ライフサイエンスコーパス: etoposide

1 apy (rituximab, ifosfamide, carboplatin, and etoposide).

2 the treatment of two drugs (doxorubicin and etoposide).

3 by 3 cycles of ICE (ifosfamide, carboplatin, etoposide).

4 plus platinum-etoposide, and 269 to platinum-etoposide).

5 chemotherapy (vincristine, carboplatin, and etoposide).

6 valuable precursors of the chemotherapeutic etoposide.

7 lar efficiency to the archetypal TOP2 poison etoposide.

8 for circumvention of acquired resistance to etoposide.

9 nced response to the topoisomerase-II poison etoposide.

10 -strand breaks in response to doxorubicin or etoposide.

11 ll sensitivity to the Topo II-targeting drug etoposide.

12 LC) are carboplatin-paclitaxel and cisplatin-etoposide.

13 or the expression of ZNF281 and treated with etoposide.

14 ders cells sensitive to the anticancer agent etoposide.

15 by treatment with the chemotherapeutic agent etoposide.

16 hemotherapeutic drugs, that is, cisplatin or etoposide.

17 e to the anti-cancer drug and TOP2 inhibitor etoposide.

18 expression levels in acquired resistance to etoposide.

19 osine arabinoside (ara-C), daunorubicin, and etoposide.

20 nsist of four cycles of a platinum agent and etoposide.

21 gnificantly improve outcomes versus platinum-etoposide.

22 d a genome-scale CRISPR knockout screen with etoposide.

23 thasone (DEX) and the chemotherapeutic agent etoposide.

24 GD3 expression sensitises an MB cell line to etoposide.

25 PEI) at total doses of platinum 420 mg/m(2), etoposide 1,200 mg/m(2), and ifosfamide 30 g/m(2).

26 cycle consisted of cisplatin 20 mg/m(2) and etoposide 100 mg/m(2) on days 1 through 5 at 21-day inte

27 rum concentration-time curve 5 on day 1 plus etoposide 100 mg/m(2) per day on days 1 to 3 every 21 da

28 atin area under the curve of 5 on day 1 plus etoposide 100 mg/m(2) per day on days 1 to 3 every 21 da

29 th equidose mesna uroprotection, followed by etoposide 100 mg/m(2) per day over 1 h on days 1-5.

30 rum concentration-time curve 4 on day 1 plus etoposide 100 mg/m(2) per day plus palifosfamide 130 mg/

31 fusions of mitoxantrone (8 mg/m(2) per day), etoposide (100 mg/m(2) per day), and cytarabine (1000 mg

32 for total doses of platinum 420 mg/m(2) and etoposide 2,040 mg/m(2).

33 o durvalumab plus tremelimumab plus platinum-etoposide, 268 to durvalumab plus platinum-etoposide, an

34 2) on days 2 through 5 (total 6 g/m(2)), and etoposide 700 mg/m(2) per day on days 2 through 4 (total

35 ith cytarabine 100 mg/m(2) daily for 5 days, etoposide 75 mg/m(2) daily for 5 days, and idarubicin 9

36 latin 700 mg/m(2) on days -5, -4, and -3 and etoposide 750 mg/m(2) on days -5, -4, and -3.

37 Platinum-etoposide consisted of etoposide 80-100 mg/m(2) on days 1-3 of each cycle with

38 In all groups, patients received etoposide 80-100 mg/m(2) on days 1-3 of each cycle with

39 s reduced by lowering the cumulative dose of etoposide (950 to 450 mg/m(2)) and intrathecal central n

40 nts with HL treated with BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, pr

41 es, encoding both coniferyl alcohol and main etoposide aglycone pathway enzymes from mayapple, in tob

42 , a late-stage biosynthetic precursor to the etoposide aglycone, using an engineered biosynthetic pat

43 o metabolite and monolignol precursor to the etoposide aglycone.

44 rovement in overall survival versus platinum-etoposide alone in patients with extensive-stage small-c

45 limumab plus platinum-etoposide; or platinum-etoposide alone.

