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1 doses of doxorubicin, cyclophosphamide, and ifosfamide).
2 183L/L209A showing 3.5-fold enhancement with ifosfamide.
3 he anti-cancer prodrugs cyclophosphamide and ifosfamide.
4 ces might be explained by toxicities with HD ifosfamide.
5 ng the anticancer drugs cyclophosphamide and ifosfamide.
6 ically activated forms of CPA and its isomer ifosfamide.
7 dehyde, a metabolite of the anti-cancer drug ifosfamide.
8 l are discussed as well the evolving role of ifosfamide.
9 vation of the prodrugs, cyclophosphamide and ifosfamide.
10 ine, vinorelbine, paclitaxel, docetaxel, and ifosfamide.
11 osphamide or seven VAI-courses with 6 g/m(2) ifosfamide.
12 xorubicin and 227 to receive doxorubicin and ifosfamide.
13 the DNA cross-linking toxin of the prodrug, ifosfamide.
14 amide (HR 0.60, 95% CI 0.51-0.71; p<0.0001), ifosfamide (0.42, 0.23-0.79; p=0.0069), procarbazine (0.
15 tin 30 mg/m(2), gemcitabine 800 mg/m(2), and ifosfamide 1 g/m(2) were given on day 1 and then repeate
16 otherapy doses were cisplatin 20 mg/m(2) and ifosfamide 1,200 mg/m(2) on days 1 to 3 and etoposide 40
17 mg/m(2) administered over 3 hours on day 1; ifosfamide 1,200 mg/m(2) on days 1 to 3; and cisplatin 2
18 The dose and schedule of ITP were constant: ifosfamide 1,500 mg/m(2) (days 1 to 3); paclitaxel 200 m
19 of regimen A alternating every 3 weeks with ifosfamide 1,800 mg/m(2)/d for 5 days and etoposide 100
22 ere vinblastine 0.11 mg/kg/d (days 1 and 2), ifosfamide 1.2 gm/m2/d (days 1 through 5), and cisplatin
23 static or unresectable TCC were treated with ifosfamide 1.5 g/m2/d for 3 days with paclitaxel 200 mg/
24 phase II dose was vinorelbine 30 mg/m2 with ifosfamide 1.6 g/m2 both given on 3 consecutive days.
25 travenously (IV) daily for 3 days (arm 1) or ifosfamide 1.6 g/m2 IV daily for 3 days plus paclitaxel
26 receive doxorubicin 60 mg/m(2) and either SD ifosfamide (1.5 g/m(2)/d, days 1 through 4) or HD ifosfa
27 mg/m(2); 25 mg/m(2) per day, days 1-3) plus ifosfamide (10 g/m(2) over 4 days with mesna and pegfilg
28 mg/m2 for previously untreated patients, or ifosfamide 12 g/m2 and etoposide 1,000 mg/m2 for previou
29 base regimen, with the addition of high-dose ifosfamide (14 g/m(2)) at 2.8 g/m(2) per day with equido
30 Random assignment to treatment was between ifosfamide 2.0 g/m2 intravenously (IV) daily for 3 days
31 (100 mg/m(2) over 2 h on day 1), intravenous ifosfamide (2 g/m(2) over 3 h on days 10, 12, and 14), p
33 es of chemotherapy (CT: mitomycin 6 mg/m(2), ifosfamide 3 g/m(2), and cisplatin 50 mg/m(2)) every 21
35 djuvant chemotherapy with mitomycin 6 mg/m2, ifosfamide 3 g/m2, and cisplatin 50 mg/m2 and received b
36 amide (1.5 g/m(2)/d, days 1 through 4) or HD ifosfamide (3.0 g/m(2), days 1 through 4) every 21 days.
