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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 l are discussed as well the evolving role of ifosfamide.
8 vation of the prodrugs, cyclophosphamide and ifosfamide.
9 ine, vinorelbine, paclitaxel, docetaxel, and ifosfamide.
10 1 prior treatment with anthracyclines and/or ifosfamide.
11 dehyde, a metabolite of the anti-cancer drug ifosfamide.
12 osphamide or seven VAI-courses with 6 g/m(2) ifosfamide.
13 xorubicin and 227 to receive doxorubicin and ifosfamide.
14  the DNA cross-linking toxin of the prodrug, ifosfamide.
15 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.
16 tin 30 mg/m(2), gemcitabine 800 mg/m(2), and ifosfamide 1 g/m(2) were given on day 1 and then repeate
17 otherapy doses were cisplatin 20 mg/m(2) and ifosfamide 1,200 mg/m(2) on days 1 to 3 and etoposide 40
18  mg/m(2) administered over 3 hours on day 1; ifosfamide 1,200 mg/m(2) on days 1 to 3; and cisplatin 2
19  The dose and schedule of ITP were constant: ifosfamide 1,500 mg/m(2) (days 1 to 3); paclitaxel 200 m
20  of regimen A alternating every 3 weeks with ifosfamide 1,800 mg/m(2)/d for 5 days and etoposide 100
21  5, and 7 consisted of 5 consecutive days of ifosfamide 1,800 mg/m2/d and etoposide 100 mg/m2/d.
22 ts were 12 lung cancer patients who received ifosfamide 1.2 g/m2 daily for 5 days.
23 ere vinblastine 0.11 mg/kg/d (days 1 and 2), ifosfamide 1.2 gm/m2/d (days 1 through 5), and cisplatin
24 static or unresectable TCC were treated with ifosfamide 1.5 g/m2/d for 3 days with paclitaxel 200 mg/
25  phase II dose was vinorelbine 30 mg/m2 with ifosfamide 1.6 g/m2 both given on 3 consecutive days.
26 travenously (IV) daily for 3 days (arm 1) or ifosfamide 1.6 g/m2 IV daily for 3 days plus paclitaxel
27 receive doxorubicin 60 mg/m(2) and either SD ifosfamide (1.5 g/m(2)/d, days 1 through 4) or HD ifosfa
28  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
29  mg/m2 for previously untreated patients, or ifosfamide 12 g/m2 and etoposide 1,000 mg/m2 for previou
30 base regimen, with the addition of high-dose ifosfamide (14 g/m(2)) at 2.8 g/m(2) per day with equido
31   Random assignment to treatment was between ifosfamide 2.0 g/m2 intravenously (IV) daily for 3 days
32 (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                            Patients received ifosfamide (2.5 g/m(2) per dose intravenously on days 1-
34                                       For SD ifosfamide, 2- and 3-year OS were 73% and 52% versus 57%
35 ateral nephrectomy (HR 4.2, 95% CI 2.3-7.7), ifosfamide (24.9, 7.4-83.5), total body irradiation (6.9
36          Chemotherapy included six cycles of ifosfamide 3 g/m(2) per dose intravenously on days 1-3 a
37 es of chemotherapy (CT: mitomycin 6 mg/m(2), ifosfamide 3 g/m(2), and cisplatin 50 mg/m(2)) every 21
38 e 9 g/m2 over 3 days continuous infusion, or ifosfamide 3 g/m2 per day in 3 hours over 3 days.
39 djuvant chemotherapy with mitomycin 6 mg/m2, ifosfamide 3 g/m2, and cisplatin 50 mg/m2 and received b
40 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.
41 um 420 mg/m(2), etoposide 1,200 mg/m(2), and ifosfamide 30 g/m(2).
42 ates of cyclophosphamide 4-hydroxylation and ifosfamide 4-hydroxylation in human liver in a manner th
43  min intravenous infusion, days 1, 2, and 3; ifosfamide 5 g/m(2) in 1000 mL in a 24 h intravenous inf
44 mg) with standard dosing of ICE on days 1-3 (ifosfamide 5 g/m(2) plus mesna 5 g/m(2) intravenously ov
45                   Four cycles of paclitaxel, ifosfamide 5 g/m(2), and cisplatin 100 mg/m(2) were give
46 ed of five cycles of doxorubicin 75 mg/m(2), ifosfamide 5 g/m(2), and lenograstim every 3 weeks.