46 valumab plus platinum-etoposide, or platinum-etoposide alone.

47 umab plus platinum-etoposide versus platinum-etoposide alone.

48 Etoposide also increased PID1 promoter reporter activity

49 B patients were treated with carboplatin and etoposide, alternating with cyclophosphamide, idarubicin

50 secondary structure regions, in response to etoposide, an inhibitor of topoisomerase II (TOP2) re-li

51 totic agents tumor necrosis factor alpha and etoposide and are the first to confirm ks-vFLIP as a tra

52 fference in response rates between cisplatin-etoposide and carboplatin-paclitaxel (58% vs 56%; P = .2

53 outcomes and toxic effects between cisplatin-etoposide and carboplatin-paclitaxel in patients with no

54 Cisplatin-etoposide and carboplatin-paclitaxel regimens were assoc

55 cancer survivors (TCSs) after four cycles of etoposide and cisplatin (EPX4) or three or four cycles o

56 une 2010, he was treated with four cycles of etoposide and cisplatin for pulmonary and thoracic lymph

57 Etoposide and cisplatin increased NFkappaB promoter repo

58 that activate p53, including 5-fluorouracil, etoposide and cisplatin.

59 and thalidomide with alternating periods of etoposide and cyclophosphamide, whereas the other arm re

60 condition for which HLH-directed therapy (as etoposide and dexamethasone) can be life-saving.

61 nd causes sensitization to DNA-damaging drug etoposide and DNA repair inhibitor olaparib.

62 Loss of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of

63 umab plus platinum-etoposide versus platinum-etoposide and for durvalumab plus tremelimumab plus plat

64 FDI6 sensitizes pancreatic cancer cells to Etoposide and Gemcitabine induced apoptosis.

65 ine key structural elements of merbarone and etoposide and generated new type II topoisomerase (topoI

66 ed to poison/inhibit TOP2A function, such as etoposide and ICRF-193, do not phenocopy the effects on

67 nterfering RNA promoted apoptosis induced by etoposide and increased EV71 release.

68 and trametinib potentiated tumor response to etoposide and increased overall survival.

69 Our results revealed the cytotoxins etoposide and ivermectin as potent inducers, allowing us

70 n-ATP-competitive inhibitors of TopoIIalpha, etoposide and merbarone, were ineffective at preventing

71 l core merges key pharmacophoric elements of etoposide and merbarone, which are two well-known topoII

72 o three chemotherapeutic drugs (vincristine, etoposide and methotrexate).

73 ansforms the topoisomerase II (TOP2) poisons etoposide and mitoxantrone to chemical forms that have a

74 and her cancer was treated with carboplatin, etoposide and radiotherapy.

75 enes was downregulated in cells treated with etoposide and silenced for ZNF281.

76 "trapped" by chemotherapeutic drugs such as etoposide and subsequently converted into irreversible T

77 Responses to platinum-etoposide and taxanes are frequent, but checkpoint inhib

78 After transformation, both platinum-etoposide and taxanes yielded high response rates, but n

79 P2ccs can be trapped by cancer drugs such as etoposide and then converted into DNA double-strand brea

80 ubicin alternating with cyclophosphamide and etoposide) and radiation therapy.

81 m-etoposide, 268 to durvalumab plus platinum-etoposide, and 269 to platinum-etoposide).

82 duction therapy with idarubicin, cytarabine, etoposide, and all-trans-retinoic acid with or without G

83 It is treated with immune suppressants, etoposide, and allogeneic hematopoietic stem cell transp

84 DNA covalent complexes less efficiently than etoposide, and at higher concentrations they suppress th

85 s (MGCT) if the administration of cisplatin, etoposide, and bleomycin (PEb) is reduced from four to t

86 up A patients were treated with vincristine, etoposide, and carboplatin (VEC) and group B patients we

87 Following IVC (vincristine, etoposide, and carboplatin), adjuvant treatments include

88 erienced a relapse after adjuvant bleomycin, etoposide, and cisplatin (BEP) from 18 centers/11 countr

89 n hypothesized for treatment with bleomycin, etoposide, and cisplatin (BEP).

