoptoticprotein Bcl-2 is increased in metastatic cells from androgen-independentprostate tissue.7 Docetaxel, a taxane used to treat a varietyof solid tumors, phosphorylates Bcl-2 in vitro, leading to itsinactivation and to eventual cell death by apoptosis.8 Estramustine,9which disrupts microtubule-associated proteins in vitro, hassynergistic activity with docetaxel against human prostate-cancercell lines.10,11 Phase 1 and 2 studies of docetaxel plus estramustinein men with androgen-independent prostate cancer demonstrateda decline in serum PSA levels of at least 50 percent in 68 to84 percent of patients, a measurable disease response in 28to 55 percent, and a median survival of up to 23 months.11,12,13,14These data provided the foundation for this prospective, randomized,phase 3 trial (Southwest Oncology Group [SWOG] Intergroup protocol99-16), which we conducted to determine whether docetaxel plusestramustine improves survival over that afforded by mitoxantroneplus prednisone in men with androgen-independent prostate cancer.
Methods
Patients
Patients were enrolled by institutions affiliated with SWOG,Cancer and Leukemia Group B, the North Central Cancer TreatmentGroup, the Clinical Trials Support Unit, and the extended participationproject program through the National Cancer Institute. Eligibilityrequired pathologically confirmed adenocarcinoma of the prostateand progressive metastatic disease (stage D1 or D2) despiteandrogen-ablative therapy and cessation of antiandrogen treatment.Criteria for progressive disease were progression of a bidimensionallymeasurable lesion, as assessed within 28 days before study registration;progression of disease that could be evaluated but not measured(e.g., by bone scanning), as assessed within 42 days beforeregistration; or an increase in the serum PSA level over thebaseline level in at least two consecutive samples obtainedat least 7 days apart.15 Antiandrogen therapy was discontinuedbefore registration, at least six weeks before in the case ofnilutamide or bicalutamide and four weeks before in the caseof flutamide or other secondary hormonal therapy. To ensurecontinued androgen ablation, patients continued taking luteinizing-hormone–releasinghormone agonists throughout study treatment. Patients were requiredto discontinue bisphosphonates at least 28 days before registration.Prior radiotherapy (to less than 30 percent of the bone marrowonly) or one prior systemic therapy (except with estramustine,taxanes, anthracyclines, or mitoxantrone) was permitted if atleast four weeks had elapsed since the completion of that therapy.Adequate renal, hepatic, and cardiac function and a SWOG performance-statusscore of 0 to 2 (a performance status of 3 was allowed if thescore was due to bone pain) were also required. Patients wereineligible if they had received prior radioisotope or anticoagulanttherapy (excluding aspirin), had active thrombophlebitis orhypercoagulability, had a history of pulmonary embolus, or pleuraleffusions or ascites.
Stratification
Patients were classified at registration according to the followingfactors: type of progression (i.e., progression of disease thatcould be measured or evaluated vs. increasing PSA level alone),grade of bone pain according to the Common Terminology Criteriaof the National Cancer Institute (grade 1 [mild, not interferingwith function] vs. grade 2 [moderate pain interfering with functionbut not interfering with the activities of daily life], grade3 [severe pain, severely interfering with the activities ofdaily living], or grade 4 [disabling pain]), and SWOG performance-statusscore (0 or 1 vs. 2 or 3).16 All patients provided written informedconsent, and the study was approved by the institutional reviewboard of each participating institution.
Treatment
Patients were randomly assigned to one of two treatments, eachgiven in 21-day cycles: 280 mg of estramustine (Emcyt, Pfizer)three times daily one hour before or two hours after meals ondays 1 through 5 plus 60 mg of docetaxel (Taxotere, Aventis)per square meter of body-surface area intravenously on day 2,preceded by 60 mg of dexamethasone orally in three divided doses,starting the night before docetaxel, or 12 mg of mitoxantrone(Novantrone, OSI) per square meter intravenously on day 1 plus5 mg of prednisone twice daily. Doses of docetaxel and mitoxantronewere increased to 70 mg per square meter and 14 mg per squaremeter, respectively, if no grade 3 or 4 adverse events wereobserved during the first cycle. A report that prophylacticanticoagulation decreased estramustine-associated vascular effectsprompted an amendment of the protocol on January 15, 2001, toinclude daily warfarin (2 mg) plus aspirin (325 mg) in the groupassigned to receive estramustine.16 Treatment continued untildisease progression or unacceptable adverse effects occurredor until a maximum of 12 cycles of docetaxel and estramustineor 144 mg of mitoxantrone per square meter had been administered.
