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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 ed camptothecin (CPT) analogs irinotecan and topotecan.
7  chemotherapy including cyclophosphamide and topotecan.
8 f random assignment was 13% on BSC and 7% on topotecan.
9 s analog 7-cyanoquinocarcinol (DX-52-1), and topotecan.
10 stoma, as a single agent or with concomitant topotecan.
11 e cytotoxic effect of the DNA-damaging agent Topotecan.
12 ) I in response to topo I inhibitors such as topotecan.
13 ther melphalan monotherapy or melphalan plus topotecan.
14 eated with the DNA topoisomerase I inhibitor topotecan.
15 gistic chemosensitisation to doxorubicin and topotecan.
16                   The MTD was established as topotecan 0.6 mg/m(2)/d and ABT-888 10 mg BID on days on
17 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
18  IV cyclophosphamide 250 mg/m(2) followed by topotecan 0.75 mg/m(2) each day for 5 days every 21 days
19 on for SSOAI received melphalan (3-6 mg) and topotecan (0.5-1 mg; doses calculated by age and weight)
20  assigned window therapy (weeks 0 to 6) with topotecan (0.75 mg/m(2) daily x 5 every 21 days) immedia
21 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
22 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
23 y 5-day topotecan (2 mg/m(2)) or combination topotecan (0.75 mg/m(2)) and cyclophosphamide (250 mg/m(
24 ) by 5 minute IV infusion on days 1 to 3, or topotecan 1.0 mg/m(2) as an continuous IV infusion on da
25 scalation to the highest planned dose level (topotecan 1.25 mg/m(2), days 1 to 5; M6620 210 mg/m(2),
26 mg/m(2) intravenously (IV) on days 1 to 3 or topotecan 1.5 mg/m(2) IV on days 1 to 5.
27 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.
28 tients were randomly assigned to either oral topotecan 1.7 mg/m2/d x 5 with IV cisplatin 60 mg/m2 on
29 5, or 7.5 mg) in every case, with additional topotecan (1 mg) and/or carboplatin (30 or 50 mg) as nec
30  the study was reopened using lower doses of topotecan (1.0 mg/m(2) or 0.8 mg/m(2) for patients with
31 nfusion, days 1 through 3, every 21 days) or topotecan (1.5 mg/m(2)/d in a 30-minute IV infusion, day
32                                         Oral topotecan (1.8 mg/m(2)/d) on a qd x 5 x 2 schedule is we
33 at affect the HIF-1alpha pathways, including topotecan, 1-benzyl-3-(5'-hydroxymethyl-2'-furyl)indazol
34 as 33.0 weeks for oral and 35.0 weeks for IV topotecan; 1- and 2-year survival rates were 32.6% and 1
35                    The antitumor efficacy of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combin
36 ors by convection-enhanced delivery (CED) of topotecan (136 mumol/L) for 1, 4, or 7 days, and then ch
37 9.1% had received liposomal doxorubicin, 25% topotecan, 15.9% both agents, and 47.7% had received thr
38  melphalan 0.4 mg/kg, carboplatin 50 mg, and topotecan 2 mg) and noting certain subtle signs of early
39 14 to 21 days; the next 33 patients received topotecan 2 mg/m(2)/d for 5 days IV every 21 days; a thi
40  were assigned to treatment with either oral topotecan 2.3 mg/m2/d on days 1 through 5 or IV topoteca
41 gimen) were randomly assigned to daily 5-day topotecan (2 mg/m(2)) or combination topotecan (0.75 mg/
42 al structures of norindenoisoquinoline 5 and topotecan (2) bound in the topoisomerase I-DNA covalent
43 s 13.9 weeks (95% CI, 11.1 to 18.6) and with topotecan, 25.9 weeks (95% CI, 18.3 to 31.6).
44 tory and randomly assigned to receive weekly topotecan 4 mg/m(2) intravenously (IV) with or without z
45 -deficient mice after an intravenous dose of topotecan (4 mg/kg).
46  resulted in a significantly higher ORR than topotecan (44% v 15%; P = .021).