47 omization to six cycles of chemotherapy with ifosfamide 5 g/m2, carboplatin 300 mg/m2, etoposide 120
48 ed to receive either cisplatin (50 mg/m(2)), ifosfamide (5 g/m(2) over 24 hours), and mesna (6 g/m(2)
49 on day 1 followed by cisplatin (50 mg/m(2)), ifosfamide (5 g/m(2) over 24 hours), and mesna (6 g/m(2)
50 re of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own
51 ycles of augmented ICE (augICE; two doses of ifosfamide 5000 mg/m(2) in combination with mesna 5000 m
52            Cumulative doses were as follows: ifosfamide 54 g/m(2) (both arms), epirubicin 450 mg/m(2)
53 n 1-year DFS comparing SD ifosfamide with HD ifosfamide (55% v 52%; P = .81).
54 atin 100 mg/m(2), etoposide 375 mg/m(2), and ifosfamide 6 g/m(2) (VIP) plus three cycles of high-dose
55    Two cycles of paclitaxel 200 mg/m(2) plus ifosfamide 6 g/m(2) were given 2 weeks apart with leukap
56 with surgery and/or radiotherapy followed by ifosfamide 6 g/m2; doxorubicin 60 mg/m2; and vincristine
57 operative CT with epirubicin 120 mg/m(2) and ifosfamide 9 g/m(2) and granulocyte colony-stimulating f
58 rative cycles of epirubicin 120 mg/m(2) plus ifosfamide 9 g/m(2), and 160 were randomly assigned to t
59             Courses 4, 5, and 7 consisted of ifosfamide 9 g/m2 and etoposide 500 mg/m2 for previously
60 standard doxorubicin 75 mg/m2 every 21 days, ifosfamide 9 g/m2 over 3 days continuous infusion, or if
61 ncluded four courses of vincristine 2 mg/m2; ifosfamide 9 g/m2; and doxorubicin 60 mg/m2 administered
62 cyclophosphamide (1.2 g/m2) alternating with ifosfamide (9 g/m2) and etoposide (500 mg/m2) for 14 cyc
63 doxorubicin (75 mg/m2), and three courses of ifosfamide (9,000 mg/m2)/etoposide (500 mg/m2).
64                       ICE chemotherapy, with ifosfamide administered as a 24-hour infusion to decreas
65              During the first 12 hours after ifosfamide administration, the amount of mesna excreted
66 are neoadjuvant standard (S) anthracycline + ifosfamide (AI) regimen with histology-tailored (HT) reg
67 re treated sequentially with doxorubicin and ifosfamide (AI), with rhTPO by a fixed dose and varying
68 tial, accelerated chemotherapy of paclitaxel/ifosfamide and carboplatin/etoposide administered with P
69  University, we recommend etoposide (VP-16), ifosfamide and cisplatin (VIPx4) instead of bleomycin, e
70 paclitaxel was evaluated in combination with ifosfamide and cisplatin as second-line chemotherapy for
71               Combinations of cisplatin plus ifosfamide and cisplatin plus mitolactol are prospective
72 posure) was a particularly potent inducer of ifosfamide and cyclophosphamide 4-hydroxylation, as well
73                   Mesna is administered with ifosfamide and cyclophosphamide to reduce the incidence
74 se Palifosfamide is the active metabolite of ifosfamide and does not require prodrug activation, ther
75 ve (regimen B) pazopanib in combination with ifosfamide and doxorubicin + preoperative radiotherapy f
76 cin (VDC), and dactinomycin alternating with ifosfamide and etoposide (IE) over VDC for patients with
77 egimens that incorporated a window of either ifosfamide and etoposide (IE) with vincristine, dactinom
78 orubicin, and methotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using concealed permute
79 A) or with these four drugs alternating with ifosfamide and etoposide (VACA-IE).
80                              The addition of ifosfamide and etoposide to a standard regimen does not
81 MOS-1 results do not support the addition of ifosfamide and etoposide to postoperative chemotherapy i
82                                       Adding ifosfamide and etoposide to standard therapy does not im
83 zed trial evaluating whether the addition of ifosfamide and etoposide to vincristine, doxorubicin, cy
84 oxorubicin, and vincristine alternating with ifosfamide and etoposide) and local control.