Evaluation
The pretreatment evaluation included a history taking, a physicalexamination in which weight and performance status were recorded,computed tomography (CT) of the abdomen and pelvis, bone scanning,nuclear ventriculography (multiple gated acquisition [MUGA]scanning), a complete blood count, and measurement of serumPSA, serum creatinine, and serum testosterone. MUGA scans wererepeated every four cycles among patients in the group givenmitoxantrone and prednisone. At every cycle, the pretreatmentevaluation was repeated (excluding MUGA scanning, measurementof serum testosterone, and baseline imaging studies). Adverseevents were evaluated by means of the Common Toxicity Criteriaof the National Cancer Institute, version 2.0. Imaging studieswere repeated every six cycles; if positive, they were repeatedevery three cycles.
Objective responses were defined on the basis of the sum ofbidimensional measurements of metastatic lesions. Confirmedobjective responses required a follow-up scan (a minimum offour weeks later) that demonstrated a continued response. Progressionwas defined by one of the following: a 50 percent increase oran increase of 10 cm2, whichever was smaller, in the sum ofmeasurements of metastatic lesions over the sum at baseline;a clear worsening of nonmeasurable disease; reappearance ofany lesion that had disappeared; appearance of any new lesion;or death.
A confirmed partial response of nonmeasurable disease was definedas a reduction by more than 50 percent over baseline in twoor more PSA measurements obtained at least four weeks apart,with no evidence of disease progression on imaging. Progressivedisease was defined as a 25 percent increase in the serum PSAlevel — to at least 5 ng per milliliter — over thelast preregistration measurement, with confirmation of the increaseat least four weeks later. For patients with a decrease in serumPSA levels during the trial, progressive disease was definedas a confirmed increase of 25 percent, to at least 5 ng permilliliter over the nadir.14
Statistical Analysis
The primary objective of the study was to compare overall survivalin the two groups. Assuming an exponential distribution of survivaltimes, 3.5 years for accrual, an additional year of follow-up,and a sample size of 310 patients per group, this study hada statistical power of 0.80 to detect an improvement of 33 percentin median survival in the group given docetaxel and estramustine,as compared with the group given mitoxantrone and prednisone,with the use of a one-sided log-rank test at a P value of 0.025.Interim analyses were to be conducted when half the patientshad been enrolled and again when enrollment was complete. Thenull and alternative hypotheses were to be tested at a one-sidedP level of 0.0025 at each analysis. The significance level forthe final analysis, performed one year after study closure,was specified as a one-sided P value of 0.02. However, in accordancewith the policy of the Journal, only two-sided P values arereported. Secondary end points included progression-free survival,the objective-response rate, the rate of PSA response (definedas a decline in the serum PSA level of at least 50 percent),and adverse events. The data set was locked and analyzed onMarch 9, 2004.
Kaplan–Meier curves were used to estimate rates of overallsurvival and progression-free survival. Survival was definedfrom the date of randomization to the date of death from anycause or censored at the date of last contact. Progression-freesurvival was defined as the time from randomization to the firstoccurrence of objective or PSA progression or death from anycause. The general chi-square test was used to compare ratesof response (objective and PSA) and adverse events between thetwo treatment groups. All analyses were performed with the useof SAS software, version 9.0.
The study was designed by the Genitourinary Committee of SWOGand was approved by the Cancer Treatment and Evaluation Programof the National Cancer Institute. The SWOG Statistical Centerreceived funding from Aventis Pharmaceuticals for the additionalcost of collecting data on the quality of life. Aventis wasallowed to review the protocol and make comments before enrollmentbegan. Aventis had no access to the data but received a semiannualsummary of enrollment and adverse events.
Results
Characteristics of the Patients
A total of 770 patients were enrolled between October 1999 andJanuary 2003. Ninety-six patients (12 percent) were found tobe ineligible: 30 owing to the lack of adequate withdrawal ofantiandrogen or other hormonal therapy, 11 because of missingdocumentation, 31 because of inadequate baseline laboratorystudies, 17 because of rising PSA levels without evidence ofmetastatic disease, and 7 for miscellaneous reasons. The baselinecharacteristics of the 674 eligible patients in both treatmentgroups were similar (Table 1). The sole evidence of diseaseprogression was a rising PSA level in 18 percent of patients.