90 etroperitoneal radiotherapy (RT); bleomycin, etoposide, and cisplatin (BEP); or more than 1 line of t

91 s less drug cost than 2 cycles of bleomycin, etoposide, and cisplatin.

92 , vincristine, cyclophosphamide, ifosfamide, etoposide, and dactinomycin and identified prognostic fa

93 o cycles of remission induction (cytarabine, etoposide, and daunorubicin [50 mg/m(2) x 3 days per cyc

94 including neocarzinostatin, gamma rays, and etoposide, and found that H3K36me3 and H4K16ac were both

95 orubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M/IVAC) for H

96 to busulfan and melphalan or to carboplatin, etoposide, and melphalan by minimisation, balancing age

97 lan group and 188 of 302 in the carboplatin, etoposide, and melphalan group had an event; 3-year even

98 d melphalan group and 11 in the carboplatin, etoposide, and melphalan group had died without relapse

99 roup vs 103 [38%] of 270 in the carboplatin, etoposide, and melphalan group), infection (55 [19%] of

100 se versus 21 (9%) of 239 in the carboplatin, etoposide, and melphalan group.

101 The carboplatin, etoposide, and melphalan regimen consisted of carboplati

102 sulfan and melphalan and 302 to carboplatin, etoposide, and melphalan.

103 halan and 29 (10%) who received carboplatin, etoposide, and melphalan.

104 severe adverse events than did carboplatin, etoposide, and melphalan.

105 fan and melphalan compared with carboplatin, etoposide, and melphalan.

106 elphalan and at least 72 h after carboplatin etoposide, and melphalan.

107 le topoisomerase II inhibitors, doxorubicin, etoposide, and pegylated liposomal doxorubicin (PLD) in

108 ese data demonstrate for the first time that etoposide- and cisplatin-induced apoptosis in medullobla

109 e activity leads to elevated accumulation of etoposide- and mitoxantrone-induced TOP2A and TOP2B-DNA

110 ly assigned to receive either cisplatin plus etoposide (arm A) or the same regimen with bevacizumab (

111 support the use of durvalumab plus platinum-etoposide as a new standard of care for the first-line t

112 one and etoposide may reduce the activity of etoposide as a TOP2 poison and thus reduce the efficacy

113 Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knock

114 ) and augmented ifosfamide, carboplatin, and etoposide (augICE), we assessed clinical factors, quanti

115 nced ABCB5 positivity after carboplatin- and etoposide-based chemotherapy, pointing to clinical signi

116 initially highly responsive to cisplatin and etoposide but in almost every case becomes rapidly chemo

117 overall survival improvement versus platinum-etoposide but the addition of tremelimumab to durvalumab

118 cytarabine, 6-thioguanine, doxorubicin, and etoposide, but not to a non-DNA damaging agent, l-aspara

119 combination of veliparib with cisplatin and etoposide (CE; CE+V) doublet in untreated, extensive-sta

120 tarting on day 22 after commencing cisplatin-etoposide chemotherapy (given as four to six cycles ever

121 ession also suppressed response to cisplatin-etoposide chemotherapy, with similar findings made upon

122 (EPX4) or three or four cycles of bleomycin, etoposide, cisplatin (BEPX3/BEPX4).

123 Treatment with bleomycin-etoposide-cisplatin (BEP; n = 1,819) was associated with

124 elapse risk were observed following TBI plus etoposide compared with chemoconditioning.

125 Platinum-etoposide consisted of etoposide 80-100 mg/m(2) on days

126 group 1 epipodophyllotoxins (teniposide and etoposide) consistently produced the greatest transducti

127 curve 4.1 mg/mL per min per day for 4 days, etoposide continuous infusion of 338 mg/m(2) per day for

128 Patients were prepared using carmustine, etoposide, cytarabine, and melphalan and received consis

129 ents underwent AHSCT using BEAM (carmustine, etoposide, cytarabine, melphalan)+antithymocyte globulin

130 sk) received autologous SCT after carmustine-etoposide-cytarabine-melphalan.

