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1 ted in the presence of the antioxidant agent amifostine.
2 oprotector to become available clinically is amifostine.
3 ioxide emission in cancer patients receiving amifostine.
4 ding the activity of dexrazoxane, mesna, and amifostine.
10 xrazoxane, three reports (two studies) each; amifostine, 33 reports (31 studies); and mesna, no publi
11 Following chemotherapy, patients received amifostine (340 mg/m2 4 days a week for 5 weeks, or 200
13 aclitaxel 175 mg/m2 over 3 hours followed by amifostine 740 mg/m2 and cisplatin 75 mg/m2 administered
15 2) and cisplatin (100 mg/m2) with or without amifostine (910 mg/m2) every 3 weeks for six cycles.
20 ts were randomly assigned at registration to amifostine (AM) 500 mg IV four times per week or no AM d
23 athologic tumor response rates were 37% with amifostine and 28% in controls, with comparable median s
25 -protectant activity-dexrazoxane, mesna, and amifostine-and questions about the role of these protect
30 oxic drugs, we conducted a phase II trial of amifostine, cisplatin, and vinblastine (ACV) in patients
32 ography-mass spectrometry confirmed that the amifostine conversion to WR-1065 was significantly more
35 findings shed new light on the mechanism of amifostine cytoprotection and encourage clinical researc
39 e, David Brizel, who worked on the phase III amifostine efficacy study, and Jens Overgaard, a vehemen
41 ifty-three percent of the patients receiving amifostine had at least one episode of nausea and/or vom
44 lines for the use of dexrazoxane, mesna, and amifostine in patients who are not enrolled on clinical
50 amifostine to its active metabolite WR-1065, amifostine may not only protect in multiple ways normal
51 clinical and clinical studies that suggested amifostine may potentiate the effects of cytotoxic drugs
52 nerally reversible and the data suggest that amifostine may protect against long-term renal insuffici
55 This study describes the direct effect of amifostine on kidney and tumor uptake of (111)In-DOTA,Ty
58 r percent of CP patients compared with 9% of amifostine plus CP patients discontinued therapy because
72 at the thiol form of the cytoprotective drug amifostine that is designated WR-1065 [2-((aminopropyl)a
73 , and Jens Overgaard, a vehement opponent of amifostine therapy, provide thought-provoking arguments
74 venous treatment with 100, 200, or 400 mg/m2 amifostine three times a week, or 740 mg/m2 weekly for t
75 d cancer cells in their abilities to convert amifostine to its active metabolite WR-1065, amifostine
77 4.5%; one-sided chi(2) test P = .005) of the amifostine-treated patients had at least grade 3 ototoxi
79 solution immunofluorescence microscopy) that amifostine treatment supports DSB repair in gamma-irradi
85 n patients with AR medulloblastoma (n = 62), amifostine would decrease the need for hearing aids (def
87 rpose of this study was to determine whether amifostine (WR-2721) prevents or ameliorates clinically
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