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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
20  5, and 7 consisted of 5 consecutive days of ifosfamide 1,800 mg/m2/d and etoposide 100 mg/m2/d.
21 ts were 12 lung cancer patients who received ifosfamide 1.2 g/m2 daily for 5 days.
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
32                                       For SD ifosfamide, 2- and 3-year OS were 73% and 52% versus 57%
33 es of chemotherapy (CT: mitomycin 6 mg/m(2), ifosfamide 3 g/m(2), and cisplatin 50 mg/m(2)) every 21
34 e 9 g/m2 over 3 days continuous infusion, or ifosfamide 3 g/m2 per day in 3 hours over 3 days.
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.
37 um 420 mg/m(2), etoposide 1,200 mg/m(2), and ifosfamide 30 g/m(2).
38 ates of cyclophosphamide 4-hydroxylation and ifosfamide 4-hydroxylation in human liver in a manner th
39                   Four cycles of paclitaxel, ifosfamide 5 g/m(2), and cisplatin 100 mg/m(2) were give
40 ed of five cycles of doxorubicin 75 mg/m(2), ifosfamide 5 g/m(2), and lenograstim every 3 weeks.
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
46            Cumulative doses were as follows: ifosfamide 54 g/m(2) (both arms), epirubicin 450 mg/m(2)
47 n 1-year DFS comparing SD ifosfamide with HD ifosfamide (55% v 52%; P = .81).
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
53             Courses 4, 5, and 7 consisted of ifosfamide 9 g/m2 and etoposide 500 mg/m2 for previously
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
57 doxorubicin (75 mg/m2), and three courses of ifosfamide (9,000 mg/m2)/etoposide (500 mg/m2).
58                       ICE chemotherapy, with ifosfamide administered as a 24-hour infusion to decreas
59              During the first 12 hours after ifosfamide administration, the amount of mesna excreted
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
64               Combinations of cisplatin plus ifosfamide and cisplatin plus mitolactol are prospective
65 posure) was a particularly potent inducer of ifosfamide and cyclophosphamide 4-hydroxylation, as well
66                   Mesna is administered with ifosfamide and cyclophosphamide to reduce the incidence
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
71 A) or with these four drugs alternating with ifosfamide and etoposide (VACA-IE).
72                              The addition of ifosfamide and etoposide to a standard regimen does not
73 MOS-1 results do not support the addition of ifosfamide and etoposide to postoperative chemotherapy i
74                                       Adding ifosfamide and etoposide to standard therapy does not im
75 zed trial evaluating whether the addition of ifosfamide and etoposide to vincristine, doxorubicin, cy
76 oxorubicin, and vincristine alternating with ifosfamide and etoposide) and local control.
77                      A new drug combination, ifosfamide and etoposide, was highly effective in patien
78 these four drugs alternating with courses of ifosfamide and etoposide.
79                         The addition of both ifosfamide and MTP resulted in a 3-year EFS rate of 78%.
80 necessary to explain the interaction between ifosfamide and MTP.
81 n involve the incorporation of drugs such as ifosfamide and taxol into conventional protocols or the
82 erved an interaction between the addition of ifosfamide and the addition of MTP.
83 ndomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 double dagger 2 factorial d
84 ndomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 x 2 factorial design.
85 of preoperative chemotherapy with mitomycin, ifosfamide, and cisplatin (MIC) on a cohort of 68 patien
86                                  Paclitaxel, ifosfamide, and cisplatin (TIP) achieved complete respon
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
91 50%) of 14 patients treated with paclitaxel, ifosfamide, and cisplatin achieved a continuous CR.
92       He received four courses of etoposide, ifosfamide, and cisplatin chemotherapy, given without bl
93                Chemotherapy with paclitaxel, ifosfamide, and cisplatin followed by surgery may be eff
94 equently received four cycles of paclitaxel, ifosfamide, and cisplatin for relapse in the lungs and m
95       The neoadjuvant regimen of paclitaxel, ifosfamide, and cisplatin induced clinically meaningful
96             With the failure of vinblastine, ifosfamide, and cisplatin to show any benefit over BEP (
97        Salvage regimens included paclitaxel, ifosfamide, and cisplatin, single agents, or a high-dose
98 bserved in patients treated with paclitaxel, ifosfamide, and cisplatin.