85                      A new drug combination, ifosfamide and etoposide, was highly effective in patien
86 these four drugs alternating with courses of ifosfamide and etoposide.
87                         The addition of both ifosfamide and MTP resulted in a 3-year EFS rate of 78%.
88 necessary to explain the interaction between ifosfamide and MTP.
89                                              Ifosfamide and other oxazaphosphorines can result in hem
90 n involve the incorporation of drugs such as ifosfamide and taxol into conventional protocols or the
91 erved an interaction between the addition of ifosfamide and the addition of MTP.
92 ndomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 double dagger 2 factorial d
93 ndomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 x 2 factorial design.
94 of preoperative chemotherapy with mitomycin, ifosfamide, and cisplatin (MIC) on a cohort of 68 patien
95                                  Paclitaxel, ifosfamide, and cisplatin (TIP) achieved complete respon
96 received three to four cycles of paclitaxel, ifosfamide, and cisplatin (TIP) chemotherapy, and respon
97  to assess the effectiveness of vinblastine, ifosfamide, and cisplatin (VeIP) as second-line therapy
98 of all histologic subtypes with vinblastine, ifosfamide, and cisplatin (VeIP) will cure approximately
99 r-risk features were treated with etoposide, ifosfamide, and cisplatin (VIP) with or without high-dos
100 50%) of 14 patients treated with paclitaxel, ifosfamide, and cisplatin achieved a continuous CR.
101       He received four courses of etoposide, ifosfamide, and cisplatin chemotherapy, given without bl
102                Chemotherapy with paclitaxel, ifosfamide, and cisplatin followed by surgery may be eff
103 equently received four cycles of paclitaxel, ifosfamide, and cisplatin for relapse in the lungs and m
104       The neoadjuvant regimen of paclitaxel, ifosfamide, and cisplatin induced clinically meaningful
105             With the failure of vinblastine, ifosfamide, and cisplatin to show any benefit over BEP (
106        Salvage regimens included paclitaxel, ifosfamide, and cisplatin, single agents, or a high-dose
107 bserved in patients treated with paclitaxel, ifosfamide, and cisplatin.
108 8-fold, particularly following procarbazine, ifosfamide, and cyclophosphamide.
109 ent contributions from each of procarbazine, ifosfamide, and cyclophosphamide.
110 emotherapy (CT; modified mesna, doxorubicin, ifosfamide, and dacarbazine [MAID]), interdigitated preo
111 active cytotoxic agents include doxorubicin, ifosfamide, and dacarbazine.
112 d ifosfamide (VAI, n = 222), or vincristine, ifosfamide, and etoposide (VIE, n = 236).
113  vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide is more effective, less toxic,
114 h-dose methotrexate, doxorubicin, cisplatin, ifosfamide, and etoposide to recognise and understand ra
115 (vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide), although the exact regimens
116 e, and etoposide v vincristine, carboplatin, ifosfamide, and etoposide).
117 y with cisplatin, doxorubicin, methotrexate, ifosfamide, and etoposide.
118 of front line regimens, such as doxorubicin, ifosfamide, and gemcitabine with docetaxel, are clearly
119 methotrexate, doxorubicin, cyclophosphamide, ifosfamide, and leucovorin dosage forms were collected b
120                The combination of cisplatin, ifosfamide, and oral etoposide (PIEo) given concurrently
121  exploring the role of taxanes, gemcitabine, ifosfamide, and platinum in double and triple combinatio
122 only CYP3A4 was induced by cyclophosphamide, ifosfamide, and rifampin.
123 , which consisted of carboplatin, etoposide, ifosfamide, and surgery.
124 eceived therapy with etoposide and high-dose ifosfamide, and to define the toxicity of this combinati
125                                              Ifosfamide- and cisplatin-containing therapy achieves a
126 azaphosphorine prodrugs cyclophosphamide and ifosfamide are activated in human liver by a 4-hydroxyla
127                  Paclitaxel, gemcitabine and ifosfamide are among the most active new agents.
128 d toxicity of cyclophosphamide compared with ifosfamide are debatable.
129     Toxicity was clearly greater with the HD ifosfamide arm, and lack of outcome differences might be
130 e 49%, 23%, and 10%, respectively, on the SD ifosfamide arm, compared with 88%, 58%, and 63%, respect
131 h 88%, 58%, and 63%, respectively, on the HD ifosfamide arm.