38 ates of cyclophosphamide 4-hydroxylation and ifosfamide 4-hydroxylation in human liver in a manner th
41 omization to six cycles of chemotherapy with ifosfamide 5 g/m2, carboplatin 300 mg/m2, etoposide 120
42 ed to receive either cisplatin (50 mg/m(2)), ifosfamide (5 g/m(2) over 24 hours), and mesna (6 g/m(2)
43 on day 1 followed by cisplatin (50 mg/m(2)), ifosfamide (5 g/m(2) over 24 hours), and mesna (6 g/m(2)
44 re of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own
45 ycles of augmented ICE (augICE; two doses of ifosfamide 5000 mg/m(2) in combination with mesna 5000 m
48 atin 100 mg/m(2), etoposide 375 mg/m(2), and ifosfamide 6 g/m(2) (VIP) plus three cycles of high-dose
49 Two cycles of paclitaxel 200 mg/m(2) plus ifosfamide 6 g/m(2) were given 2 weeks apart with leukap
50 with surgery and/or radiotherapy followed by ifosfamide 6 g/m2; doxorubicin 60 mg/m2; and vincristine
51 operative CT with epirubicin 120 mg/m(2) and ifosfamide 9 g/m(2) and granulocyte colony-stimulating f
52 rative cycles of epirubicin 120 mg/m(2) plus ifosfamide 9 g/m(2), and 160 were randomly assigned to t
54 standard doxorubicin 75 mg/m2 every 21 days, ifosfamide 9 g/m2 over 3 days continuous infusion, or if
55 ncluded four courses of vincristine 2 mg/m2; ifosfamide 9 g/m2; and doxorubicin 60 mg/m2 administered
56 cyclophosphamide (1.2 g/m2) alternating with ifosfamide (9 g/m2) and etoposide (500 mg/m2) for 14 cyc
60 re treated sequentially with doxorubicin and ifosfamide (AI), with rhTPO by a fixed dose and varying
61 tial, accelerated chemotherapy of paclitaxel/ifosfamide and carboplatin/etoposide administered with P
62 University, we recommend etoposide (VP-16), ifosfamide and cisplatin (VIPx4) instead of bleomycin, e
63 paclitaxel was evaluated in combination with ifosfamide and cisplatin as second-line chemotherapy for
65 posure) was a particularly potent inducer of ifosfamide and cyclophosphamide 4-hydroxylation, as well
67 se Palifosfamide is the active metabolite of ifosfamide and does not require prodrug activation, ther
68 cin (VDC), and dactinomycin alternating with ifosfamide and etoposide (IE) over VDC for patients with
69 egimens that incorporated a window of either ifosfamide and etoposide (IE) with vincristine, dactinom
70 orubicin, and methotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using concealed permute
73 MOS-1 results do not support the addition of ifosfamide and etoposide to postoperative chemotherapy i
75 zed trial evaluating whether the addition of ifosfamide and etoposide to vincristine, doxorubicin, cy
81 n involve the incorporation of drugs such as ifosfamide and taxol into conventional protocols or the
83 ndomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 double dagger 2 factorial d
85 of preoperative chemotherapy with mitomycin, ifosfamide, and cisplatin (MIC) on a cohort of 68 patien
87 received three to four cycles of paclitaxel, ifosfamide, and cisplatin (TIP) chemotherapy, and respon
88 to assess the effectiveness of vinblastine, ifosfamide, and cisplatin (VeIP) as second-line therapy
89 of all histologic subtypes with vinblastine, ifosfamide, and cisplatin (VeIP) will cure approximately
90 r-risk features were treated with etoposide, ifosfamide, and cisplatin (VIP) with or without high-dos
94 equently received four cycles of paclitaxel, ifosfamide, and cisplatin for relapse in the lungs and m
99 emotherapy (CT; modified mesna, doxorubicin, ifosfamide, and dacarbazine [MAID]), interdigitated preo
102 h-dose methotrexate, doxorubicin, cisplatin, ifosfamide, and etoposide to recognise and understand ra
103 (vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide), although the exact regimens
106 of front line regimens, such as doxorubicin, ifosfamide, and gemcitabine with docetaxel, are clearly
108 exploring the role of taxanes, gemcitabine, ifosfamide, and platinum in double and triple combinatio
111 eceived therapy with etoposide and high-dose ifosfamide, and to define the toxicity of this combinati
113 azaphosphorine prodrugs cyclophosphamide and ifosfamide are activated in human liver by a 4-hydroxyla
116 Toxicity was clearly greater with the HD ifosfamide arm, and lack of outcome differences might be
117 e 49%, 23%, and 10%, respectively, on the SD ifosfamide arm, compared with 88%, 58%, and 63%, respect
121 crosis increased to 48% with the addition of ifosfamide as compared with 13% of the patients in all t
125 A group of 23 children who had received ifosfamide at age 2.1-16.2 years (median 6.9) for variou
126 Sixty-three (26%) patients were treated with ifosfamide based chemotherapy (IF), 83 (34%) with doxoru
127 phosphamide or vincristine, actinomycin, and ifosfamide-based chemotherapy and proton radiation.