Table 1. Baseline Characteristics of the Patients.
Treatment
There were 11 major protocol deviations. Six patients in thegroup given docetaxel and estramustine and four patients inthe group given mitoxantrone and prednisone did not receivethe assigned treatment and were not included in the evaluationof adverse events. One patient in the latter group who receivedintermittent radiotherapy while receiving the assigned treatment,a major protocol deviation, was included in the evaluation ofadverse events. Six patients who discontinued treatment withinone week after starting mitoxantrone and prednisone (four men)or docetaxel and estramustine (two men) were not included inthe evaluation of adverse events; however, in the case of allthese men, the reported results and statistical analyses arebased on the treatment group to which the patients were assigned.
Response and Survival
During a median follow-up of 32 months, 217 of the 338 patientsin the group given docetaxel and estramustine died (64 percent),as did 235 of the 336 patients in the group given mitoxantroneand prednisone (70 percent). According to the intention-to-treatanalysis, the median survival was 17.5 months among the patientsassigned to docetaxel and estramustine and 15.6 months amongthe patients assigned to mitoxantrone and prednisone (P=0.02)(Figure 1); the corresponding hazard ratio for death was 0.80(95 percent confidence interval, 0.67 to 0.97). The median timeto progression was 6.3 months in the group given docetaxel andestramustine and 3.2 months in the group given mitoxantroneand prednisone (P<0.001) (Figure 2).
Figure 1. Kaplan–Meier Estimates of Overall Survival among Men with Androgen-Independent Prostate Cancer Treated with Mitoxantrone and Prednisone or Docetaxel and Estramustine.
Figure 2. Kaplan–Meier Estimates of Progression-free Survival among Men with Androgen-Independent Prostate Cancer Treated with Mitoxantrone and Prednisone or Docetaxel and Estramustine.
Declines in serum PSA levels of at least 50 percent occurredmore frequently after treatment with docetaxel and estramustine(155 of 309 patients, or 50 percent) than after treatment withmitoxantrone and prednisone (82 of 303 patients, or 27 percent;P<0.001). A partial response in measurable disease occurredin 17 percent of patients in the group given docetaxel and estramustine(17 of 103, 4 unconfirmed) and 11 percent of patients in thegroup given mitoxantrone and prednisone (10 of 93, 4 unconfirmed).This difference was not significant (P=0.30). Patients withan inadequate assessment were assumed to have had no response.There was no significant difference in pain relief, as reportedby the patients, between the two groups (data not shown).
Adverse Events
As of December 2003, all surviving patients had stopped theprotocol treatment. Adverse events led to the withdrawal of54 patients in the group assigned to docetaxel and estramustine(16 percent) and 32 patients in the group assigned to mitoxantroneand prednisone (10 percent). The rates of severe or life-threatening(grade 3 or 4) and fatal (grade 5) adverse events are summarizedin Table 2. The rate of grade 3, 4, or 5 neutropenia in thegroup given mitoxantrone and prednisone did not differ significantlyfrom that in the group given docetaxel and estramustine (12.5percent vs. 16.1 percent, P=0.22). As compared with the groupgiven mitoxantrone and prednisone, the group given docetaxeland estramustine had significantly higher rates of grade 3 or4 neutropenic fevers (5 percent vs. 2 percent, P=0.01), cardiovascularevents (15 percent vs. 7 percent, P=0.001), nausea and vomiting(20 percent vs. 5 percent, P<0.001), metabolic disturbances(6 percent vs. 1 percent, P<0.001), and neurologic events(7 percent vs. 2 percent, P=0.001). There were eight treatment-relateddeaths in the group given docetaxel and estramustine: threeare still under review, a fourth was due to gastrointestinalbleeding thought to be due to aspirin, a fifth was caused bysepsis arising from necrotic prostate tissue, a sixth (due toliver and renal failure, atrial fibrillation, and pulmonaryedema) occurred within a week after treatment was started, aseventh was associated with granulocytopenia and neutropenia,and the eighth was caused by a respiratory tract infection.Four patients had grade 5 adverse events attributed to mitoxantroneand prednisone. Three died within 30 days of receiving protocoltreatment, and another died from a respiratory tract infectionand grade 4 anorexia. Vascular complications and their relationshipto prophylactic warfarin treatment in the group given docetaxeland estramustine are shown in Table 3; these findings are observationaland were not part of the planned primary analysis.
Table 3. Adverse Events among Patients Receiving Docetaxel and Estramustine, According to Whether They Were Receiving Prophylactic Anticoagulation.
