FCCC LOGO Faculty Publications
Carlson RW , O'Neill AM , Goldstein LJ , Sikic BI , Abramson N , Stewart JA , Davidson NE , Wood WC
A pilot phase II trial of valspodar modulation of multidrug resistance to paclitaxel in the treatment of metastatic carcinoma of the breast (E1195): A trial of the eastern cooperative oncology group
Cancer Investigation. 2006 Nov;24(7) :677-681
PMID: ISI:000242207700003   
Back to previous list
Abstract
Background: To assess the activity and toxicity of valspodar (PSC-833) in combination with paclitaxel in women with anthracycline refractory, metastatic breast cancer. Patients and Methods: Limited, multi-institutional, Phase II trial of valspodar at 5 mg/kg/dose orally every 6 hours for 12 doses in combination with paclitaxel 70 mg/m(2) administered intravenously as a 3-hour infusion beginning 4 hours after the fifth dose of valspodar, every 3 weeks. Eligible patients had bi-dimensionally measurable metastatic carcinoma of the breast, prior anthracycline therapy or a medical contraindication to anthracycline therapy, no more than one prior chemotherapy for recurrent or metastatic breast cancer, and adequate organ function. Treatment was continued until disease progression or unacceptable toxicity. Results: Thirty-four patients are evaluable for response and 37 for toxicity. Two (6 percent) patients achieved a complete response and 5 (15 percent) a partial response for an objective response rate of 21 percent (95 percent confidence interval of 9 to 38 percent). Median duration of response was 9.7 months (95 percent confidence interval 8.0-17.2 months), median time to progression was 3.3 months (95 percent confidence interval 2.0-4.2 months), and median survival was 12 months (95 percent confidence interval 8.1-17.3 months). The toxicity experienced was acceptable. Conclusions: Combination valspodar plus paclitaxel is an active regimen and has acceptable toxicity. The combination is not clearly more active than single agent paclitaxel.
Notes
ISI Document Delivery No.: 107YU Times Cited: 0 Cited Reference Count: 25 Cited References: BOESCH D, 1991, CANCER RES, V51, P4226 COLLINS HL, 1995, P AM SOC CLIN ONCOL, V14 COX DR, 1989, ANAL BINARY DATA, P26 FRACASSO PM, 1995, P AM SOC CLIN ONCOL, V14 FRACASSO PM, 2001, J CLIN ONCOL, V19, P2975 GOLDSTEIN LJ, 1989, J NATL CANCER I, V81, P116 GOLDSTEIN LJ, 1992, CRIT REV ONCOL HEMAT, V12, P243 HOLMES FA, 1993, MONOGR NATL CANCER I, V15, P161 HOLMES FA, 1998, P AN M AM SOC CLIN, V17, A110 JACHEZ B, 1993, J NATL CANCER I, V85, P478 KAPLAN EL, 1958, J AM STAT ASSOC, V53, P457 LEONESSA F, 2003, ENDOCR-RELAT CANCER, V10, P43 PEREZ EA, 2001, J CLIN ONCOL, V19, P4216 REICHMAN BS, 1993, J CLIN ONCOL, V11, P1943 SANGRAJRANG S, 2000, CHEMOTHERAPY, V46, P327 SCHILLER JH, 1994, J CLIN ONCOL, V12, P241 SEIDMAN AD, 1995, J CLIN ONCOL, V13, P2575 SIKIC BI, 1993, J CLIN ONCOL, V11, P1629 SIKIC BI, 1997, CANCER CHEMOTH PHARM, V40, P13 SLEDGE GW, 1997, P AN M AM SOC CLIN, V16, A1 SLEDGE GW, 2003, J CLIN ONCOL, V21, P588 SMITH RE, 1999, J CLIN ONCOL, V17, P3403 TROCK BJ, 1997, J NATL CANCER I, V89, P917 TWENTYMANN PR, 1992, EUR J CANCER, V27, P1639 YUSUF RZ, 2003, CURR CANCER DRUG TAR, V3, P1