131 Recent shortages of etoposide demonstrate the need for a more dependable pro

132 of tremelimumab to durvalumab plus platinum-etoposide did not significantly improve outcomes versus

133 he chemotherapeutical agents gemcitabine and etoposide distinctively.

134 CTx was predominantly bleomycin, etoposide, doxorubicin cyclophosphamide, vincristine, pr

135 ated with six to eight courses of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

136 n PET2 were switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

137 w-up, 106 months), superiority of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

138 atients switched to two cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

139 to 5) were switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

140 fter two cycles received BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

141 We hypothesized that dose-adjusted etoposide, doxorubicin, cyclophosphamide, vincristine, p

142 s two standard cycles of BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p

143 strate that the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rituximab, and th

144 DSBs, as well as for cellular resistance to etoposide during genomic DNA replication.

145 s durvalumab plus tremelimumab plus platinum-etoposide, durvalumab plus platinum-etoposide, or platin

146 n a 1:1:1 ratio) to durvalumab plus platinum-etoposide; durvalumab plus tremelimumab plus platinum-et

147 g of 700 mg/m(2) carboplatin and 750 mg/m(2) etoposide, each for 3 consecutive days, and each followe

148 ly imprinted polymer (MIP) was presented for etoposide (ETO) detection.

149 Etoposide (ETO) is a commonly used chemotherapeutic drug

150 duced by topoisomerase inhibitors, including etoposide (ETO), results in a potent block to HIV-1 infe

151 poisons, such as the chemotherapeutic agent etoposide (ETO).

152 group received up to six cycles of platinum-etoposide every 3 weeks and optional prophylactic crania

153 rapy groups and up to six cycles of platinum-etoposide every 3 weeks plus prophylactic cranial irradi

154 TOP2 cells treated with etoposide exhibit the same mutation signature, as do cel

155 terial gyrase, GSK299423, ciprofloxacin, and etoposide exhibited 15-, 57-, and 3-fold selectivity for

156 We therefore recommend TBI plus etoposide for patients > 4 years old with high-risk ALL

157 -line recommendations or using platinum plus etoposide for those with large-cell neuroendocrine carci

158 s and doxorubicin had a higher efficacy than etoposide for treating hepatocellular carcinoma.

159 ing bevacizumab to first-line cisplatin plus etoposide for treatment of extensive-disease (ED) small-

160 Indeed, the etoposide formulated as a nanosuspension by a bottom-up

161 2%) patients in the durvalumab plus platinum-etoposide group (cardiac arrest, dehydration, hepatotoxi

162 e durvalumab plus tremelimumab plus platinum-etoposide group (death, febrile neutropenia, and pulmona

163 is [n=1 each]), and two (1%) in the platinum-etoposide group (pancytopenia and thrombocytopenia [n=1

164 ted patients in the durvalumab plus platinum-etoposide group and 166 (62%) of 266 in the platinum-eto

165 re allocated to the durvalumab plus platinum-etoposide group and 269 to the platinum-etoposide group.

166 platinum-etoposide group versus the platinum-etoposide group from a planned interim analysis.

167 Patients in the platinum-etoposide group received up to six cycles of platinum-et

168 I 11.5-14.8) in the durvalumab plus platinum-etoposide group versus 10.3 months (9.3-11.2) in the pla

169 ort results for the durvalumab plus platinum-etoposide group versus the platinum-etoposide group from

170 and 88 [33%] of 266 patients in the platinum-etoposide group) and anaemia (34 [13%], 24 [9%], and 48

171 e durvalumab plus tremelimumab plus platinum-etoposide group, 64 [24%] of 265 patients in the durvalu

172 e durvalumab plus tremelimumab plus platinum-etoposide group, 85 (32%) in the durvalumab plus platinu

173 265 patients in the durvalumab plus platinum-etoposide group, and 88 [33%] of 266 patients in the pla

174 up, 85 (32%) in the durvalumab plus platinum-etoposide group, and 97 (36%) in the platinum-etoposide

175 ersus 10.3 months (9.3-11.2) in the platinum-etoposide group, with 34% (26.9-41.0) versus 25% (18.4-3

176 (investigator's discretion) in the platinum-etoposide group.