99 emotherapy (CT; modified mesna, doxorubicin, ifosfamide, and dacarbazine [MAID]), interdigitated preo
100 active cytotoxic agents include doxorubicin, ifosfamide, and dacarbazine.
101 d ifosfamide (VAI, n = 222), or vincristine, ifosfamide, and etoposide (VIE, n = 236).
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
104 e, and etoposide v vincristine, carboplatin, ifosfamide, and etoposide).
105 y with cisplatin, doxorubicin, methotrexate, ifosfamide, and etoposide.
106 of front line regimens, such as doxorubicin, ifosfamide, and gemcitabine with docetaxel, are clearly
107                The combination of cisplatin, ifosfamide, and oral etoposide (PIEo) given concurrently
108  exploring the role of taxanes, gemcitabine, ifosfamide, and platinum in double and triple combinatio
109 only CYP3A4 was induced by cyclophosphamide, ifosfamide, and rifampin.
110 , which consisted of carboplatin, etoposide, ifosfamide, and surgery.
111 eceived therapy with etoposide and high-dose ifosfamide, and to define the toxicity of this combinati
112                                              Ifosfamide- and cisplatin-containing therapy achieves a
113 azaphosphorine prodrugs cyclophosphamide and ifosfamide are activated in human liver by a 4-hydroxyla
114                  Paclitaxel, gemcitabine and ifosfamide are among the most active new agents.
115 d toxicity of cyclophosphamide compared with ifosfamide are debatable.
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
118 h 88%, 58%, and 63%, respectively, on the HD ifosfamide arm.
119  There were five early deaths, all on the HD ifosfamide arm.
120 and encephalopathy were more frequent in the ifosfamide arms.
121 crosis increased to 48% with the addition of ifosfamide as compared with 13% of the patients in all t
122          To determine if paclitaxel added to ifosfamide as first-line treatment for advanced uterine
123 nctional monomer, and an anticancerous drug, ifosfamide, as a print molecule (test analyte).
124 d to decrease the incidence of standard-dose ifosfamide-associated urothelial toxicity.
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.
128                                              Ifosfamide-based chemotherapy was associated with an imp
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
133 d HD, were treated with 2 biweekly cycles of ifosfamide, carboplatin, and etoposide (ICE).
134 h brentuximab vedotin, followed by augmented ifosfamide, carboplatin, and etoposide (ICE).
135 ssive disease were successfully rescued with ifosfamide, carboplatin, and etoposide therapy.
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
140 ne, prednisone) followed by 3 cycles of ICE (ifosfamide, carboplatin, etoposide).
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
145 in, epirubicin, mitomycin, cyclophosphamide, ifosfamide, cisplatin, and carboplatin.
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
148 treated with conventional-dose cisplatin-and-ifosfamide combination chemotherapy.
149                These results suggest that HD ifosfamide combination regimens should not be used as fi
150 robably caused by the use of higher doses of ifosfamide compared with relatively low doses of cycloph
151                                         This ifosfamide-containing regimen is tolerable and effective
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
154    Pretreatment of rats with up to 100 mg/kg ifosfamide did not impair hepatic dimesna reduction.
155           When combined with doxorubicin, HD ifosfamide did not improve 1-year DFS and OS.
156  the dose-schedule employed to cisplatin and ifosfamide did not improve outcome in patients with adva
157             The relative value of increasing ifosfamide dose in combination chemotherapy for patients
158                             The median total ifosfamide dose was 100.8 (9.0-160.4) g/m2 over a median
159  analysed by multiple regression, only total ifosfamide dose was associated with proximal tubular tox
160                                   High total ifosfamide dose was the only risk factor we identified.
161 es equaled 20% and 40%, respectively, of the ifosfamide dose.
