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1 etween cancer cell 'A549_LUNG' and compound 'Topotecan'.
2 roved camptothecin analogues (irinotecan and topotecan).
3  observed in patients receiving ABT-888 with topotecan.
4 n, and 26 patients were randomly assigned to topotecan.
5 ads to a greater proportion of intracellular topotecan.
6 stoma, as a single agent or with concomitant topotecan.
7 ed camptothecin (CPT) analogs irinotecan and topotecan.
8  chemotherapy including cyclophosphamide and topotecan.
9 f random assignment was 13% on BSC and 7% on topotecan.
10 s analog 7-cyanoquinocarcinol (DX-52-1), and topotecan.
11 e cytotoxic effect of the DNA-damaging agent Topotecan.
12 ) I in response to topo I inhibitors such as topotecan.
13 tion with cytarabine (ara-C), idarubicin, or topotecan.
14 gistic chemosensitisation to doxorubicin and topotecan.
15                   The MTD was established as topotecan 0.6 mg/m(2)/d and ABT-888 10 mg BID on days on
16 weeks (CPT); cisplatin 50 mg/m(2) day 1 plus topotecan 0.75 mg/m(2) days 1 to 3 every 3 weeks (CT); o
17  IV cyclophosphamide 250 mg/m(2) followed by topotecan 0.75 mg/m(2) each day for 5 days every 21 days
18 on for SSOAI received melphalan (3-6 mg) and topotecan (0.5-1 mg; doses calculated by age and weight)
19  assigned window therapy (weeks 0 to 6) with topotecan (0.75 mg/m(2) daily x 5 every 21 days) immedia
20 clitaxel (175 mg/m(2) over 3 h on day 1) and topotecan (0.75 mg/m(2) for 30 min on days 1-3) with or
21 xel (135 mg/m(2) or 175 mg/m(2) on day 1) or topotecan (0.75 mg/m(2) on days 1-3) plus paclitaxel (17
22 y 5-day topotecan (2 mg/m(2)) or combination topotecan (0.75 mg/m(2)) and cyclophosphamide (250 mg/m(
23 ) by 5 minute IV infusion on days 1 to 3, or topotecan 1.0 mg/m(2) as an continuous IV infusion on da
24 scalation to the highest planned dose level (topotecan 1.25 mg/m(2), days 1 to 5; M6620 210 mg/m(2),
25 mg/m(2) intravenously (IV) on days 1 to 3 or topotecan 1.5 mg/m(2) IV on days 1 to 5.
26 otecan 2.3 mg/m2/d on days 1 through 5 or IV topotecan 1.5 mg/m2/d on days 1 through 5 every 21 days.
27 tients were randomly assigned to either oral topotecan 1.7 mg/m2/d x 5 with IV cisplatin 60 mg/m2 on
28 5, or 7.5 mg) in every case, with additional topotecan (1 mg) and/or carboplatin (30 or 50 mg) as nec
29  the study was reopened using lower doses of topotecan (1.0 mg/m(2) or 0.8 mg/m(2) for patients with
30 nfusion, days 1 through 3, every 21 days) or topotecan (1.5 mg/m(2)/d in a 30-minute IV infusion, day
31                                         Oral topotecan (1.8 mg/m(2)/d) on a qd x 5 x 2 schedule is we
32 at affect the HIF-1alpha pathways, including topotecan, 1-benzyl-3-(5'-hydroxymethyl-2'-furyl)indazol
33 as 33.0 weeks for oral and 35.0 weeks for IV topotecan; 1- and 2-year survival rates were 32.6% and 1
34                    The antitumor efficacy of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combin
35 ors by convection-enhanced delivery (CED) of topotecan (136 mumol/L) for 1, 4, or 7 days, and then ch
36 9.1% had received liposomal doxorubicin, 25% topotecan, 15.9% both agents, and 47.7% had received thr
37 14 to 21 days; the next 33 patients received topotecan 2 mg/m(2)/d for 5 days IV every 21 days; a thi
38  were assigned to treatment with either oral topotecan 2.3 mg/m2/d on days 1 through 5 or IV topoteca
39 gimen) were randomly assigned to daily 5-day topotecan (2 mg/m(2)) or combination topotecan (0.75 mg/
40 al structures of norindenoisoquinoline 5 and topotecan (2) bound in the topoisomerase I-DNA covalent
41 s 13.9 weeks (95% CI, 11.1 to 18.6) and with topotecan, 25.9 weeks (95% CI, 18.3 to 31.6).