Discussion
This randomized trial demonstrated that the treatment of androgen-independentmetastatic prostate cancer with estramustine and docetaxel resultsin a longer median survival than treatment with mitoxantroneand prednisone (17.5 months vs. 15.6 months, P=0.02). The hazardratios for death (0.80 and 0.76, respectively) and median survivalrates (17.5 months and 18.9 months, respectively) were similarin our docetaxel group and the group given docetaxel every threeweeks in the study reported by Tannock et al.17 elsewhere inthis issue of the Journal. Although we did not meet our primaryaim of detecting a 33 percent improvement in median survivalwith estramustine and docetaxel, this trial had reasonable powerto detect smaller differences in survival. Relative to mitoxantroneand prednisone, docetaxel and estramustine reduced the mortalityrate by 20 percent (95 percent confidence interval, 3 to 33percent). The rates of reduced PSA levels and progression-freesurvival were significantly higher in the group given docetaxeland estramustine than in the group given mitoxantrone and prednisone.The survival estimate of the group given estramustine and docetaxelin our trial fell within the confidence intervals of smallerphase 1 and 2 studies of this combination.11,12,13,14
The median survival of 15.6 months among patients treated withmitoxantrone and prednisone is longer than that reported byTannock et al. (12 months),5 Kantoff et al. (12.3 months),6or Ernst et al. (11.5 months).18 The median survival was similarto that reported in the current study by Tannock et al. (16.5months). This difference may be due in part to the use of differenteligibility criteria, in particular the requirement for symptomaticdisease in the studies by Tannock et al. and Ernst et al. Incontrast, in a randomized trial of 101 asymptomatic men witha rising serum PSA level, Berry et al. found a nonsignificant4-month difference in median survival: 23 months among men treatedwith mitoxantrone and prednisone, as compared with 19 monthsamong men treated with prednisone alone.19 In our trial, 18percent of patients had an increase in PSA but were asymptomaticwith metastatic disease. The median PSA level at entry (87 ngper milliliter) was somewhat lower than in the studies by Kantoffet al. (150 ng per milliliter),6 Tannock et al. (158 ng permilliliter),5 and Ernst et al. (150 ng per milliliter),18 butpretreatment PSA levels do not predict survival in this patientpopulation, although they probably reflect tumor burden.
Crossover treatment may also partially account for the smalldifference in survival between the two treatment groups. Ofall the patients we treated, about half received at least oneother antineoplastic regimen after having had no response tothe assigned treatment. It is difficult to judge the effectof these additional treatments on overall survival, becausemultiple variables influence response and survival after crossovertreatment.
Continuous corticosteroid treatment can reduce serum PSA levelsby at least 50 percent in 20 to 74 percent of men with hormone-refractoryprostate cancer,20 but the regimen of premedication with dexamethasone(60 mg every three weeks) that we used is unlikely to have affectedthe results. In a phase 2 study, the same dose and scheduleof dexamethasone that we used were employed until the serumPSA level rose at least 25 percent over baseline levels or clinicalprogression occurred, at which point docetaxel and estramustinewere given. None of the patients treated with dexamethasonehad a decline in PSA of at least 50 percent (the level actuallyincreased by a median of 47 percent). After progression duringdexamethasone therapy, 92 percent of patients treated with docetaxeland estramustine had a decline in serum PSA levels of at least50 percent.21
In phase 2 studies, estramustine was associated with an increasedrisk of nausea, thromboembolic events, and cardiovascular events.11,12,13,14,22In our trial, cardiovascular and gastrointestinal events weremore frequent among patients given docetaxel and estramustinethan among those given mitoxantrone and prednisone. However,this difference was not associated with an increased rate oftreatment-related deaths or discontinuation of treatment inthe former group.
In conclusion, treatment with estramustine and docetaxel moderatelyincreases survival at the cost of an increased rate of adverseevents. These factors must be balanced when one is consideringthe use of docetaxel and estramustine as first-line therapyfor men with metastatic androgen-independent prostate cancer.