177 inum-etoposide group and 269 to the platinum-etoposide group.

178 toposide group, and 97 (36%) in the platinum-etoposide group.

179 e group and 166 (62%) of 266 in the platinum-etoposide group; adverse events leading to death occurre

180 re included from 31 studies in the cisplatin-etoposide groups (median age, 61 years; 65% male; 40% sq

181 y metastases, age, or doses of cisplatin and etoposide had no influence on follow-up PFT, and renal f

182 rovement in overall survival versus platinum-etoposide (hazard ratio [HR] 0.82 [95% CI 0.68-1.00]; p=

183 ) or high-dose cytarabine, daunorubicin, and etoposide (HD-ADE, n = 133) as induction I.

184 sing cells recovered from cytotoxic doses of etoposide; however, LMP1 expression was sufficient for t

185 rovement in overall survival versus platinum-etoposide (HR 0.75 [95% CI 0.62-0.91]; nominal p=0.0032)

186 ed by augmented ifosfamide, carboplatin, and etoposide (ICE).

187 He received four courses of etoposide, ifosfamide, and cisplatin chemotherapy, given

188 at inhibition of TOP2 religation activity by etoposide in AIRE-expressing cells had a synergistic eff

189 addition of palifosfamide to carboplatin and etoposide in extensive stage (ES) small-cell lung cancer

190 ory has characterized acquired resistance to etoposide in human leukemia K562 cells.

191 eased the apoptosis induced by cisplatin and etoposide in medulloblastoma and glioblastoma cell lines

192 might reduce the need for anthracycline and etoposide in pediatric patients with acute myeloid leuke

193 The addition of bevacizumab to cisplatin and etoposide in the first-line treatment of ED-SCLC had an

194 umab plus platinum-etoposide versus platinum-etoposide in the intention-to-treat population.

195 ally survived treatment with carboplatin and etoposide in vitro and in human MCC xenograft-bearing mi

196 us either cisplatin or carboplatin (platinum-etoposide) in treatment-naive patients with ES-SCLC.

197 Cisplatin and etoposide increased phosphorylation of AKT (S473) and GR

198 nd find that cisplatin, cyclophosphamide and etoposide induce extra base substitutions with distinct

199 ased NFkappaB promoter reporter activity and etoposide induced nuclear translocation of NFkappaB.

200 ons, protecting up to 80% of neurons against etoposide-induced apoptosis at concentrations as low as

201 GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown.

202 d proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell line

203 and to their protection from cisplatin- and etoposide-induced apoptosis.

204 bile salt-induced apoptosis (BSIA) but also etoposide-induced apoptosis.

205 In biodistribution studies, etoposide-induced cell death in a SW1222 xenograft model

206 iesterase activity and is protective against etoposide-induced cell death, but co-immunoprecipitates

207 ated with leukemic transformation, including etoposide-induced chromosomal breaks at the MLL and RUNX

208 Consistent with this, isoeugenol exacerbated etoposide-induced cytotoxicity, which generates TOP2-med

209 OP2alpha/170 mRNA and resulted in attenuated etoposide-induced DNA damage (gain-of-miRNA-inhibitory f

210 0 mRNA levels and resulted in enhancement of etoposide-induced DNA damage (loss-of-miRNA-inhibitory f

211 We found that etoposide-induced DSBs are efficiently resected into 3'

212 nce the initial appearance of radiation- and etoposide-induced gammaH2AX and 53BP1 foci, it markedly

213 itination was required for the liberation of etoposide-induced protein-free DSBs and is therefore an

214 P2-DNA complexes, and doxorubicin suppressed etoposide-induced TOP2-DNA complexes.

215 he defects in Mre11 compromise the repair of etoposide-induced Top2-DNA covalent complexes, and MRE11

