Ixabepilone, mitoxantrone, and prednisone for metastatic castration-resistant prostate cancer after docetaxel-based therapy
dc.contributor.author | Harzstark, Andrea L. | en_US |
dc.contributor.author | Rosenberg, Jonathan E. | en_US |
dc.contributor.author | Weinberg, Vivian K. | en_US |
dc.contributor.author | Sharib, Jeremy | en_US |
dc.contributor.author | Ryan, Charles J. | en_US |
dc.contributor.author | Smith, David C. | en_US |
dc.contributor.author | Pagliaro, Lance C. | en_US |
dc.contributor.author | Beer, Tomasz M. | en_US |
dc.contributor.author | Liu, Glenn | en_US |
dc.contributor.author | Small, Eric J. | en_US |
dc.date.accessioned | 2011-06-10T14:21:40Z | |
dc.date.available | 2012-07-12T17:42:23Z | en_US |
dc.date.issued | 2011-06-01 | en_US |
dc.identifier.citation | Harzstark, Andrea L.; Rosenberg, Jonathan E.; Weinberg, Vivian K.; Sharib, Jeremy; Ryan, Charles J.; Smith, David C.; Pagliaro, Lance C.; Beer, Tomasz M.; Liu, Glenn; Small, Eric J. (2011). "Ixabepilone, mitoxantrone, and prednisone for metastatic castration-resistant prostate cancer after docetaxel-based therapy." Cancer 117(11): 2419-2425. <http://hdl.handle.net/2027.42/84416> | en_US |
dc.identifier.issn | 0008-543X | en_US |
dc.identifier.issn | 1097-0142 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/84416 | |
dc.description.abstract | BACKGROUND: Mitoxantrone plus prednisone and ixabepilone each have modest activity as monotherapy for second-line chemotherapy in patients with docetaxel-refractory castration-resistant prostate cancer. Clinical noncross- resistance was previously observed. Phase 1 testing determined the maximum tolerated dose and dose-limiting toxicities with the combination regimen; a phase 2 study was conducted to evaluate the activity of the combination. METHODS: Patients with metastatic progressive castration-resistant prostate cancer during or after 3 or more cycles of taxane-based chemotherapy enrolled in a phase 2 multicenter study of ixabepilone 35 mg/m 2 and mitoxantrone 12 mg/m 2 administered on Day 1 every 21 days with pegfilgrastim support, along with prednisone 5 mg twice daily. Patients were evaluated for disease response and toxicity. RESULTS: Results are reported for the 56 evaluable patients. Twenty-five (45%; 95% confidence interval [CI], 31%-59%) experienced confirmed ≥50% prostate-specific antigen (PSA) declines, 33 (59%; 95% CI, 45%-72%) experienced confirmed ≥30% PSA declines, and 8 of 36 patients (22%; 95% CI, 10%-39%) with measurable disease experienced objective responses. Median time to PSA or objective progression was 4.4 months (95% CI, 3.5-5.6), and median progression-free survival was also 4.4 months (95% CI, 3.0-6.0). Median overall survival was 12.5 months (95% CI, 10.2-15.9). Thirty-two percent of patients experienced grade 3 of 4 neutropenia, and 11% experienced grade 3 or higher neutropenic infections, including 1 treatment-related death. Grade 2 and 3 neuropathy occurred in 11% and 12.5% of patients, respectively. CONCLUSIONS: These results suggest that the combination of ixabepilone and mitoxantrone is both feasible and active in castration-resistant prostate cancer and requires dosing with pegfilgrastim. Cancer 2011;. © 2010 American Cancer Society. | en_US |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cancer Research, Oncology and Pathology | en_US |
dc.title | Ixabepilone, mitoxantrone, and prednisone for metastatic castration-resistant prostate cancer after docetaxel-based therapy | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Oncology and Hematology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California ; The first 2 authors contributed equally to this article. ; Fax: (415) 353-7779 ; Department of Medicine, University of California, San Francisco; Helen Diller Family Comprehensive Cancer Center, 1600 Divisadero Street, Box 1711, San Francisco, CA 94143-1711 | en_US |
dc.contributor.affiliationother | Dana Farber Cancer Institute, Boston, Massachusetts | en_US |
dc.contributor.affiliationother | Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California | en_US |
dc.contributor.affiliationother | Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California | en_US |
dc.contributor.affiliationother | Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California | en_US |
dc.contributor.affiliationother | The University of Texas M. D. Anderson Cancer Center, Houston, Texas | en_US |
dc.contributor.affiliationother | Oregon Health and Science University Knight Cancer Institute, Portland, Oregon | en_US |
dc.contributor.affiliationother | University of Wisconsin Carbone Cancer Center, Madison, Wisconsin | en_US |
dc.contributor.affiliationother | Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California | en_US |
dc.identifier.pmid | 24048789 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/84416/1/25810_ftp.pdf | |
dc.identifier.doi | 10.1002/cncr.25810 | en_US |
dc.identifier.source | Cancer | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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