132  There were five early deaths, all on the HD ifosfamide arm.
133 and encephalopathy were more frequent in the ifosfamide arms.
134 crosis increased to 48% with the addition of ifosfamide as compared with 13% of the patients in all t
135          To determine if paclitaxel added to ifosfamide as first-line treatment for advanced uterine
136 nctional monomer, and an anticancerous drug, ifosfamide, as a print molecule (test analyte).
137 d to decrease the incidence of standard-dose ifosfamide-associated urothelial toxicity.
138      A group of 23 children who had received ifosfamide at age 2.1-16.2 years (median 6.9) for variou
139 Sixty-three (26%) patients were treated with ifosfamide based chemotherapy (IF), 83 (34%) with doxoru
140 phosphamide or vincristine, actinomycin, and ifosfamide-based chemotherapy and proton radiation.
141                                              Ifosfamide-based chemotherapy was associated with an imp
142 the responsiveness of tumor cells to CPA and ifosfamide, both in the context of conventional chemothe
143  with brentuximab vedotin (BV) and augmented ifosfamide, carboplatin, and etoposide (augICE), we asse
144 to evaluate the addition of pembrolizumab to ifosfamide, carboplatin, and etoposide (ICE) chemotherap
145 imab and platinum-based chemotherapy, either ifosfamide, carboplatin, and etoposide (ICE) or dexameth
146 le prognosis were treated with six cycles of ifosfamide, carboplatin, and etoposide (ICE), at 4-week
147 d HD, were treated with 2 biweekly cycles of ifosfamide, carboplatin, and etoposide (ICE).
148 h brentuximab vedotin, followed by augmented ifosfamide, carboplatin, and etoposide (ICE).
149 ssive disease were successfully rescued with ifosfamide, carboplatin, and etoposide therapy.
150 tive, patients received three cycles of ICE (ifosfamide, carboplatin, and etoposide) consolidation th
151 ients with chemosensitive disease after ICE (ifosfamide, carboplatin, and etoposide)-based salvage th
152 tor (itacitinib) or chemotherapy (rituximab, ifosfamide, carboplatin, and etoposide).
153 ther active agents in bladder cancer include ifosfamide, carboplatin, docetaxel, and vinorelbine, and
154 transplantation-eligible patients undergoing ifosfamide, carboplatin, etoposide (ICE) second-line che
155 ne, prednisone) followed by 3 cycles of ICE (ifosfamide, carboplatin, etoposide).
156 investigated whether adding rituximab to the ifosfamide-carboplatin-etoposide (ICE) chemotherapy regi
157 /m2 orally on days 2 to 6, or cisplatin plus ifosfamide (CIFX) 5 g/m2 given as a 24-hour infusion plu
158  life in localized, unresectable (mitomycin, ifosfamide, cisplatin [MIC]1 trial) and extensive (MIC2
159 us chemotherapy (CCRT-VIPD [etoposide/vp-16, ifosfamide, cisplatin and dexamethasone), 16.2 months fo
160 d every 2-5 years for survivors treated with ifosfamide, cisplatin, abdominal radiotherapy, total bod
161 in, vincristine, cisplatin [BOP])/etoposide, ifosfamide, cisplatin, and bleomycin [VIP-B]), compared
162 in, epirubicin, mitomycin, cyclophosphamide, ifosfamide, cisplatin, and carboplatin.
163 eated with a salvage chemotherapy regimen of ifosfamide, cisplatin, and either vinblastine or etoposi
164   This pilot trial suggests that carboplatin/ifosfamide combination chemotherapy has substantial anti
165 treated with conventional-dose cisplatin-and-ifosfamide combination chemotherapy.
166                These results suggest that HD ifosfamide combination regimens should not be used as fi
167 robably caused by the use of higher doses of ifosfamide compared with relatively low doses of cycloph
168 previous line of anthracycline-containing or ifosfamide-containing chemotherapy.