42 tory and randomly assigned to receive weekly topotecan 4 mg/m(2) intravenously (IV) with or without z
43 -deficient mice after an intravenous dose of topotecan (4 mg/kg).
44  resulted in a significantly higher ORR than topotecan (44% v 15%; P = .021).
45 e documented in 67% of children who received topotecan, 76% after topo-cyclo, and 25% after paclitaxe
46                    Tdp1-/- mice treated with topotecan, a drug that increases levels of Top1-DNA comp
47 sorption and decreased systemic clearance of topotecan, a model substrate, indicating that additional
48  ATR inhibitor M6620 (previously VX-970) and topotecan, a selective TOP1 inhibitor, would be tolerabl
49                                              Topotecan, a soluble analog of CPT and FDA-approved anti
50 53 knockout counterpart after treatment with topotecan, a specific topoisomerase I inhibitor.
51 al extracellular fluid (ECF) accumulation of topotecan, a substrate of the ATP-binding cassette (ABC)
52                            Here we find that topotecan, a topoisomerase 1 (TOP1) inhibitor, dose-depe
53                We have previously shown that topotecan, a topoisomerase I poison, inhibits hypoxia-in
54 arib), a PARP inhibitor, in combination with topotecan, a topoisomerase I-targeted agent, was carried
55                                              Topotecan, a topoisomerase inhibitor, killed both hair c
56 osage of NSC 19630 and the chemotherapy drug topotecan acted synergistically to inhibit cell prolifer
57 le of Ube3a in neurons, but the mechanism of topotecan action on the PWS/AS locus is unknown.
58 lly binding to the enzyme-substrate complex, Topotecan acts as an uncompetitive inhibitor.
59 sults demonstrate that the AS candidate drug topotecan acts predominantly through stabilizing R loops
60    Three treatment schedules were evaluated: topotecan administered 24 h before, 24 h after, or simul
61                                              Topotecan administered on a protracted schedule is activ
62                                  Concomitant topotecan administration did not influence melphalan pha
63 s no effect of the sequence of melphalan and topotecan administration in plasma pharmacokinetics.
64                                              Topotecan after cyclophosphamide is a combination that i
65 as higher with combination therapy than with topotecan alone in patients who had platinum-sensitive d
66 l lung cancer, which tends not to respond to topotecan alone.
67 dvantage compared with subjects treated with topotecan alone.
68 uality of life; however, only cisplatin plus topotecan also improved overall survival.
69 nation of zoledronic acid + cyclophosphamide/topotecan also significantly improved survival (P < 0.00
70                                              Topotecan also suppressed spontaneous network activity w
71                             However, whether topotecan alters synaptic protein levels and synapse fun
72 dies also demonstrate promise for the use of topotecan and 2-deoxy-D-glucose in children.
73  cytotoxicity of the topoisomerase I poisons topotecan and camptothecin (CPT).
74 ingle-agent topotecan (TOPO) and combination topotecan and cyclophosphamide (TOPO/CTX) were compared
75   ABCG2 function was determined by measuring topotecan and doxorubicin efflux using flow cytometry, i
76 eloma cell lines increased after exposure to topotecan and doxorubicin, and was greater in logphase c
77                                              Topotecan and irinotecan are already in widespread use i
78                                              Topotecan and irinotecan are two CPTs that are approved
79 ced by anticancer camptothecins (CPTs) (e.g. topotecan and irinotecan) as well as structurally pertur
80 on induced by anticancer camptothecins (e.g. topotecan and irinotecan) as well as structurally pertur
81            Camptothecin and its derivatives, topotecan and irinotecan, are specific topoisomerase I (
82 tothecin (CPT) and its clinical derivatives, topotecan and irinotecan.