Supported in part by grants (CA38926, CA32102, CA37135, CA25224,CA46441, CA37981, CA45808, CA27057, CA12644, CA68183, CA22433,CA35261, CA58861, CA20319, CA46113, CA58882, CA76447, CA04919,CA16385, CA35090, CA03096, CA67663, CA45450, CA35431, CA45807,CA58416, CA14028, CA45377, CA63845, CA42777, CA46136, CA11083,CA35119, CA58658, CA46282, CA76129, CA46368, CA35176, CA86780,CA46462, CA35192, CA35178, CA67575, CA63844, CA12213, CA74647,CA35128, CA35996, CA58686, CA13612, CA45461, CA58723, CA63848,CA35281, CA63850, CA76132, and CA74811) from the National CancerInstitute, Department of Health and Human Services, and by Aventis.
Drs. Petrylak and Taplin report having received grant support,lecture fees, and consulting fees from Aventis; Dr. Hussainconsulting fees and lecture fees from and having equity in Aventis;Dr. Lara lecture fees from Aventis and AstraZeneca; Dr. Bensonlecture fees from Aventis; Drs. Small and Raghavan consultingfees from Aventis; Dr. Crawford consulting fees and lecturefees from Aventis; and Dr. Moinpour consulting fees from AstraZeneca.
We are indebted to Dr. Robert Fine and Dr. Karen Antman forhelpful comments during the preparation of this manuscript.
Source Information
From Columbia University, Herbert Irving Comprehensive Cancer Center, New York (D.P.P., M.C.B.); Southwest Oncology Group Statistical Center, Seattle (C.M.T., C.M.); the University of Michigan Comprehensive Cancer Center, Ann Arbor (M.H.A.H.); the University of California, Davis, Sacramento (P.N.L.); Baylor College of Medicine, Houston (J.A.J.); the University of Massachusetts Medical Center, Worcester (M.E.T.); the Mayo Clinic, Rochester, Minn. (P.A.B.); Biobehavioral Nursing and Health Systems, University of Washington, Seattle (D.B.); the University of Arkansas for Medical Science, Little Rock (M.K.); the University of California, San Francisco, Cancer Center, San Francisco (E.J.S.); the Cleveland Clinic Foundation, Cleveland (D.R.); and the University of Colorado Health Science Center, Denver (E.D.C.).
Address reprint requests to the Southwest Oncology Group (S9916) Operations Office, 14980 Omicron Dr., San Antonio, TX 78245-3217, or at pubs{at}swog.org.
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Howard, D. N, Chambers, C., Cusano, F.
(2008). Efficacy vs. effectiveness -- docetaxel and prednisone in hormone refractory prostate cancer. J Oncol Pharm Pract
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(2008). Tumor-targeting nanodelivery enhances the anticancer activity of a novel quinazolinone analogue. Molecular Cancer Therapeutics
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Hu, H., Li, G.-x., Wang, L., Watts, J., Combs, G. F. Jr., Lu, J.
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Roach, M. III, Bae, K., Speight, J., Wolkov, H. B., Rubin, P., Lee, R. J., Lawton, C., Valicenti, R., Grignon, D., Pilepich, M. V.
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(2007). Adaptive Therapy for Androgen-Independent Prostate Cancer: A Randomized Selection Trial of Four Regimens. JNCI J Natl Cancer Inst
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(2007). Do General Dimensions of Quality of Life Add Clinical Value to Symptom Data?. J Natl Cancer Inst Monogr
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(2007). Molecular Alterations in Prostate Carcinomas that Associate with In vivo Exposure to Chemotherapy: Identification of a Cytoprotective Mechanism Involving Growth Differentiation Factor 15. Clin. Cancer Res.
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Armstrong, A. J., Garrett-Mayer, E., Ou Yang, Y.-C., Carducci, M. A., Tannock, I., de Wit, R., Eisenberger, M.
(2007). Prostate-Specific Antigen and Pain Surrogacy Analysis in Metastatic Hormone-Refractory Prostate Cancer. JCO
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(2007). Three-weekly Docetaxel with Prednisone is Feasible for Japanese Patients with Hormone-refractory Prostate Cancer: A Retrospective Comparative Study with Weekly Docetaxel Alone. Jpn J Clin Oncol
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(2007). A bifunctional colchicinoid that binds to the androgen receptor. Molecular Cancer Therapeutics
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Quintero, I. B., Araujo, C. L., Pulkka, A. E., Wirkkala, R. S., Herrala, A. M., Eskelinen, E.-L., Jokitalo, E., Hellstrom, P. A., Tuominen, H. J., Hirvikoski, P. P., Vihko, P. T.
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Agarwal, C., Veluri, R., Kaur, M., Chou, S.-C., Thompson, J. A., Agarwal, R.
