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1 toxicity of, SN38 (the active metabolite of irinotecan).
2 isting of a platinum agent plus etoposide or irinotecan.
3 nsitivity to SN-38, the active metabolite of irinotecan.
4 tic index of SN-38, the active metabolite of irinotecan.
5 s active metabolite SN-38 compared with free irinotecan.
6 luding a fluoropyrimidine and oxaliplatin or irinotecan.
7 otype can be used to individualize dosing of irinotecan.
8 n PFS between treatment arms with or without irinotecan.
9 imination of SN-38, the active metabolite of irinotecan.
10 ded dosing on efficacy in patients receiving irinotecan.
11 droxycamptothecin), the active metabolite of irinotecan.
12 ess the distribution of the anticancer drug, irinotecan.
13 FL118 shows structural similarity to irinotecan.
14 rs as a single agent and in combination with irinotecan.
15 stemic chemotherapy including oxaliplatin or irinotecan.
16 and its clinical derivatives, topotecan and irinotecan.
17 n two repeat dose schedules, was superior to irinotecan.
18 ent of malignant glioma with bevacizumab and irinotecan.
19 s systemic chemotherapy with oxaliplatin and irinotecan.
20 icantly enhances the bioavailability of oral irinotecan.
21 ation, particularly with orally administered irinotecan.
22 o those reported with protracted intravenous irinotecan.
23 rontline colorectal cancer chemotherapy drug irinotecan.
24 delivery of SN-38, the active metabolite of irinotecan.
25 osis, and were refractory to oxaliplatin and irinotecan.
26 combinatorial treatment of Pitavastatin and Irinotecan.
27 ther cetuximab monotherapy or cetuximab plus irinotecan.
28 8-a prodrug of the topoisomerase I inhibitor irinotecan.
30 emotherapy and had relapsed disease received irinotecan 150 mg/m(2) and carboplatin AUC of 5 (arm B).
33 5, 150, 250 mg/m(2)) in a 3 + 3 design, plus irinotecan (16 or 20 mg/m(2)/d) for 5 days for 2 consecu
34 received adjuvant oxaliplatin could receive irinotecan 180 mg/m(2) intravenously over 30 min with fl
36 er FOLFIRINOX alone (oxaliplatin 85 mg/m(2), irinotecan 180 mg/m(2), leucovorin 400 mg/m(2), and bolu
37 ay cycle consisted of bevacizumab (5 mg/kg), irinotecan (180 mg/m(2)), bolus FU (400 mg/m(2)), and le
38 receive FOLFIRINOX (oxaliplatin, 85 mg/m(2); irinotecan, 180 mg/m(2); leucovorin, 400 mg/m(2); and fl
39 otecan with vincristine: regimen 1A included irinotecan 20 mg/m(2)/d intravenously for 5 days at week
40 tients with extensive SCLC were treated with irinotecan 200 mg/m(2) and carboplatin area under the cu
42 d with bevacizumab alone or bevacizumab plus irinotecan, 46.4% and 65.8%, respectively, experienced g
43 80 mg/m(2) per day on days 1 to 7 along with irinotecan 50 mg/m(2) intravenously and temozolomide 100
44 of weeks 1, 2, 4, and 5; regimen 1B included irinotecan 50 mg/m(2)/d intravenously for 5 days at week
46 omide (100 mg/m(2) per dose) and intravenous irinotecan (50 mg/m(2) per dose) on days 1-5 of 21-day c
48 the second oxaliplatin (5 mg/kg), the third irinotecan (80 mg/kg) plus oxaliplatin (5 mg/kg), and th
51 with distinct circadian toxicity patterns of irinotecan, a topoisomerase I inhibitor active against c
53 administered at doses 5-fold lower than free irinotecan achieved similar intratumoral exposure of SN-
54 se (MTD) and dose limiting toxicity (DLT) of irinotecan administered in combination with vincristine,
57 ealed that compound 18a was more potent than irinotecan against HT-29 cells and was as potent as irin
59 n with panitumumab) vs 4.4 [2.8-6.7] months (irinotecan alone); HR, 0.38 [95% CI, 0.24-0.61]; P < .00
61 hese lines were tested for their response to irinotecan and a Chk1 inhibitor (either UCN-01 or AZD776
63 4 (MRP4), such as the anti-colon cancer drug irinotecan and an anti-retroviral used to treat HIV infe
65 trial to evaluate a novel 21-day schedule of irinotecan and carboplatin in patients with relapsed or
67 phase II trial evaluating the combination of irinotecan and cetuximab every second week, as third-lin
69 ntified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinom
70 ve higher intratumoral levels of the prodrug irinotecan and its active metabolite SN-38 compared with
71 cted the abundance change of anticancer drug irinotecan and its metabolites inside spheroids treated
74 FOLFIRINOX (leucovorin and fluorouracil plus irinotecan and oxaliplatin) in patients with locally adv
76 learance (an inverse measure of exposure) of irinotecan and SN-38 by 37% and 38%, respectively (P < .