169                                         This ifosfamide-containing regimen is tolerable and effective
170  of relapse, and relative tolerability as an ifosfamide-containing salvage regimen for testicular GCT
171 therapy comprised two additional carboplatin/ifosfamide cycles, doxorubicin, and high-dose methotrexa
172    Pretreatment of rats with up to 100 mg/kg ifosfamide did not impair hepatic dimesna reduction.
173           When combined with doxorubicin, HD ifosfamide did not improve 1-year DFS and OS.
174  the dose-schedule employed to cisplatin and ifosfamide did not improve outcome in patients with adva
175             The relative value of increasing ifosfamide dose in combination chemotherapy for patients
176                             The median total ifosfamide dose was 100.8 (9.0-160.4) g/m2 over a median
177  analysed by multiple regression, only total ifosfamide dose was associated with proximal tubular tox
178                                   High total ifosfamide dose was the only risk factor we identified.
179 es equaled 20% and 40%, respectively, of the ifosfamide dose.
180 of mesna to prevent urothelial toxicity with ifosfamide doses that exceed 2.5 g/m(2)/d.
181 x patients were treated with EIA (etoposide, ifosfamide, doxorubicin)+RHT (>/=5 cycles: 69.7%) versus
182 consisted of high-dose methotrexate (HDMTX), ifosfamide, doxorubicin, and cisplatin.
183 hemotherapy with six courses of vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) and one co
184 duction chemotherapy containing vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) in standar
185 ly diagnosed Ewing sarcoma than vincristine, ifosfamide, doxorubicin, and etoposide induction and sho
186  active agents for ES/PNET-cyclophosphamide, ifosfamide, doxorubicin, dactinomycin, vincristine, etop
187 nto IRS-III and the ifosfamide/etoposide and ifosfamide/doxorubicin trials fared best.
188  that of a historic group that received only ifosfamide during the initial window evaluation.
189 ing of the intensity of cyclophosphamide (or ifosfamide equivalent) dosing per cycle between IRS-III
190  doxorubicin, vincristine, cyclophosphamide, ifosfamide, etoposide, and dactinomycin and identified p
191 ristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M
192 esults provide a rationale for incorporating ifosfamide, etoposide, doxorubicin, and topoisomerase I
193                       Induction consisted of ifosfamide, etoposide, doxorubicin, dactinomycin, cyclop
194                   The novel regimen IVE/MTX (ifosfamide, etoposide, epirubicin/methotrexate)-ASCT [co
195 M), and a new drug combination consisting of ifosfamide, etoposide, high-dose cytarabine (ara-C), and
196 r to a comparator (vinorelbine, oxaliplatin, ifosfamide, etoposide, mitoxantrone, or gemcitabine) giv
197 vincristine-doxorubicin-cyclophosphamide and ifosfamide-etoposide cycles and primary tumor treatment
198 oxorubicin-cyclophosphamide; cycles 2 and 4: ifosfamide-etoposide).
199 ntenance included four alternating cycles of ifosfamide/etoposide and doxorubicin/CTX, with randomiza
200 048); patients enrolled onto IRS-III and the ifosfamide/etoposide and ifosfamide/doxorubicin trials f
201          Induction comprised three cycles of ifosfamide/etoposide on days 1 to 3 and cyclophosphamide
202 gn that progress is not linear, 2 cousins of ifosfamide failed to show benefit in phase 3 trials, des
203 d an I.V. mesna dose given concurrently with ifosfamide, followed 2 and 8 hours later by oral adminis
204                          The substitution of ifosfamide for bleomycin, however, was associated with s
205 k factors for long-term nephrotoxicity after ifosfamide for childhood cancers are not fully known.
206 pport the use of intensified doxorubicin and ifosfamide for palliation of advanced soft-tissue sarcom