47 e documented in 67% of children who received topotecan, 76% after topo-cyclo, and 25% after paclitaxe
48                    Tdp1-/- mice treated with topotecan, a drug that increases levels of Top1-DNA comp
49 sorption and decreased systemic clearance of topotecan, a model substrate, indicating that additional
50  ATR inhibitor M6620 (previously VX-970) and topotecan, a selective TOP1 inhibitor, would be tolerabl
51                                              Topotecan, a soluble analog of CPT and FDA-approved anti
52 al extracellular fluid (ECF) accumulation of topotecan, a substrate of the ATP-binding cassette (ABC)
53                            Here we find that topotecan, a topoisomerase 1 (TOP1) inhibitor, dose-depe
54                We have previously shown that topotecan, a topoisomerase I poison, inhibits hypoxia-in
55 arib), a PARP inhibitor, in combination with topotecan, a topoisomerase I-targeted agent, was carried
56                                              Topotecan, a topoisomerase inhibitor, killed both hair c
57 osage of NSC 19630 and the chemotherapy drug topotecan acted synergistically to inhibit cell prolifer
58 le of Ube3a in neurons, but the mechanism of topotecan action on the PWS/AS locus is unknown.
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 linically used camptothecin anticancer drugs topotecan and irinotecan.
83 tothecin (CPT) and its clinical derivatives, topotecan and irinotecan.
84 to the FDA-approved topoisomerase inhibitors topotecan and irinotecan.
85 nalogues that are used clinically, including topotecan and irinotecan.
86 s are more sensitive to the topo I inhibitor topotecan and other anticancer agents such as VM-26 and
87 n vitro, only simultaneous administration of topotecan and PJ34 or PJ34 and (131)I-MIBG induced supra
88 tently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumula
89 rsing resistance to camptothecin derivatives topotecan and SN-38.
90                              Combinations of topotecan and the PARP-1 inhibitor PJ34 were assessed fo
91                                              Topotecan and topo-cyclo are active in children with NB,
92  and protein expression after treatment with topotecan, and at relapse.
93 eated with VAC alternating with vincristine, topotecan, and cyclophosphamide (VAC/VTC).
94 C alone or VAC alternating with vincristine, topotecan, and cyclophosphamide.
95                In contrast, while cisplatin, topotecan, and gemcitabine each activated Chk1, RNAi-med
96 itors, such as the camptothecin derivatives, topotecan, and irinotecan, which are used to treat human
97  no effect on cell sensitivity to cisplatin, topotecan, and methotrexate.
98  drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.
99 ant to other Top1 inhibitors, including CPT, topotecan, and the indenoisoquinolines MJ-III-65 (NSC 70
100 ology Group conducted a study of paclitaxel, topotecan, and topotecan-cyclophosphamide (topo-cyclo) i
101 sensitize BRCA1-depleted cells to cisplatin, topotecan, and veliparib beyond the potent sensitization
102                                              Topotecan- and paclitaxel-resistant prostate cancer line
103 therapeutics derived from it, irinotecan and topotecan, are highly specific inhibitors of human nucle
104 deaths occurred in four patients (6%) in the topotecan arm.
105 emergent adverse events in the amrubicin and topotecan arms were: neutropenia (41% v 54%; P = .004),
106     Herein we describe the identification of topotecan as a novel inhibitor of global SUMOylation.
107 orresponding to the anatomic distribution of topotecan as predicted by MRI of a surrogate tracer.
108  the safety and efficacy of amrubicin versus topotecan as second-line treatment for SCLC.
109 n ORR of 44% compared with an ORR of 15% for topotecan as second-line treatment in patients with SCLC
110  a dose of 135 or 175 mg per square meter or topotecan at a dose of 0.75 mg per square meter on days
111 r low (0.1 microM)- and high (1 microM)-dose topotecan at multiple time points within the first 6 h o
112 e presence of camptothecin or its derivative topotecan, ATP (at up to 2 mM) inhibited PARP-1/NAD-faci
113                                       Target topotecan AUCs were achieved in 92 (72%) of the 127 meas
114                          Purpose To evaluate topotecan-based therapy for advanced intraocular retinob
115                                              Topotecan blocked the IGF-I-stimulated increase in HIF-1
116                          Gefitinib increased topotecan brain ECF penetration but decreased the ventri
117                               In conclusion, topotecan brain ECF penetration was lower compared with
118                      Eight patients received topotecan capsules during course 2 only.
119 l active transport of topotecan lactone over topotecan carboxylate was shown in vivo by vCSF lactone-
120      Concomitant with HIF-1alpha inhibition, topotecan caused a significant tumor growth inhibition a
121          To study the effect of gefitinib on topotecan CNS penetration, 200 mg/kg gefitinib was admin
122 lood-cerebrospinal fluid barriers to enhance topotecan CNS penetration.
123                     The PJ34 and (131)I-MIBG/topotecan combination treatment induced G(2) arrest in a
124 y of topotecan, (131)I-MIBG, and (131)I-MIBG/topotecan combination treatment was increased by PARP-1
125 ash, and mucositis on the troxacitabine plus topotecan combination.