77 dose for 7 days is tolerable with a standard irinotecan and temozolomide backbone and has promising r
78 ine the response rate associated with use of irinotecan and temozolomide for children with relapsed/r
83 as used to randomly assign patients (1:1) to irinotecan and temozolomide plus either temsirolimus or
87 he cancer chemotherapeutics derived from it, irinotecan and topotecan, are highly specific inhibitors
89 y of 5c with SN-38 (the active metabolite of irinotecan) and 5-fluorouracil on cell proliferation und
90 tween FOLFIRI (fluorouracil, leucovorin, and irinotecan) and ECX (epirubicin, cisplatin,and capecitab
93 a randomized clinical trial of panitumumab, irinotecan, and ciclosporin in colorectal cancer (PICCOL
94 therapy (comprising oxaliplatin, leucovorin, irinotecan, and fluorouracil) in patients with metastati
96 of folinic acid (leucovorin), fluorouracil, irinotecan, and oxaliplatin (FOLFIRINOX), restrict their
97 tatic setting (eg, fluorouracil, leucovorin, irinotecan, and oxaliplatin and gemcitabine plus nanopar
98 mbinations such as fluorouracil, leucovorin, irinotecan, and oxaliplatin as well as gemcitabine/nab-p
99 OX (fluorouracil, folinic acid [leucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nanopa
101 e combination of a WEE1 inhibitor (AZD1775), irinotecan, and vincristine can lead to complete respons
102 ptothecin and its derivatives, topotecan and irinotecan, are specific topoisomerase I (Top1) inhibito
105 cer camptothecins (CPTs) (e.g. topotecan and irinotecan) as well as structurally perturbed DNAs (e.g.
107 in at 65 mg/m(2), leucovorin at 400 mg/m(2), irinotecan at 140 mg/m(2), and fluorouracil 400 mg/m(2)
110 urve (AUCs; r(2) = 0.0003; P = .97), but the irinotecan AUC was correlated with the actual dose (r(2)
112 can (80 mg/m(2), equivalent to 70 mg/m(2) of irinotecan base) with fluorouracil and folinic acid ever
113 antage of bevacizumab was more apparent with irinotecan-based chemotherapy (HR, 0.80; 95% CI, 0.66 to
114 re aggressive intervention (oxaliplatin- and irinotecan-based chemotherapy and/or surgery for recurre
115 ed to be candidates for oxaliplatin-based or irinotecan-based chemotherapy regimens, were randomly as
116 h mCRC treated with bev plus oxaliplatin- or irinotecan-based chemotherapy, and correlated treatment
117 and 2011 and treated with oxaliplatin and/or irinotecan-based preoperative chemotherapy were eligible
119 management of treatment with bevacizumab and irinotecan (BEV/IR) in patients with recurrent high-grad
121 itinib increased the bioavailability of oral irinotecan by four-fold over that observed in historical
122 ur work shows how liposomal encapsulation of irinotecan can safely improve its antitumor activity in
123 with p65 siRNA photothermal transfection and irinotecan caused substantially enhanced tumor apoptosis
125 -erbalpha and Bmal1 mRNA expressions and for irinotecan chronotoxicity in clock-altered Per2(m/m) mic
128 ant KRAS tumors indicated that the anti-DLL4/irinotecan combination produced a significant decrease i
129 ties for the clinical translation of PDT and irinotecan combination therapy for effective pancreatic
130 erval, pretreatment with an 80 mg/kg dose of irinotecan combined with 2 fractions of 4.5 Gy in a 24-h
131 ine the maximum-tolerated dose (MTD) of oral irinotecan combined with temozolomide in children with r
132 ds Eligible patients with at least one prior irinotecan-containing therapy received labetuzumab govit
133 re recruited to a three-arm design including irinotecan (control), irinotecan plus ciclosporin, and i
134 Here, we prepared PEG conjugates of the irinotecan (CPT-11) active metabolite SN-38 via a phenyl
135 orphism, that can explain the variability in irinotecan (CPT-11) pharmacokinetics and neutropenia in
136 expression is associated with resistance to irinotecan (CPT-11) therapy in preclinical colorectal ca
137 A phase II study of bevacizumab (BVZ) plus irinotecan (CPT-11) was conducted in children with recur
143 both groups received 350 mg/m(2) intravenous irinotecan every 3 weeks (300 mg/m(2) if aged >/=70 year
144 as infusional fluorouracil, leucovorin, and irinotecan (FOLFIRI) or fluorouracil, leucovorin, and ox
145 ith first-line fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Com
146 ith first-line fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Com
147 combination of leucovorin, fluorouracil, and irinotecan (FOLFIRI) regimen is superior as first-line t
148 f cetuximab to fluorouracil, leucovorin, and irinotecan (FOLFIRI) significantly improved overall surv
150 h fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) showed superior efficacy as compa
151 r sensitivity to FOLFIRI [5-fluorouracil(FU)+irinotecan+folinic acid] than to FOLFOX (5-FU+oxaliplati
152 e combination regimen was 15 mg/m(2)/d of IV irinotecan for 5 days of 2 consecutive weeks and 112.5 m
153 -line FOLFIRI (leucovorin, fluorouracil, and irinotecan) for metastatic colorectal cancer in patients
154 tudy design included two dose levels (DL) of irinotecan given intravenously once daily for 5 consecut
156 ents (3.8%) patients in the bevacizumab-plus-irinotecan group (grades 1, 2, and 4, respectively).