216 Here, we have quantified etoposide-induced trapping of TOP2ccs, their conversion

217 intensification 1 (high-dose cytarabine and etoposide), intensification 2 (high-dose cytarabine and

218 Etoposide is a plant-derived drug used clinically to tre

219 Because the toxicity of etoposide is pH-independent, there could be a more gener

220 type induced by DNA damage reagents, such as Etoposide, is at least in part mediated by MDM2-dependen

221 termediate by chemotherapeutic drugs such as etoposide leads to persistent and potentially toxic DSBs

222 e, adding MTAs to radiation, doxorubicin, or etoposide led to more sustained gamma-H2AX levels.

223 ethotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using concealed permuted blocks with t

224 ontaining anthracyclines or mitoxantrone and etoposide may reduce the activity of etoposide as a TOP2

225 phamide followed by dose-reduced carboplatin/etoposide/melphalan (n = 176) or single transplant with

226 = 176) or single transplant with carboplatin/etoposide/melphalan (n = 179).

227 These drugs include etoposide, mitoxantrone, and the anthracyclines doxorubi

228 sing for future clinical evaluation of these etoposide nanosuspensions.

229 onstrate that DSBs induced in pre-B cells by etoposide or bleomycin inhibit recombination of Igkappa

230 preparations of mammalian cells treated with etoposide or electrochemically induced DNA damage condit

231 n stimulated with apoptotic triggers such as etoposide or vesicular stomatitis virus infection, but d

232 d epithelial cells with DNA-damaging agents, etoposide or zeocin, induces HSATII RNA expression, and

233 how that DSBs induced by ionizing radiation, etoposide, or bleomycin suppress Rag1 and Rag2 mRNA leve

234 platinum-etoposide, durvalumab plus platinum-etoposide, or platinum-etoposide alone.

235 is was induced by exposure to actinomycin D, etoposide, or tunicamycin, with each agent triggering a

236 ; durvalumab plus tremelimumab plus platinum-etoposide; or platinum-etoposide alone.

237 to two chemotherapeutic drugs, bleomycin and etoposide (P < 0.001).

238 se (GR) received four cycles of platinum and etoposide (PE), for total doses of platinum 420 mg/m(2)

239 us ART (week 48 PFS 50%, 32 to 67; n=59) and etoposide plus ART (20%, 6 to 33; n=59), and -20% (-33%

240 el plus ART showing superiority to both oral etoposide plus ART and bleomycin and vincristine plus AR

241 The etoposide plus ART arm also closed due to inferiority in

242 ort our experience with 2 cycles of adjuvant etoposide plus cisplatin (EPx2) after therapeutic primar

243 r placebo, combined with up to six cycles of etoposide plus cisplatin or carboplatin every 3 weeks, u

244 rapy groups received four cycles of platinum-etoposide plus durvalumab 1500 mg with or without tremel

245 ients received up to four cycles of platinum-etoposide plus durvalumab 1500 mg with or without tremel

246 or without tremelimumab, in combination with etoposide plus either cisplatin or carboplatin (platinum

247 gh-dose prolonged-infusion ifosfamide in SS; etoposide plus ifosfamide in MPNST; and gemcitabine plus

248 cristine, doxorubicin, cyclophosphamide, and etoposide plus radiotherapy) would improve patient outco

249 a third course, MACE (amsacrine, Ara-C, and etoposide), plus a fourth course of MidAc (mitoxantrone

250 n, vincristine, and prednisone or rituximab, etoposide, prednisone, vincristine, cyclophosphamide, an

251 EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, an

252 oup, phase III study, compared dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, do

253 s caused by methyl methanesulfonate (MMS) or etoposide promote the formation of Ku70-Pol-beta complex