83 nalogues that are used clinically, including topotecan and irinotecan.
84 s are more sensitive to the topo I inhibitor topotecan and other anticancer agents such as VM-26 and
85 n vitro, only simultaneous administration of topotecan and PJ34 or PJ34 and (131)I-MIBG induced supra
86 tently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumula
87 rsing resistance to camptothecin derivatives topotecan and SN-38.
88                              Combinations of topotecan and the PARP-1 inhibitor PJ34 were assessed fo
89                                              Topotecan and topo-cyclo are active in children with NB,
90  and protein expression after treatment with topotecan, and at relapse.
91 eated with VAC alternating with vincristine, topotecan, and cyclophosphamide (VAC/VTC).
92 C alone or VAC alternating with vincristine, topotecan, and cyclophosphamide.
93                In contrast, while cisplatin, topotecan, and gemcitabine each activated Chk1, RNAi-med
94 itors, such as the camptothecin derivatives, topotecan, and irinotecan, which are used to treat human
95  no effect on cell sensitivity to cisplatin, topotecan, and methotrexate.
96  drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.
97 ant to other Top1 inhibitors, including CPT, topotecan, and the indenoisoquinolines MJ-III-65 (NSC 70
98 ology Group conducted a study of paclitaxel, topotecan, and topotecan-cyclophosphamide (topo-cyclo) i
99 sensitize BRCA1-depleted cells to cisplatin, topotecan, and veliparib beyond the potent sensitization
100                                              Topotecan- and paclitaxel-resistant prostate cancer line
101 therapeutics derived from it, irinotecan and topotecan, are highly specific inhibitors of human nucle
102 deaths occurred in four patients (6%) in the topotecan arm.
103 emergent adverse events in the amrubicin and topotecan arms were: neutropenia (41% v 54%; P = .004),
104     Herein we describe the identification of topotecan as a novel inhibitor of global SUMOylation.
105 orresponding to the anatomic distribution of topotecan as predicted by MRI of a surrogate tracer.
106  the safety and efficacy of amrubicin versus topotecan as second-line treatment for SCLC.
107 n ORR of 44% compared with an ORR of 15% for topotecan as second-line treatment in patients with SCLC
108  a dose of 135 or 175 mg per square meter or topotecan at a dose of 0.75 mg per square meter on days
109 r low (0.1 microM)- and high (1 microM)-dose topotecan at multiple time points within the first 6 h o
110 e presence of camptothecin or its derivative topotecan, ATP (at up to 2 mM) inhibited PARP-1/NAD-faci
111                                       Target topotecan AUCs were achieved in 92 (72%) of the 127 meas
112                          Purpose To evaluate topotecan-based therapy for advanced intraocular retinob
113                                              Topotecan blocked the IGF-I-stimulated increase in HIF-1
114                          Gefitinib increased topotecan brain ECF penetration but decreased the ventri
115                               In conclusion, topotecan brain ECF penetration was lower compared with
116                      Eight patients received topotecan capsules during course 2 only.
117 l active transport of topotecan lactone over topotecan carboxylate was shown in vivo by vCSF lactone-
118      Concomitant with HIF-1alpha inhibition, topotecan caused a significant tumor growth inhibition a
119          To study the effect of gefitinib on topotecan CNS penetration, 200 mg/kg gefitinib was admin
120 lood-cerebrospinal fluid barriers to enhance topotecan CNS penetration.
121                     The PJ34 and (131)I-MIBG/topotecan combination treatment induced G(2) arrest in a
122 y of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combination treatment was increased by PARP-1
123 ash, and mucositis on the troxacitabine plus topotecan combination.
124                                   Conclusion Topotecan combined with vincristine, carboplatin, and ag
125 as similar with combined ziv-aflibercept and topotecan compared with topotecan in both strata.
126 ntiated neurons and show a reduced effect of topotecan compared with wild-type neurons.