126                                   Conclusion Topotecan combined with vincristine, carboplatin, and ag
127 as similar with combined ziv-aflibercept and topotecan compared with topotecan in both strata.
128 ntiated neurons and show a reduced effect of topotecan compared with wild-type neurons.
129 ht, new injection site location, addition of topotecan, concomitant focal treatment, and time interva
130                                              Topotecan concomitantly downregulated expression of the
131 rebrospinal fluid barrier, resulting in high topotecan CSF penetration.
132              Mucositis rarely occurred after topotecan cycles (9.7%) in contrast to 30% after MSKCC c
133 ducted a study of paclitaxel, topotecan, and topotecan-cyclophosphamide (topo-cyclo) in newly diagnos
134 the efficacy and toxicity of carboplatin +/- topotecan delivered by ophthalmic artery chemosurgery wh
135                                         Oral topotecan demonstrates activity and tolerability similar
136  we report that in primary cortical neurons, topotecan depleted synaptic proteins that are encoded by
137                                              Topotecan did not alter the pharmacokinetics of ABT-888.
138 on topotecan tECF penetration and intratumor topotecan distribution.
139                                   The median topotecan dosage required to achieve the target AUC was
140 3 status) and the treatment effect (i.e., of topotecan dose and time of exposure).
141 ysis, neither increasing maximum carboplatin/topotecan dose nor cumulative carboplatin/topotecan dose
142 in/topotecan dose nor cumulative carboplatin/topotecan dose was associated with statistically signifi
143                   Pharmacokinetically guided topotecan dosing (target systemic exposure with area und
144 ograft models in comparison with irinotecan, topotecan, doxorubicin, 5-FU, gemcitabine, docetaxel, ox
145  and in vivo, to further enhance (131)I-MIBG/topotecan efficacy.
146                              The desired CSF topotecan exposure was achieved in seven of eight pharma
147                         At equivalent plasma topotecan exposures, we found that P(tumor) after gefiti
148            A regimen combining melphalan and topotecan for SSOAI treatment of retinoblastoma is activ
149 ic inhibitors in combination with cisplatin, topotecan, gemcitabine, and the PARP inhibitor veliparib
150 ase I trial of the injectable formulation of topotecan given orally once daily for 5 days for 2 conse
151 val (primary end point) was prolonged in the topotecan group (log-rank P = .0104).
152 ocytopenia seemed to be more frequent in the topotecan group as compared with the amrubicin group (78
153 orse neutropenia and thrombocytopenia in the topotecan group as compared with the amrubicin group.
154                Myeloma patients treated with topotecan had an increase in ABCG2 mRNA and protein expr
155                                  Patients on topotecan had slower quality of life deterioration and g
156                                  DX-52-1 and topotecan have been previously established as HIF-1 inhi
157 months with amrubicin versus 7.8 months with topotecan (hazard ratio [HR], 0.880; P = .170); in refra
158 .1 months with amrubicin and 3.5 months with topotecan (HR, 0.802; P = .018).
159 esolution) in ternary complexes with DNA and topotecan (Hycamtin), a camptothecin analogue currently
160  microg in 0.04 mL of diluent) combined with topotecan hydrochloride (8-20 microg in 0.04 mL of balan
161          A well-known chemotherapeutic drug, topotecan hydrochloride, was used to investigate the eff
162 d by several agents (bleomycin, doxorubicin, topotecan, hydrogen peroxide, UV, photosensitized reacti
163 as administered orally 1 hour before 4 mg/kg topotecan i.v.
164                          After 4 and 8 mg/kg topotecan i.v., the brain ECF to plasma AUC ratio of unb
165  I study tested the combination of M6620 and topotecan in 3-week cycles using 3 + 3 dose escalation.
166  ziv-aflibercept and topotecan compared with topotecan in both strata.
167 nhanced accumulation of the anticancer agent topotecan in brain tissue and cerebrospinal fluid (CSF).
168 ates activity and tolerability similar to IV topotecan in chemotherapy-sensitive SCLC patients and of
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 omized, phase III study compared oral and IV topotecan in patients with SCLC sensitive to initial che
176 nd efficacy of single-agent amrubicin versus topotecan in patients with small-cell lung cancer (SCLC)
177 ucted to evaluate the activity and safety of topotecan in pediatric patients with recurrent Wilms' tu
178 ed superior levels of activity compared with topotecan in preclinical models.
179  did not improve survival when compared with topotecan in the second-line treatment of patients with
180 rmined the volume of distribution of unbound topotecan in tumor (V(u,tumor)) and found that it was si
181 rugs (eg, pegylated liposomal doxorubicin or topotecan) in platinum-resistant ovarian cancer.