162 e bevacizumab-alone and the bevacizumab-plus-irinotecan groups, estimated 6-month progression-free su
165 n with panitumumab) vs 4.0 [2.7-7.5] months (irinotecan); HR, 0.93 [95% CI, 0.64-1.37]; P = .73; inte
166 tment (85 mg/m2 of oxaliplatin, 180 mg/m2 of irinotecan hydrochloride, 400 mg/m2 of leucovorin calciu
167 identified a patient prescribed a regimen of irinotecan hydrochloride, cetuximab, and ramucirumab for
168 is of new liver and lung metastases in 2010, irinotecan in 2011, and then cetuximab until progression
169 in combination with cisplatin, docetaxel, or irinotecan in a multi-institutional, randomized, phase I
171 lus cetuximab in the Cetuximab Combined With Irinotecan in First-line Therapy for Metastatic Colorect
172 lus cetuximab in the Cetuximab Combined With Irinotecan in First-line Therapy for Metastatic Colorect
173 se (MTD) and dose-limiting toxicity (DLT) of irinotecan in patients with advanced solid tumors strati
174 ated adjuvant chemotherapy containing FU and irinotecan in patients with MMR deficient (MMR-D) colon
175 ess cetuximab monotherapy and cetuximab plus irinotecan in patients with molecularly selected (G13D m
176 was to assess the addition of panitumumab to irinotecan in pretreated advanced colorectal cancer.
177 e the cytotoxicity of the DNA damaging agent irinotecan in TNBC using xenotransplant tumor models.
179 0203, FOLFIRI (fluorouracil, leucovorin, and irinotecan) in study 20050181, or best supportive care i
180 f bevacizumab, alone and in combination with irinotecan, in patients with recurrent glioblastoma in a
181 irmed by encapsulating a cancer therapeutic, irinotecan, in the compartment containing the acetal-mod
182 l (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD)
188 otherapy either alone or in combination with irinotecan (IRI) in the Federation Francophone de Cancer
189 rms were evaluated: IFL (fluorouracil [FU] + irinotecan [IRN]), FOLFOX (FU + oxaliplatin), and IROX (
191 e/dexamethasone and systemic oxaliplatin and irinotecan is an effective regimen for the treatment of
193 use protracted administration of intravenous irinotecan is costly and inconvenient, we sought to dete
194 sk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant th
197 ct, and it was increased in combination with irinotecan, leading to tumor regression and replacement
198 leucovorin, and oxaliplatin was superior to irinotecan, leucovorin, and fluorouracil as a first-line
200 nfusion via a hepatic arterial pump or port, irinotecan-loaded drug-eluting beads, and radioembolizat
201 In this issue of the JCI, Liu et al. use irinotecan-loaded nanoparticles to treat pancreatic aden
202 nistration of iRGD enhanced the uptake of an irinotecan-loaded silicasome carrier that comprises lipi
203 monstrate that iRGD enhances the efficacy of irinotecan-loaded silicasome-based therapy and may be a
204 served with the combination of cetuximab and irinotecan may reflect true drug synergy or persistent i
205 ral location to receive either nanoliposomal irinotecan monotherapy (120 mg/m(2) every 3 weeks, equiv
206 acil and folinic acid (n=117), nanoliposomal irinotecan monotherapy (n=151), or fluorouracil and foli
207 ffer between patients assigned nanoliposomal irinotecan monotherapy and those allocated fluorouracil
208 received fluoropyrimidines, oxaliplatin, and irinotecan; most [91%] had also received cetuximab) were
210 tic cancer, combining PDP with nanoliposomal irinotecan (nal-IRI) prevented tumor relapse, reduced me
219 itabine and/or bevacizumab, cetuximab and/or irinotecan, or erlotinib resulted in increased antitumor
220 dity profile; fluorouracil plus oxaliplatin, irinotecan, or nanoliposomal irinotecan should be offere
222 rectal radiotherapy, and the use of combined irinotecan/oxaliplatin chemotherapy were more frequent i
223 4.3 months (95% CI, 12.0 to 15.9 months) for irinotecan (P = .38; hazard ratio = 0.92; 95% CI, 0.8 to
224 nitial dose, then 250 mg/m(2) per week) plus irinotecan, patients with </= grade 1 skin reactions wer
225 ombination of fluorouracil, oxaliplatin, and irinotecan plus bevacizumab (FOLFOXIRI-Bev) is an establ
