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- W2806419148 abstract "4714 While conventional therapies have lead to significant improvement in overall survival for patients with Ewing’s sarcoma, patients with metastatic disease and relapsed disease remain largely incurable with even the most intensive therapy. There is an ongoing need for new agents with activity in Ewing’s sarcoma (ES). Maintenance of a neoplastic phenotype in tumor cells often requires signaling through the mammalian target of rapamycin (MTOR), which functions as a sensor of mitogen, energy and nutrient levels, and a gatekeeper for cell cycle progression from G 1 to S. A recent report by Mateo-Lozano, et. al. (Oncogene. 2003;22:9282-7) demonstrates that rapamycin leads to decreased proliferation of ES cells, down-regulation of EWS-FLI-1 levels, and a restoration of TGF-β type-2 receptor, which is repressed by EWS-FLI-1. Inhibition of MTOR may be an effective anti-neoplastic strategy in the treatment Ewing’s sarcoma. The cytotoxicity of rapamycin in ES was evaluated in a panel of Ewing’s sarcoma cell lines. Cells were incubated in the presence of drug at various concentrations for 3 to 7 days. The IC50 in all lines tested is in the range of 1-10ng/ml. In vivo response was determined in SCID xenograft models of ES implanted heterotopically. Treatment groups consisted of 5 to 8 mice. Each animal received either rapamycin (7mg/kg) or normal saline orally for 2 weeks starting when tumors reached a volume of 1cm 3 . There was complete inhibition of tumor growth in the rapamycin-treated mice with no tumor re-growth for the duration of therapy. At day 14 of treatment the mean tumor volume for the rapamycin treated group was 115mm 3 and for the control group 3155 mm 3 (p" @default.
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- W2806419148 date "2005-05-01" @default.
- W2806419148 modified "2023-09-24" @default.
- W2806419148 title "The MTOR inhibitor, rapamycin, inhibits growth of Ewing’s sarcoma in vitro and in vivo" @default.
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