127 ht, new injection site location, addition of topotecan, concomitant focal treatment, and time interva
128                                              Topotecan concomitantly downregulated expression of the
129 rebrospinal fluid barrier, resulting in high topotecan CSF penetration.
130              Mucositis rarely occurred after topotecan cycles (9.7%) in contrast to 30% after MSKCC c
131 ducted a study of paclitaxel, topotecan, and topotecan-cyclophosphamide (topo-cyclo) in newly diagnos
132 the efficacy and toxicity of carboplatin +/- topotecan delivered by ophthalmic artery chemosurgery wh
133                                         Oral topotecan demonstrates activity and tolerability similar
134  we report that in primary cortical neurons, topotecan depleted synaptic proteins that are encoded by
135                                              Topotecan did not alter the pharmacokinetics of ABT-888.
136 on topotecan tECF penetration and intratumor topotecan distribution.
137                                   The median topotecan dosage required to achieve the target AUC was
138 3 status) and the treatment effect (i.e., of topotecan dose and time of exposure).
139 ysis, neither increasing maximum carboplatin/topotecan dose nor cumulative carboplatin/topotecan dose
140 in/topotecan dose nor cumulative carboplatin/topotecan dose was associated with statistically signifi
141                   Pharmacokinetically guided topotecan dosing (target systemic exposure with area und
142 ograft models in comparison with irinotecan, topotecan, doxorubicin, 5-FU, gemcitabine, docetaxel, ox
143  and in vivo, to further enhance (131)I-MIBG/topotecan efficacy.
144 h platinum and a taxane; these drugs include topotecan, etoposide, pegylated liposomal doxorubicin, e
145                              The desired CSF topotecan exposure was achieved in seven of eight pharma
146                         At equivalent plasma topotecan exposures, we found that P(tumor) after gefiti
147            A regimen combining melphalan and topotecan for SSOAI treatment of retinoblastoma is activ
148 ic inhibitors in combination with cisplatin, topotecan, gemcitabine, and the PARP inhibitor veliparib
149 ase I trial of the injectable formulation of topotecan given orally once daily for 5 days for 2 conse
150 val (primary end point) was prolonged in the topotecan group (log-rank P = .0104).
151 ocytopenia seemed to be more frequent in the topotecan group as compared with the amrubicin group (78
152 orse neutropenia and thrombocytopenia in the topotecan group as compared with the amrubicin group.
153                Myeloma patients treated with topotecan had an increase in ABCG2 mRNA and protein expr
154                                  Patients on topotecan had slower quality of life deterioration and g
155                                  DX-52-1 and topotecan have been previously established as HIF-1 inhi
156 months with amrubicin versus 7.8 months with topotecan (hazard ratio [HR], 0.880; P = .170); in refra
157 .1 months with amrubicin and 3.5 months with topotecan (HR, 0.802; P = .018).
158 esolution) in ternary complexes with DNA and topotecan (Hycamtin), a camptothecin analogue currently
159  microg in 0.04 mL of diluent) combined with topotecan hydrochloride (8-20 microg in 0.04 mL of balan
160          A well-known chemotherapeutic drug, topotecan hydrochloride, was used to investigate the eff
161 as administered orally 1 hour before 4 mg/kg topotecan i.v.
162                          After 4 and 8 mg/kg topotecan i.v., the brain ECF to plasma AUC ratio of unb
163  I study tested the combination of M6620 and topotecan in 3-week cycles using 3 + 3 dose escalation.
164 werful chemopotentiators of temozolomide and topotecan in both A549 and LoVo cell lines.
165  ziv-aflibercept and topotecan compared with topotecan in both strata.
166 nhanced accumulation of the anticancer agent topotecan in brain tissue and cerebrospinal fluid (CSF).
167 ates activity and tolerability similar to IV topotecan in chemotherapy-sensitive SCLC patients and of
168                       A phase II trial of IT topotecan in children with neoplastic meningitis is in p
169 s provide a compelling rationale for testing topotecan in clinical trials to target HIF-1 in cancer p
170   Varying schedules and doses of intravenous topotecan in combination with ABT-888 (10 mg) administer
171 ts received 66 cycles of SSOAI melphalan and topotecan in combination.