129 the responsiveness of tumor cells to CPA and ifosfamide, both in the context of conventional chemothe
130 with brentuximab vedotin (BV) and augmented ifosfamide, carboplatin, and etoposide (augICE), we asse
131 imab and platinum-based chemotherapy, either ifosfamide, carboplatin, and etoposide (ICE) or dexameth
132 le prognosis were treated with six cycles of ifosfamide, carboplatin, and etoposide (ICE), at 4-week
136 tive, patients received three cycles of ICE (ifosfamide, carboplatin, and etoposide) consolidation th
137 ients with chemosensitive disease after ICE (ifosfamide, carboplatin, and etoposide)-based salvage th
138 ther active agents in bladder cancer include ifosfamide, carboplatin, docetaxel, and vinorelbine, and
139 transplantation-eligible patients undergoing ifosfamide, carboplatin, etoposide (ICE) second-line che
141 investigated whether adding rituximab to the ifosfamide-carboplatin-etoposide (ICE) chemotherapy regi
142 /m2 orally on days 2 to 6, or cisplatin plus ifosfamide (CIFX) 5 g/m2 given as a 24-hour infusion plu
143 life in localized, unresectable (mitomycin, ifosfamide, cisplatin [MIC]1 trial) and extensive (MIC2
144 in, vincristine, cisplatin [BOP])/etoposide, ifosfamide, cisplatin, and bleomycin [VIP-B]), compared
146 eated with a salvage chemotherapy regimen of ifosfamide, cisplatin, and either vinblastine or etoposi
147 This pilot trial suggests that carboplatin/ifosfamide combination chemotherapy has substantial anti
150 robably caused by the use of higher doses of ifosfamide compared with relatively low doses of cycloph
152 of relapse, and relative tolerability as an ifosfamide-containing salvage regimen for testicular GCT
153 therapy comprised two additional carboplatin/ifosfamide cycles, doxorubicin, and high-dose methotrexa
156 the dose-schedule employed to cisplatin and ifosfamide did not improve outcome in patients with adva
159 analysed by multiple regression, only total ifosfamide dose was associated with proximal tubular tox
163 x patients were treated with EIA (etoposide, ifosfamide, doxorubicin)+RHT (>/=5 cycles: 69.7%) versus
165 duction chemotherapy containing vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) in standar
166 active agents for ES/PNET-cyclophosphamide, ifosfamide, doxorubicin, dactinomycin, vincristine, etop
169 ing of the intensity of cyclophosphamide (or ifosfamide equivalent) dosing per cycle between IRS-III
170 doxorubicin, vincristine, cyclophosphamide, ifosfamide, etoposide, and dactinomycin and identified p
171 ristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M
172 esults provide a rationale for incorporating ifosfamide, etoposide, doxorubicin, and topoisomerase I
175 M), and a new drug combination consisting of ifosfamide, etoposide, high-dose cytarabine (ara-C), and
176 r to a comparator (vinorelbine, oxaliplatin, ifosfamide, etoposide, mitoxantrone, or gemcitabine) giv
177 vincristine-doxorubicin-cyclophosphamide and ifosfamide-etoposide cycles and primary tumor treatment
179 ntenance included four alternating cycles of ifosfamide/etoposide and doxorubicin/CTX, with randomiza
180 048); patients enrolled onto IRS-III and the ifosfamide/etoposide and ifosfamide/doxorubicin trials f
182 gn that progress is not linear, 2 cousins of ifosfamide failed to show benefit in phase 3 trials, des
183 d an I.V. mesna dose given concurrently with ifosfamide, followed 2 and 8 hours later by oral adminis
185 k factors for long-term nephrotoxicity after ifosfamide for childhood cancers are not fully known.
186 pport the use of intensified doxorubicin and ifosfamide for palliation of advanced soft-tissue sarcom
188 significantly higher for the doxorubicin and ifosfamide group (7.4 months [95% CI 6.6-8.3]) than for
190 .3 months [12.5-16.5] in the doxorubicin and ifosfamide group; hazard ratio [HR] 0.83 [95.5% CI 0.67-
191 Combining doxorubicin with standard-dose ifosfamide has not been shown to improve survival and is
192 Cisplatin, mitolactol (dibromodulcitol), and ifosfamide have been the most active single agents in sq
193 of additional cytotoxic chemotherapy such as ifosfamide have not definitively improved the survival o
194 al of the TI-CE regimen (paclitaxel [T] plus ifosfamide [I] followed by high-dose carboplatin [C] plu
195 neurotoxic metabolite of the anticancer drug ifosfamide (IFA) and is a dose-limiting factor in IFA-ba
196 agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that requ
199 (CDP), and doxorubicin (ADM) with or without ifosfamide (IFO) in patients with nonmetastatic osteosar
204 her dose intensification of doxorubicin with ifosfamide improves survival of patients with advanced s
205 l asked whether cyclophosphamide may replace ifosfamide in combination with vincristine and dactinomy
206 Cyclophosphamide may be able to replace ifosfamide in consolidation treatment of standard-risk E
208 combination with low doses of cisplatin and ifosfamide in previously treated patients with advanced
209 y applicable to the ultratrace evaluation of ifosfamide in real (biological/pharmaceutical) samples w
210 Adjuvant chemotherapy with doxorubicin and ifosfamide in resected soft-tissue sarcoma showed no ben
212 ) over 24 hours), and mesna (6 g/m(2) during ifosfamide infusion and the following 12 hours) (CI) ver
213 ) over 24 hours), and mesna (6 g/m(2) during ifosfamide infusion and the following 12 hours) (CIB).