226 e-arm design including irinotecan (control), irinotecan plus ciclosporin, and irinotecan plus panitum
227 and continuous-infusion fluorouracil (ECF), irinotecan plus cisplatin (IC), or FOLFOX (oxaliplatin,
229 were randomly assigned either nanoliposomal irinotecan plus fluorouracil and folinic acid (n=117), n
230 survival in patients assigned nanoliposomal irinotecan plus fluorouracil and folinic acid was 6.1 mo
231 y in the 117 patients assigned nanoliposomal irinotecan plus fluorouracil and folinic acid were neutr
233 incidence of early nausea for patients given irinotecan plus oxaliplatin (IROX) compared with those g
234 had longer overall survival than both IROX [irinotecan plus oxaliplatin] and IFL [irinotecan and bol
236 toneal dosing of the clinically used prodrug irinotecan produces high initial and local concentration
238 inotecan treatment, we also demonstrate that irinotecan reduced the tumoral expression of monocarboxy
239 f cetuximab dose escalation in patients with irinotecan-refractory metastatic colorectal cancer who h
241 n systemic chemotherapy using oxaliplatin or irinotecan remains unknown for patients with resected li
242 identify perturbed chromatin acetylation in irinotecan resistance and establish HDAC inhibitors as p
243 ated colorectal cancer (CRC) cell models for irinotecan resistance and report that resistance is neit
248 us oxaliplatin, irinotecan, or nanoliposomal irinotecan should be offered to patients with first-line
250 FL118 was no better than the active form of irinotecan, SN-38 at 1 microM, FL118 effectively inhibit
251 PDT and a subclinical dose of nanoliposomal irinotecan synergistically inhibited tumor growth by 70%
252 e addition of temsirolimus or dinutuximab to irinotecan-temozolomide in patients with relapsed or ref
257 ng 35 patients, 18 were randomly assigned to irinotecan-temozolomide-temsirolimus and 17 to irinoteca
261 anthracycline, 4 cisplatin, 1 paclitaxel, 1 irinotecan) that meet inclusion criteria, with a total o
262 which tested the addition of panitumumab to irinotecan therapy in patients with KRAS wt aCRC who exp
263 e mCRC who had progressed within 6 months of irinotecan therapy were randomly assigned to cetuximab 4
266 ownregulation of the main cellular target of irinotecan TOP1 nor upregulation of the key TOP1 PDB rep
267 an tumor xenograft models in comparison with irinotecan, topotecan, doxorubicin, 5-FU, gemcitabine, d
272 The net result of combined lurbinectedin and irinotecan treatment was a complete reversal of EWS-FLI1
273 ere euthanized 7 days after the beginning of irinotecan treatment, and small intestines were collecte
277 umors in a phase II study of bevacizumab and irinotecan underwent brain MR and (18)F-FDG PET within 2
281 ts: Of the 696 PICCOLO trial patients in the irinotecan-vs-irinotecan with panitumumab randomization,
285 y in combination with the DSB-inducing agent irinotecan was observed in a disease relevant model.
288 plus FOLFIRI (fluorouracil, leucovorin, and irinotecan) was superior to placebo plus FOLFIRI in prev
289 Bevacizumab, alone or in combination with irinotecan, was well tolerated and active in recurrent g
290 inations of oxaliplatin, 5-fluorouracil, and irinotecan were investigated for metastatic colorectal c
291 ontaining fluorouracil, capecitabine, and/or irinotecan were randomly assigned to receive octreotide
293 s 23% (95% CI, 9% to 40%) for cetuximab plus irinotecan with a hazard ratio of 0.74 (95% CI, 0.42 to
294 and subsequent fluorouracil, leucovorin, and irinotecan with or without bevacizumab in the second-lin
295 PICCOLO trial patients in the irinotecan-vs-irinotecan with panitumumab randomization, 331 had suffi
296 , median (IQR) PFS was 3.2 [2.7-8.1] months (irinotecan with panitumumab) vs 4.0 [2.7-7.5] months (ir
297 range [IQR]) PFS was 8.3 [4.0-11.0] months (irinotecan with panitumumab) vs 4.4 [2.8-6.7] months (ir
299 ssigned to one of two treatment schedules of irinotecan with vincristine: regimen 1A included irinote
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