182                          Both paclitaxel and topotecan, in combination with cisplatin, yielded superi
183 , ABT-888, with a topoisomerase I inhibitor, topotecan, in PBMCs, tumor, and CTCs.
184 31)I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DNA damage and supraadditive
185 heduled combinations of PJ34 and (131)I-MIBG/topotecan induced supraadditive toxicity and increased D
186 plexes, phospho-H2AX and Rad51 suggests that topotecan-induced DNA double-strand breaks occur at site
187                                              Topotecan-induced topo I-DNA complexes peak at 15-30 min
188                           57 carboplatin +/- topotecan infusions (of 111 total) were performed in 31
189                              Carboplatin +/- topotecan infusions are effective for ophthalmic artery
190                                              Topotecan inhibited HIF-1 activity only at cytotoxic con
191 Here, we report that daily administration of topotecan inhibits HIF-1alpha protein expression in U251
192 esults suggest that Bcrp1 and P-gp transport topotecan into vCSF and out of brain parenchyma through
193 d, multicenter phase III study compared oral topotecan/intravenous cisplatin (TC) with intravenous (I
194                         These drugs included topotecan, irinotecan, etoposide and dexrazoxane (ICRF-1
195 e combination of Nutlin-3a(OC) with systemic topotecan is a significantly better treatment for retino
196                                              Topotecan is a substrate of the ATP-binding cassette tra
197                                              Topotecan is a topoisomerase 1 (TOP1) inhibitor that is
198                                              Topotecan is active against neuroblastoma when it is adm
199                                              Topotecan is an effective agent against pediatric medull
200                Single-agent intravenous (IV) topotecan is an effective treatment for small-cell lung
201                       Chemotherapy with oral topotecan is associated with prolongation of survival an
202 e evidence that inhibition of SUMOylation by topotecan is associated with reduced levels of CDK6 and
203 s were individualized to attain a single-day topotecan lactone area under the plasma concentration-ti
204  studies were conducted on day 1 to attain a topotecan lactone area under the plasma concentration-ti
205 nder the plasma concentration-time curve for topotecan lactone at this dosage was 20.9 +/- 8.4 ng/mL.
206 The brain ECF to plasma AUC ratio of unbound topotecan lactone increased by 1.6-fold to 0.35 +/- 0.04
207             Preferential active transport of topotecan lactone over topotecan carboxylate was shown i
208 the brain ECF to plasma AUC ratio of unbound topotecan lactone was 0.21 +/- 0.04 and 0.61 +/- 0.16, r
209                                              Topotecan lactone was below detectable limits in the ECF
210                  vCSF penetration of unbound topotecan lactone was measured as the ratio of vCSF-to-p
211            These agents include gemcitabine, topotecan, liposomal doxorubicin, and prolonged oral eto
212            The combination of melphalan plus topotecan (MPT) was used to treat 149 patients and 158 e
213 h oral topotecan (n = 153) and 21.9% with IV topotecan (n = 151), with a difference (oral -IV) of -3.
214 nalysis, response rates were 18.3% with oral topotecan (n = 153) and 21.9% with IV topotecan (n = 151
215  coadminister ABT-888 with standard doses of topotecan, necessitating dose reductions.
216      BCRP substrates include numerous drugs (topotecan, nitrofurantoin, cimetidine) as well as food c
217  ORR was 31.1% with amrubicin and 16.9% with topotecan (odds ratio, 2.223; P < .001).
218 e tested the effects of locally administered topotecan on a rat model of glioblastoma that is induced
219  and significantly increases accumulation of topotecan only in cells expressing functional ABCG2.
220 stoma patients whom received carboplatin +/- topotecan ophthalmic artery chemosurgery.
221 during, or within 3 months of discontinuing, topotecan or liposomal doxorubicin.
222 that hypersensitivity of ATM-mutant cells to topotecan or the poly-(ADP-ribose) polymerase (PARP) inh
223 eloped grade 3 to 4 marrow suppression after topotecan or topo-cyclo.
224 toma receiving 630 intravitreous (melphalan, topotecan) or topotecan periocular injections.
225 oisomerase (Topo) I inhibitor (camptothecin, topotecan, or SN-38) and tumor necrosis factor-related a
226 h to characterize the effect of gefitinib on topotecan P(tumor).