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Agus, D. B., Sweeney, C. J., Morris, M. J., Mendelson, D. S., McNeel, D. G., Ahmann, F. R., Wang, J., Derynck, M. K., Ng, K., Lyons, B., Allison, D. E., Kattan, M. W., Scher, H. I.
(2007). Efficacy and Safety of Single-Agent Pertuzumab (rhuMAb 2C4), a Human Epidermal Growth Factor Receptor Dimerization Inhibitor, in Castration-Resistant Prostate Cancer After Progression From Taxane-Based Therapy. JCO
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Wu, J. D., Haugk, K., Coleman, I., Woodke, L., Vessella, R., Nelson, P., Montgomery, R. B., Ludwig, D. L., Plymate, S. R.
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Gulley, J. L., Figg, W. D., Dahut, W.
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Small, E. J., Schellhammer, P. F., Higano, C. S., Redfern, C. H., Nemunaitis, J. J., Valone, F. H., Verjee, S. S., Jones, L. A., Hershberg, R. M.
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Adess, M., Eisner, R., Nand, S., Godwin, J., Messmore, H. L. Jr, Wehrmacher, W. H.
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Berry, D. L., Moinpour, C. M., Jiang, C. S., Ankerst, D. P., Petrylak, D. P., Vinson, L. V., Lara, P. N., Jones, S., Taplin, M. E., Burch, P. A., Hussain, M. H.A., Crawford, E. D.
(2006). Quality of Life and Pain in Advanced Stage Prostate Cancer: Results of a Southwest Oncology Group Randomized Trial Comparing Docetaxel and Estramustine to Mitoxantrone and Prednisone. JCO
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Kampa, M., Kogia, C., Theodoropoulos, P. A., Anezinis, P., Charalampopoulos, I., Papakonstanti, E. A., Stathopoulos, E. N., Hatzoglou, A., Stournaras, C., Gravanis, A., Castanas, E.
(2006). Activation of membrane androgen receptors potentiates the antiproliferative effects of paclitaxel on human prostate cancer cells. Molecular Cancer Therapeutics
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Tarassoff, C. P., Arlen, P. M., Gulley, J. L.
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Petrylak, D. P., Ankerst, D. P., Jiang, C. S., Tangen, C. M., Hussain, M. H. A., Lara, P. N. Jr., Jones, J. A., Taplin, M. E., Burch, P. A., Kohli, M., Benson, M. C., Small, E. J., Raghavan, D., Crawford, E. D.
(2006). Evaluation of prostate-specific antigen declines for surrogacy in patients treated on SWOG 99-16.. JNCI J Natl Cancer Inst
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Farokhzad, O. C., Cheng, J., Teply, B. A., Sherifi, I., Jon, S., Kantoff, P. W., Richie, J. P., Langer, R.
(2006). Targeted nanoparticle-aptamer bioconjugates for cancer chemotherapy in vivo. Proc. Natl. Acad. Sci. USA
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Ma, D., Hopf, C. E., Malewicz, A. D., Donovan, G. P., Senter, P. D., Goeckeler, W. F., Maddon, P. J., Olson, W. C.
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Wagmiller, J. A., Griggs, J. J., Dick, A. W., Sahasrabudhe, D. M.
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Lara, P. N. Jr., Stadler, W. M., Longmate, J., Quinn, D. I., Wexler, J., Van Loan, M., Twardowski, P., Gumerlock, P. H., Vogelzang, N. J., Vokes, E. E., Lenz, H. J., Doroshow, J. H., Gandara, D. R.
(2006). A Randomized Phase II Trial of the Matrix Metalloproteinase Inhibitor BMS-275291 in Hormone-Refractory Prostate Cancer Patients with Bone Metastases. Clin. Cancer Res.
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Arlen, P. M., Gulley, J. L., Parker, C., Skarupa, L., Pazdur, M., Panicali, D., Beetham, P., Tsang, K. Y., Grosenbach, D. W., Feldman, J., Steinberg, S. M., Jones, E., Chen, C., Marte, J., Schlom, J., Dahut, W.
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Huff, C. A., Matsui, W., Smith, B. D., Jones, R. J.
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Tang, Y., Khan, M. A., Goloubeva, O., Lee, D. I., Jelovac, D., Brodie, A. M., Hussain, A.
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Hussein, M.A. H., Bird, B. R., O'Sullivan, M. J., Kalimuthu, S. G., O'Sullivan, G. C., O'Reilly, S., Breathnach, O. S.
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