162 of mesna to prevent urothelial toxicity with ifosfamide doses that exceed 2.5 g/m(2)/d.
163 x patients were treated with EIA (etoposide, ifosfamide, doxorubicin)+RHT (>/=5 cycles: 69.7%) versus
164 consisted of high-dose methotrexate (HDMTX), ifosfamide, doxorubicin, and cisplatin.
165 duction chemotherapy containing vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) in standar
166  active agents for ES/PNET-cyclophosphamide, ifosfamide, doxorubicin, dactinomycin, vincristine, etop
167 nto IRS-III and the ifosfamide/etoposide and ifosfamide/doxorubicin trials fared best.
168  that of a historic group that received only ifosfamide during the initial window evaluation.
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
173                       Induction consisted of ifosfamide, etoposide, doxorubicin, dactinomycin, cyclop
174                   The novel regimen IVE/MTX (ifosfamide, etoposide, epirubicin/methotrexate)-ASCT [co
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
178 oxorubicin-cyclophosphamide; cycles 2 and 4: ifosfamide-etoposide).
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
181          Induction comprised three cycles of ifosfamide/etoposide on days 1 to 3 and cyclophosphamide
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
184                          The substitution of ifosfamide for bleomycin, however, was associated with s
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
187                       Increasing exposure to ifosfamide from 90 to 140 g/m2, cyclophosphamide from 9.
188 significantly higher for the doxorubicin and ifosfamide group (7.4 months [95% CI 6.6-8.3]) than for
189         More patients in the doxorubicin and ifosfamide group than in the doxorubicin group had an ov
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
197                   Cyclophosphamide (CPA) and ifosfamide (IFA) are oxazaphosphorine anticancer prodrug
198                   Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer prodrugs tha
199 (CDP), and doxorubicin (ADM) with or without ifosfamide (IFO) in patients with nonmetastatic osteosar
200                              The efficacy of ifosfamide (IFO), an antineoplastic drug, is severely li
201                               In the case of ifosfamide (IFO), the bioactivation produces two toxic m
202                                              Ifosfamide (IFX) is an agent as yet unstudied in advance
203                          On the first cycle, ifosfamide (IFX), 2 gm/m2; carboplatin, 400 mg/m2; and e
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
207 h-dose (HD) ifosfamide or standard-dose (SD) ifosfamide in patients with STS.
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
211                              The addition of ifosfamide in this dose schedule to standard chemotherap
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
218 s not known whether higher dose single-agent ifosfamide is superior to doxorubicin.
219 high-dose cytarabine (ara-C), etoposide, and ifosfamide (IVAC) for a total of four cycles.
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
222 ifosfamide but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein.
223 other OAPs but not to phosphoramide mustard, ifosfamide mustard, melphalan, or acrolein.
224 d treatment-related risk factors for chronic ifosfamide nephrotoxicity.
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
227 S were 73% and 52% versus 57% and 49% for HD ifosfamide (P = .34).
228 e (AG) followed by the three-drug regimen of ifosfamide, paclitaxel, and cisplatin (ITP) in patients
229                          A phase II trial of ifosfamide, paclitaxel, and cisplatin (ITP) was conducte
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
236                                              Ifosfamide plus paclitaxel is the regimen with establish
237                            Chemotherapy from ifosfamide produces a specific pattern of injury to the
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
240 these 4 drugs alternating with etoposide and ifosfamide (regimen B).
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
247                              The addition of ifosfamide to cisplatin, doxorubicin, and methotrexate d
248                              The addition of ifosfamide to standard chemotherapy achieved a 3-year EF
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
252                                              Ifosfamide treatment significantly inhibited oxidative p
253  to the other regimen on days 2 through 5 of ifosfamide treatment.
254 ) versus a control regimen of vinorelbine or ifosfamide (V/I).
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
257 ived three cycles of PE plus three cycles of ifosfamide, vinblastine, and bleomycin.
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
261                Two cycles of paclitaxel plus ifosfamide were administered with leukapheresis, followe
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).
267                                 Inclusion of ifosfamide with or without etoposide made no difference

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