227 gimen (melphalan vs. combined melphalan plus topotecan; P < 0.05), catheterization route (internal ca
228 mbining bevacizumab/A4.6.1 with doxorubicin, topotecan, paclitaxel, docetaxel, or radiotherapy result
229                                              Topotecan-paclitaxel was not superior to cisplatin-pacli
230 liposomal doxorubicin, weekly paclitaxel, or topotecan), patients were randomly assigned to single-ag
231                                We found that topotecan penetration (P(tumor)) of U87 was 0.96 +/- 0.2
232 e effect of modulating these transporters on topotecan penetration in gliomas has not been thoroughly
233                        This study focused on topotecan penetration into the brain extracellular fluid
234  To define the role of these transporters in topotecan penetration into the ventricular cerebrospinal
235  630 intravitreous (melphalan, topotecan) or topotecan periocular injections.
236 en of eight pharmacokinetic studies when the topotecan plasma AUC was within target range.
237 ments in progression-free survival, but only topotecan plus cisplatin has demonstrated an improvement
238 astine, doxorubicin, and cisplatin (MVAC) or topotecan plus cisplatin in advanced cervix cancer, we u
239                          The maximum dose of topotecan plus M6620 is tolerable.
240 onths) received chemotherapy: two courses of topotecan plus vincristine followed by three alternating
241 boplatin and vincristine for two courses and topotecan plus vincristine for one course, with optional
242 al administration of melphalan combined with topotecan produced complete control of vitreous seeds in
243 ntiate responses to the clinically used drug topotecan, producing a more than 9-fold suppression of c
244 nt to enhance antiproliferative responses to topotecan, producing a significant survival advantage co
245 nrolled and received a total of 94 cycles of topotecan (range, one to six cycles).
246                       We recently found that topotecan reduces the expression of multiple long genes,
247     DDR evoked by the topoisomerase I poison topotecan remained unaffected by lovastatin.
248                                          The topotecan resistance of cells overexpressing Mrp4 and th
249 r of the BRCA1-A complex specifically confer topotecan resistance to ATM-deficient cells.
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 VW/NAT xenografts, compared with (131)I-MIBG/topotecan therapy.
261 perienced disease progression during initial topotecan therapy.
262  (P = .002 and P = .018, respectively) after topotecan therapy.
263         In this case series, the addition of topotecan to melphalan did not alter the IAC side effect
264 nsporting the 9-dimethylaminomethyl group of topotecan to the 10-position of the norindenoisoquinolin
265 tential strategy to increase the efficacy of topotecan to treat central nervous system (CNS) malignan
266                                 Single-agent topotecan (TOPO) and combination topotecan and cyclophos
267 mal release kinetics of the anticancer agent topotecan (TPT) in physiological fluids and subsequently
268                                              Topotecan (TPT) is a topoisomerase I inhibitor that unde
269           We demonstrate that in addition to topotecan (TPT), a known inhibitor of HIF-1alpha, UVC, b
270 wn previously that the camptothecin analogue topotecan (TPT), a topoisomerase I (Top 1) poison, inhib
271 h ISG15 expression that is comparable to the topotecan (TPT)-sensitive NSCLC cell lines was found in
272 eveloped a method to efficiently encapsulate topotecan (TPT, 1), an important cytotoxic drug, in biod
273 r resistance protein 1 (Bcrp1), an efficient topotecan transporter, was detected at the apical aspect
274                                              Topotecan treatment reduced GFP(+) cells about 10-fold a
275                    Here, we demonstrate that topotecan treatment stabilizes the formation of RNA:DNA
276 ons for at least 12 weeks after cessation of topotecan treatment, indicating that transient topoisome
277 th was observed with combination miR-34a and topotecan treatment.
278 c human gliomas (U87 and MT330) and assessed topotecan tumor ECF (tECF) penetration and the effect of
279                   When administered in vivo, topotecan unsilenced the paternal Ube3a allele in severa
280                  These results indicate that topotecan unsilences Ube3a in cis by reducing transcript
281                 At nanomolar concentrations, topotecan upregulated catalytically active UBE3A in neur
282 , vincristine, and etoposide with or without topotecan, vincristine, and doxorubicin) and achieved an
283                                  Response to topotecan was 7% partial and 44% stable disease.
284 says, ABCG2-mediated resistance to SN-38 and topotecan was abrogated in ABCG2-transfected HEK-293 cel
285                                              Topotecan was administered at 1.5 mg/m(2) (or 1.2 mg/m(2
286          In this prospective phase II trial, topotecan was administered intravenously daily for 5 day
287                                              Topotecan was administered intravenously over 30 minutes
288            Further studies demonstrated that topotecan was an Mrp4 substrate and that cells overexpre
289 oxicity in patients who received oral and IV topotecan was as follows: neutropenia in 47% and 64%, th
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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