172 ation of combined intravitreal melphalan and topotecan in eyes not subsequently enucleated appears to
173                                 Inclusion of topotecan in front-line clinical trials for patients wit
174 ased the cell cycle and cytotoxic effects of topotecan in multiple cell line models.
175  The MTD and recommended phase II dose of IT topotecan in patients who are 3 years or older is 0.4 mg
176 omized, phase III study compared oral and IV topotecan in patients with SCLC sensitive to initial che
177 nd efficacy of single-agent amrubicin versus topotecan in patients with small-cell lung cancer (SCLC)
178 ucted to evaluate the activity and safety of topotecan in pediatric patients with recurrent Wilms' tu
179 ed superior levels of activity compared with topotecan in preclinical models.
180 ts were up- or down-regulated in response to topotecan in the p53+/+ cells, whereas only 1% of the tr
181  did not improve survival when compared with topotecan in the second-line treatment of patients with
182 odel, and compared favorably with CPT-11 and topotecan in the SKNEP anaplastic Wilms' tumor model.
183 rmined the volume of distribution of unbound topotecan in tumor (V(u,tumor)) and found that it was si
184 rugs (eg, pegylated liposomal doxorubicin or topotecan) in platinum-resistant ovarian cancer.
185                          Both paclitaxel and topotecan, in combination with cisplatin, yielded superi
186 , ABT-888, with a topoisomerase I inhibitor, topotecan, in PBMCs, tumor, and CTCs.
187 31)I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DNA damage and supraadditive
188 heduled combinations of PJ34 and (131)I-MIBG/topotecan induced supraadditive toxicity and increased D
189 plexes, phospho-H2AX and Rad51 suggests that topotecan-induced DNA double-strand breaks occur at site
190                                              Topotecan-induced topo I-DNA complexes peak at 15-30 min
191                           57 carboplatin +/- topotecan infusions (of 111 total) were performed in 31
192                              Carboplatin +/- topotecan infusions are effective for ophthalmic artery
193                                              Topotecan inhibited HIF-1 activity only at cytotoxic con
194 Here, we report that daily administration of topotecan inhibits HIF-1alpha protein expression in U251
195 esults suggest that Bcrp1 and P-gp transport topotecan into vCSF and out of brain parenchyma through
196 d, multicenter phase III study compared oral topotecan/intravenous cisplatin (TC) with intravenous (I
197                         These drugs included topotecan, irinotecan, etoposide and dexrazoxane (ICRF-1
198 e combination of Nutlin-3a(OC) with systemic topotecan is a significantly better treatment for retino
199                                              Topotecan is a substrate of the ATP-binding cassette tra
200                                              Topotecan is a topoisomerase 1 (TOP1) inhibitor that is
201                                              Topotecan is active against neuroblastoma when it is adm
202                                              Topotecan is an active agent for the treatment of advanc
203                                              Topotecan is an effective agent against pediatric medull
204                Single-agent intravenous (IV) topotecan is an effective treatment for small-cell lung
205                       Chemotherapy with oral topotecan is associated with prolongation of survival an
206 e evidence that inhibition of SUMOylation by topotecan is associated with reduced levels of CDK6 and
207 s were individualized to attain a single-day topotecan lactone area under the plasma concentration-ti
208  studies were conducted on day 1 to attain a topotecan lactone area under the plasma concentration-ti
209 nder the plasma concentration-time curve for topotecan lactone at this dosage was 20.9 +/- 8.4 ng/mL.
210 The brain ECF to plasma AUC ratio of unbound topotecan lactone increased by 1.6-fold to 0.35 +/- 0.04
211             Preferential active transport of topotecan lactone over topotecan carboxylate was shown i
212 the brain ECF to plasma AUC ratio of unbound topotecan lactone was 0.21 +/- 0.04 and 0.61 +/- 0.16, r
213                                              Topotecan lactone was below detectable limits in the ECF
214                  vCSF penetration of unbound topotecan lactone was measured as the ratio of vCSF-to-p
215            These agents include gemcitabine, topotecan, liposomal doxorubicin, and prolonged oral eto
216 h oral topotecan (n = 153) and 21.9% with IV topotecan (n = 151), with a difference (oral -IV) of -3.