214 sna 6 g/m2 during and for 12 hours after the ifosfamide infusion, every 3 weeks for up to six courses
215 rapy regimen used (methotrexate with/without ifosfamide), intrinsic methodological problems and lack
216 The combination of etoposide and high-dose ifosfamide is effective induction chemotherapy for patie
217 This regimen of cisplatin, gemcitabine, and ifosfamide is not feasible for weekly administration bec
220 leomycin to the combination of cisplatin and ifosfamide may improve response rates and possible survi
221 rrow transplantation or up to four cycles of ifosfamide, mesna, and etoposide alternating with DECAL
225 dnisone followed by cycles containing either ifosfamide or cyclophosphamide; high-dose methotrexate,
226 toxicity of doxorubicin with high-dose (HD) ifosfamide or standard-dose (SD) ifosfamide in patients
228 e (AG) followed by the three-drug regimen of ifosfamide, paclitaxel, and cisplatin (ITP) in patients
230 doxorubicin and gemcitabine (AG) followed by ifosfamide, paclitaxel, and cisplatin (ITP) was previous
231 HR) with a GR received four cycles of PE and ifosfamide (PEI) at total doses of platinum 420 mg/m(2),
232 static GCTs were treated with paclitaxel and ifosfamide plus cisplatin (TIP) as second-line therapy.
233 reated GCTs were treated with paclitaxel and ifosfamide plus cisplatin (TIP) as second-line therapy.
234 with one or two courses of vinblastine plus ifosfamide plus cisplatin preceded the high-dose chemoth
235 ative options in the salvage setting include ifosfamide plus cisplatin-containing standard dose thera
238 ed CR with a conventional-dose cisplatin and ifosfamide program, and six experienced CR after high-do
239 osfamide, the combination of carboplatin and ifosfamide reduced the progressive disease rate at week
241 n, we found that the addition of carboplatin/ifosfamide resulted in patient outcomes comparable to tr
242 alone or the combination of doxorubicin and ifosfamide should be used routinely is still controversi
243 transformation pathways of cyclophosphamide, ifosfamide, tamoxifen, docetaxel, paclitaxel, and irinot
244 ch were all more common with doxorubicin and ifosfamide than with doxorubicin alone-were leucopenia (
245 th the historic population who received only ifosfamide, the combination of carboplatin and ifosfamid
246 injury caused by the chemotherapeutic agent ifosfamide, the problem of analgesic nephropathy, and th
249 rmation continues to support the addition of ifosfamide to standard chemotherapy regimens and help fu
250 compared with topoisomerase I poison trials, ifosfamide/topoisomerase II inhibitor trials had superio
251 ase, chemotherapy with anthracyclines and/or ifosfamide, trabectedin, or pazopanib has been demonstra
255 d cyclophosphamide (VAC, n = 235), or VA and ifosfamide (VAI, n = 222), or vincristine, ifosfamide, a
256 amide [VAC] v vincristine, dactinomycin, and ifosfamide [VAI]) after an intensive induction chemother
258 RMS were randomly assigned to receive either ifosfamide, vincristine, and dactinomycin (IVA) or a six
259 response rate to three cycles of carboplatin/ifosfamide was 67.7% (95% confidence interval, 55.0% to
260 pilot study in which the same total dose of ifosfamide was administered by a bolus schedule, along w
262 ly received treatment with anthracycline and ifosfamide were randomly assigned (1:1) to intravenous i
263 ilable for most sarcomas and doxorubicin and ifosfamide-which have been used to treat soft-tissue sar
264 nal work on chemotherapy regimens containing ifosfamide will undoubtedly stimulate interest in a new
265 on a novel (daily-times-three) schedule with ifosfamide with granulocyte colony-stimulating factor (G
266 ficant difference in 1-year DFS comparing SD ifosfamide with HD ifosfamide (55% v 52%; P = .81).
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