207                       Increasing exposure to ifosfamide from 90 to 140 g/m2, cyclophosphamide from 9.
208 significantly higher for the doxorubicin and ifosfamide group (7.4 months [95% CI 6.6-8.3]) than for
209         More patients in the doxorubicin and ifosfamide group than in the doxorubicin group had an ov
210 .3 months [12.5-16.5] in the doxorubicin and ifosfamide group; hazard ratio [HR] 0.83 [95.5% CI 0.67-
211     Combining doxorubicin with standard-dose ifosfamide has not been shown to improve survival and is
212 Cisplatin, mitolactol (dibromodulcitol), and ifosfamide have been the most active single agents in sq
213 of additional cytotoxic chemotherapy such as ifosfamide have not definitively improved the survival o
214 al of the TI-CE regimen (paclitaxel [T] plus ifosfamide [I] followed by high-dose carboplatin [C] plu
215 neurotoxic metabolite of the anticancer drug ifosfamide (IFA) and is a dose-limiting factor in IFA-ba
216  agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that requ
217                   Cyclophosphamide (CPA) and ifosfamide (IFA) are oxazaphosphorine anticancer prodrug
218                   Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer prodrugs tha
219 (CDP), and doxorubicin (ADM) with or without ifosfamide (IFO) in patients with nonmetastatic osteosar
220                              The efficacy of ifosfamide (IFO), an antineoplastic drug, is severely li
221                               In the case of ifosfamide (IFO), the bioactivation produces two toxic m
222                                              Ifosfamide (IFX) is an agent as yet unstudied in advance
223                          On the first cycle, ifosfamide (IFX), 2 gm/m2; carboplatin, 400 mg/m2; and e
224 drug sensitivity of oxaliplatin, carmustine, ifosfamide, imexon, lomustine, and BN-2629, indicating t
225 her dose intensification of doxorubicin with ifosfamide improves survival of patients with advanced s
226 l asked whether cyclophosphamide may replace ifosfamide in combination with vincristine and dactinomy
227      Cyclophosphamide may be able to replace ifosfamide in consolidation treatment of standard-risk E
228 ed-infusion ifosfamide in SS; etoposide plus ifosfamide in MPNST; and gemcitabine plus docetaxel in U
229 h-dose (HD) ifosfamide or standard-dose (SD) ifosfamide in patients with STS.
230  combination with low doses of cisplatin and ifosfamide in previously treated patients with advanced
231 y applicable to the ultratrace evaluation of ifosfamide in real (biological/pharmaceutical) samples w
232   Adjuvant chemotherapy with doxorubicin and ifosfamide in resected soft-tissue sarcoma showed no ben
233 rbazine in LMS; high-dose prolonged-infusion ifosfamide in SS; etoposide plus ifosfamide in MPNST; an
234                              The addition of ifosfamide in this dose schedule to standard chemotherap
235 could be therapeutically targeted to prevent ifosfamide-induced hemorrhagic cystitis.
236 ) over 24 hours), and mesna (6 g/m(2) during ifosfamide infusion and the following 12 hours) (CI) ver
237 ) over 24 hours), and mesna (6 g/m(2) during ifosfamide infusion and the following 12 hours) (CIB).
238 sna 6 g/m2 during and for 12 hours after the ifosfamide infusion, every 3 weeks for up to six courses
239 e-phase inflammation and oxidative stress in ifosfamide-injured bladder, which are reversed by pretre
240 rapy regimen used (methotrexate with/without ifosfamide), intrinsic methodological problems and lack
241   The combination of etoposide and high-dose ifosfamide is effective induction chemotherapy for patie
242  This regimen of cisplatin, gemcitabine, and ifosfamide is not feasible for weekly administration bec
243 s not known whether higher dose single-agent ifosfamide is superior to doxorubicin.
244 high-dose cytarabine (ara-C), etoposide, and ifosfamide (IVAC) for a total of four cycles.
245 leomycin to the combination of cisplatin and ifosfamide may improve response rates and possible survi
246 rrow transplantation or up to four cycles of ifosfamide, mesna, and etoposide alternating with DECAL
247 ifosfamide but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein.
248 other OAPs but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein.
249 ents randomly assigned to anthracycline plus ifosfamide (n = 98), sclerohyalinosis greater than 20% r
250 d treatment-related risk factors for chronic ifosfamide nephrotoxicity.
251 dnisone followed by cycles containing either ifosfamide or cyclophosphamide; high-dose methotrexate,
252  toxicity of doxorubicin with high-dose (HD) ifosfamide or standard-dose (SD) ifosfamide in patients
253 included methotrexate, bleomycin, etoposide, ifosfamide, oral morphine, and allopurinol.
254 S were 73% and 52% versus 57% and 49% for HD ifosfamide (P = .34).
255 e (AG) followed by the three-drug regimen of ifosfamide, paclitaxel, and cisplatin (ITP) in patients
256                          A phase II trial of ifosfamide, paclitaxel, and cisplatin (ITP) was conducte
257 doxorubicin and gemcitabine (AG) followed by ifosfamide, paclitaxel, and cisplatin (ITP) was previous
258 HR) with a GR received four cycles of PE and ifosfamide (PEI) at total doses of platinum 420 mg/m(2),
259 static GCTs were treated with paclitaxel and ifosfamide plus cisplatin (TIP) as second-line therapy.