254 Carboplatin- and etoposide-resistant MCC cell lines exhibited increased e

255 In these cells, etoposide robustly induced TOP2B covalent complexes, but

256 Our data show etoposide's antibacterial activity is due to DNA gyrase

257 Durvalumab plus platinum-etoposide showed sustained improvement in overall surviv

258 First-line durvalumab plus platinum-etoposide showed sustained overall survival improvement

259 th either cisplatin or carboplatin (platinum-etoposide) showed a significant improvement in overall s

260 First-line durvalumab plus platinum-etoposide significantly improved overall survival in pat

261 Like etoposide, since PR-619 affected TOP2 enzyme activity in

262 de optimized formulations for nanostructured etoposide solutions and validate by means of in vitro an

263 In vitro, etoposide-stabilized DNA cleavage was attenuated by doxo

264 d reduce tumor growth and sensitize cells to etoposide, suggesting a clinical application of miRNAs a

265 evious analogue 4a toward the treatment with etoposide, suggesting that these analogues could serve a

266 synthesis and DNA damage were implicated in etoposide susceptibility.

267 ntravenous bleomycin and vincristine or oral etoposide (the investigational arms), or intravenous pac

268 o not support the addition of ifosfamide and etoposide to postoperative chemotherapy in patients with

269 iferation and increase in differentiation in etoposide-treated neurospheres.

270 served when p53 was activated in response to etoposide treatment and remained lower than those measur

271 Etoposide treatment combined with FAIM2 inhibition also

272 cancer cells to ionizing radiation (IR) and etoposide treatment, as assessed by clonogenic survival

273 f topoisomerase I and II by camptothecin and etoposide treatment, respectively, increased DSBs at the

274 le-stranded break (DSB) sites in response to etoposide treatment.

275 f DNA-PK at serine 2056 in response to IR or etoposide treatment.

276 ed with those expressing WT SMURF2 following etoposide treatment.

277 rosporine, taxol, doxorubicin, cisplatin and etoposide, utilized as controls, neferine was shown to i

278 conditioning with fractionated 12 Gy TBI and etoposide versus fludarabine, thiotepa, and either busul

279 h durvalumab plus tremelimumab plus platinum-etoposide versus platinum-etoposide alone.

280 verall survival for durvalumab plus platinum-etoposide versus platinum-etoposide and for durvalumab p

281 r durvalumab plus tremelimumab plus platinum-etoposide versus platinum-etoposide in the intention-to-

282 of vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) and one course of vincristine, dactinom

283 ncluding 19 treated with modified infusional etoposide, vincristine, and doxorubicin with cyclophosph

284 apeutic agents such as doxorubicin (Dox) and etoposide (VP-16).

285 , GSK2830371 enhanced doxorubicin- (Dox) and etoposide- (VP-16) induced cytotoxicity in a subset of N

286 d DNA single-strand breaks (SSBs) induced by etoposide (VP16) in vivo.

287 For cisplatin-etoposide vs carboplatin-paclitaxel, there was no signif

288 Durvalumab plus platinum-etoposide was associated with a significant improvement

289 Cisplatin-etoposide was associated with higher grade 3 to 4 hemato

290 Durvalumab plus tremelimumab plus platinum-etoposide was not associated with a significant improvem

291 RT) with carboplatin-paclitaxel or cisplatin-etoposide were identified using electronic databases (ME

292 Doses of doxorubicin, cyclophosphamide, and etoposide were reduced midstudy because of nonhematologi

293 TOP2-DNA complexes stabilized by etoposide were shown to be conjugated to ubiquitin, and

294 However, in contrast to etoposide, which induces TOP2-DNA complexes with a pan-n

295 Etoposide, which is largely used as an anti-cancerous ag

296 First-line durvalumab plus etoposide with either cisplatin or carboplatin (platinum

297 r first-line chemotherapy with cisplatin and etoposide with or without bleomycin.

298 boplatin, cyclophosphamide, vincristine, and etoposide with or without topotecan, vincristine, and do

299 antibacterial QPT-1 and the anticancer drug etoposide with Staphylococcus aureus DNA gyrase, showing

300 an IC(50) = 120 muM for the anticancer drug etoposide] with excellent metabolic stability and solubi