217 nalysis, response rates were 18.3% with oral topotecan (n = 153) and 21.9% with IV topotecan (n = 151
218  coadminister ABT-888 with standard doses of topotecan, necessitating dose reductions.
219      BCRP substrates include numerous drugs (topotecan, nitrofurantoin, cimetidine) as well as food c
220  ORR was 31.1% with amrubicin and 16.9% with topotecan (odds ratio, 2.223; P < .001).
221 e tested the effects of locally administered topotecan on a rat model of glioblastoma that is induced
222  and significantly increases accumulation of topotecan only in cells expressing functional ABCG2.
223 stoma patients whom received carboplatin +/- topotecan ophthalmic artery chemosurgery.
224 during, or within 3 months of discontinuing, topotecan or liposomal doxorubicin.
225 eloped grade 3 to 4 marrow suppression after topotecan or topo-cyclo.
226 toma receiving 630 intravitreous (melphalan, topotecan) or topotecan periocular injections.
227 oisomerase (Topo) I inhibitor (camptothecin, topotecan, or SN-38) and tumor necrosis factor-related a
228 h to characterize the effect of gefitinib on topotecan P(tumor).
229 mbining bevacizumab/A4.6.1 with doxorubicin, topotecan, paclitaxel, docetaxel, or radiotherapy result
230                                              Topotecan-paclitaxel was not superior to cisplatin-pacli
231 liposomal doxorubicin, weekly paclitaxel, or topotecan), patients were randomly assigned to single-ag
232                                We found that topotecan penetration (P(tumor)) of U87 was 0.96 +/- 0.2
233 e effect of modulating these transporters on topotecan penetration in gliomas has not been thoroughly
234                        This study focused on topotecan penetration into the brain extracellular fluid
235  To define the role of these transporters in topotecan penetration into the ventricular cerebrospinal
236  630 intravitreous (melphalan, topotecan) or topotecan periocular injections.
237 en of eight pharmacokinetic studies when the topotecan plasma AUC was within target range.
238 ments in progression-free survival, but only topotecan plus cisplatin has demonstrated an improvement
239 astine, doxorubicin, and cisplatin (MVAC) or topotecan plus cisplatin in advanced cervix cancer, we u
240                          The maximum dose of topotecan plus M6620 is tolerable.
241 onths) received chemotherapy: two courses of topotecan plus vincristine followed by three alternating
242 boplatin and vincristine for two courses and topotecan plus vincristine for one course, with optional
243 al administration of melphalan combined with topotecan produced complete control of vitreous seeds in
244 ntiate responses to the clinically used drug topotecan, producing a more than 9-fold suppression of c
245 nt to enhance antiproliferative responses to topotecan, producing a significant survival advantage co
246 nrolled and received a total of 94 cycles of topotecan (range, one to six cycles).
247                       We recently found that topotecan reduces the expression of multiple long genes,
248     DDR evoked by the topoisomerase I poison topotecan remained unaffected by lovastatin.
249                                          The topotecan resistance of cells overexpressing Mrp4 and th
250 survival rates were 32.6% and 12.4% for oral topotecan, respectively, and 29.2% and 7.1% for IV topot
251 amrubicin and 3.3 months and 7.6 months with topotecan, respectively.
252 can, respectively, and 29.2% and 7.1% for IV topotecan, respectively.
253 somerase, DNA, and the chemotherapeutic drug topotecan show important differences in the mechanisms f
254 neous administration of PJ34 and (131)I-MIBG/topotecan significantly delayed the growth of SK-N-BE(2c
255 vealed that two of the six, flubendazole and topotecan, significantly suppress hair cell regeneration
256                                              Topotecan strongly suppressed inhibitory neurotransmissi
257                              On the basis of topotecan systemic clearance, doses were individualized
258                                     Targeted topotecan systemic exposure was achieved in 26 (84%) of
259 ) penetration and the effect of gefitinib on topotecan tECF penetration and intratumor topotecan dist
260 perienced disease progression during initial topotecan therapy.
