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Originally published as JCO Early Release 10.1200/JCO.2008.20.5054 on May 18 2009 © 2009 American Society of Clinical Oncology.
Phase II Multicenter Trial of Imatinib in 10 Histologic Subtypes of Sarcoma Using a Bayesian Hierarchical Statistical ModelFrom the Department of Internal Medicine, University of Michigan, Ann Arbor, MI; The University of Texas M. D. Anderson Cancer Center, Houston, TX; Memorial Sloan-Kettering Cancer Center; New York, NY; Washington Cancer Institute, Washington, DC; and Kootenai Cancer Center, Coeur d'Alene, ID. Corresponding author: Rashmi Chugh, MD, 1500 E Medical Center Dr, C407 Med Inn, SPC 5843, Ann Arbor, MI 48109-5843; e-mail: rashmim{at}umich.edu. Purpose The purpose of this trial was to assess the efficacy of imatinib in patients with one of 10 different subtypes of advanced sarcoma.
Patients and Methods Eligible patients were treated daily with imatinib dosed at 300 mg twice a day (for body-surface area Results One hundred eighty-five assessable patients with one of 10 subtypes of sarcoma were treated. One CR and three PRs were achieved. A CBR was achieved in 28 patients treated overall and by subtype: two angiosarcomas (n = 16), 0 Ewing (n = 13), one fibrosarcoma (n = 12), six leiomyosarcomas (n = 29), seven liposarcomas (n = 31), three malignant fibrous histiocytomas (n = 30), five osteosarcomas (n = 27), one malignant peripheral-nerve sheath tumor (n = 7), 0 rhabdomyosarcoma (n = 2), and three synovial sarcomas (n = 22). Variable expression and mutations within the KIT/PDGFR pathway were observed. Conclusion This is the first phase II study of a new agent in sarcoma to include sufficient patients with each of the common histologic subtypes to permit generalizable conclusions. The BHM is an effective method for studying rare diseases and their subtypes, when it is reasonable to assume that their response rates are exchangeable. Although rare dramatic responses were seen, imatinib is not an active agent in advanced sarcoma in these subtypes. Supported by Novartis Pharmaceuticals. Presented in part at the 40th Annual Meeting of the American Society of Clinical Oncology, June 5-8, 2004, New Orleans, LA. Authors' disclosures of potential conflicts of interest and author contributions are found at the end of this article. Clinical Trials repository link available JCO.org. Clinical trial information can be found for the following: NCT00031915 [ClinicalTrials.gov] .
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Copyright © 2009 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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1.5 m2). The primary end point was response (clinical benefit response [CBR]), defined as complete (CR) or partial response (PR) at 2 months, or stable disease, CR, or PR at 4 months. Rules for early termination within each disease type were based on a Bayesian hierarchical probability model (BHM) accounting for correlation of the responses of the 10 subtypes. Available tissue samples were analyzed for molecules within the KIT/platelet-derived growth factor receptor (PDGFR) signal transduction pathway. 