260 reated GCTs were treated with paclitaxel and ifosfamide plus cisplatin (TIP) as second-line therapy.
261  with one or two courses of vinblastine plus ifosfamide plus cisplatin preceded the high-dose chemoth
262 ative options in the salvage setting include ifosfamide plus cisplatin-containing standard dose thera
263                                              Ifosfamide plus paclitaxel is the regimen with establish
264                            Chemotherapy from ifosfamide produces a specific pattern of injury to the
265 ed CR with a conventional-dose cisplatin and ifosfamide program, and six experienced CR after high-do
266 osfamide, the combination of carboplatin and ifosfamide reduced the progressive disease rate at week
267 these 4 drugs alternating with etoposide and ifosfamide (regimen B).
268 ived host modulatory protein, can ameliorate ifosfamide-related cystitis; however, the mechanisms und
269 n, we found that the addition of carboplatin/ifosfamide resulted in patient outcomes comparable to tr
270  alone or the combination of doxorubicin and ifosfamide should be used routinely is still controversi
271 transformation pathways of cyclophosphamide, ifosfamide, tamoxifen, docetaxel, paclitaxel, and irinot
272 ch were all more common with doxorubicin and ifosfamide than with doxorubicin alone-were leucopenia (
273 th the historic population who received only ifosfamide, the combination of carboplatin and ifosfamid
274  injury caused by the chemotherapeutic agent ifosfamide, the problem of analgesic nephropathy, and th
275                              The addition of ifosfamide to cisplatin, doxorubicin, and methotrexate d
276                              The addition of ifosfamide to standard chemotherapy achieved a 3-year EF
277 rmation continues to support the addition of ifosfamide to standard chemotherapy regimens and help fu
278 compared with topoisomerase I poison trials, ifosfamide/topoisomerase II inhibitor trials had superio
279 ase, chemotherapy with anthracyclines and/or ifosfamide, trabectedin, or pazopanib has been demonstra
280 k transcriptional profiling of bladders from ifosfamide-treated mice, with or without pretreatment wi
281                                              Ifosfamide treatment significantly inhibited oxidative p
282                                              Ifosfamide treatment upregulated a range of proinflammat
283  to the other regimen on days 2 through 5 of ifosfamide treatment.
284 ) versus a control regimen of vinorelbine or ifosfamide (V/I).
285 one course of vincristine, dactinomycin, and ifosfamide (VAI) before either BuMel or seven courses of
286 d cyclophosphamide (VAC, n = 235), or VA and ifosfamide (VAI, n = 222), or vincristine, ifosfamide, a
287 amide [VAC] v vincristine, dactinomycin, and ifosfamide [VAI]) after an intensive induction chemother
288 ived three cycles of PE plus three cycles of ifosfamide, vinblastine, and bleomycin.
289        Beginning in 2007, the IVADo regimen (ifosfamide, vincristine, actinomycin-D, and doxorubicin)
290 RMS were randomly assigned to receive either ifosfamide, vincristine, and dactinomycin (IVA) or a six
291 ion after standard treatment (nine cycles of ifosfamide, vincristine, dactinomycin with or without do
292 response rate to three cycles of carboplatin/ifosfamide was 67.7% (95% confidence interval, 55.0% to
293  pilot study in which the same total dose of ifosfamide was administered by a bolus schedule, along w
294                Two cycles of paclitaxel plus ifosfamide were administered with leukapheresis, followe
295 ly received treatment with anthracycline and ifosfamide were randomly assigned (1:1) to intravenous i
296 ilable for most sarcomas and doxorubicin and ifosfamide-which have been used to treat soft-tissue sar
297 nal work on chemotherapy regimens containing ifosfamide will undoubtedly stimulate interest in a new
298 on a novel (daily-times-three) schedule with ifosfamide with granulocyte colony-stimulating factor (G
299 ficant difference in 1-year DFS comparing SD ifosfamide with HD ifosfamide (55% v 52%; P = .81).
300                                 Inclusion of ifosfamide with or without etoposide made no difference

 
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