261  (P = .002 and P = .018, respectively) after topotecan therapy.
262 VW/NAT xenografts, compared with (131)I-MIBG/topotecan therapy.
263 nsporting the 9-dimethylaminomethyl group of topotecan to the 10-position of the norindenoisoquinolin
264 tential strategy to increase the efficacy of topotecan to treat central nervous system (CNS) malignan
265                                 Single-agent topotecan (TOPO) and combination topotecan and cyclophos
266 mal release kinetics of the anticancer agent topotecan (TPT) in physiological fluids and subsequently
267                                              Topotecan (TPT) is a topoisomerase I inhibitor that unde
268           We demonstrate that in addition to topotecan (TPT), a known inhibitor of HIF-1alpha, UVC, b
269 wn previously that the camptothecin analogue topotecan (TPT), a topoisomerase I (Top 1) poison, inhib
270 h ISG15 expression that is comparable to the topotecan (TPT)-sensitive NSCLC cell lines was found in
271 eveloped a method to efficiently encapsulate topotecan (TPT, 1), an important cytotoxic drug, in biod
272 r resistance protein 1 (Bcrp1), an efficient topotecan transporter, was detected at the apical aspect
273                                              Topotecan treatment reduced GFP(+) cells about 10-fold a
274                    Here, we demonstrate that topotecan treatment stabilizes the formation of RNA:DNA
275 ons for at least 12 weeks after cessation of topotecan treatment, indicating that transient topoisome
276 th was observed with combination miR-34a and topotecan treatment.
277 c human gliomas (U87 and MT330) and assessed topotecan tumor ECF (tECF) penetration and the effect of
278                   When administered in vivo, topotecan unsilenced the paternal Ube3a allele in severa
279                  These results indicate that topotecan unsilences Ube3a in cis by reducing transcript
280                 At nanomolar concentrations, topotecan upregulated catalytically active UBE3A in neur
281 , vincristine, and etoposide with or without topotecan, vincristine, and doxorubicin) and achieved an
282                                  Response to topotecan was 7% partial and 44% stable disease.
283 says, ABCG2-mediated resistance to SN-38 and topotecan was abrogated in ABCG2-transfected HEK-293 cel
284                                              Topotecan was administered at 1.5 mg/m(2) (or 1.2 mg/m(2
285          In this prospective phase II trial, topotecan was administered intravenously daily for 5 day
286                                              Topotecan was administered intravenously over 30 minutes
287            Further studies demonstrated that topotecan was an Mrp4 substrate and that cells overexpre
288 oxicity in patients who received oral and IV topotecan was as follows: neutropenia in 47% and 64%, th
289          A phase I trial of intrathecal (IT) topotecan was performed to determine the optimal dose, t
290 ater-mediated contact between the enzyme and topotecan, we were surprised to find that a well-ordered
291 n of the chemotherapy backbone (single-agent topotecan, weekly paclitaxel, or gemcitabine), patients
292  and (131)I-MIBG and of PJ34 and (131)I-MIBG/topotecan were also assessed using similar scheduling.
293 ry properties of miR-34a in combination with topotecan were determined by cell growth assay.
294                    Principal toxicities with topotecan were hematological: grade 4 neutropenia, 33%;
295  substrates of ABCG2 such as mitoxantrone or topotecan were not identified, we characterized three no
296 stingly, topoisomerase inhibitors, including topotecan, were recently identified in an unbiased drug
297                                          The topotecan window consisted of two cycles, administered i
298                                    Comparing topotecan with BSC, infection grade 2 was 14% versus 12%
299                                         Oral topotecan with cisplatin provides similar efficacy and t
300 cribe a randomized, phase II trial of weekly topotecan with or without ziv-aflibercept (VEGF-trap) in

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