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1 the treatment of two drugs (doxorubicin and etoposide).
2 by 3 cycles of ICE (ifosfamide, carboplatin, etoposide).
3 e to the anti-cancer drug and TOP2 inhibitor etoposide.
4 osine arabinoside (ara-C), daunorubicin, and etoposide.
5 nsist of four cycles of a platinum agent and etoposide.
6 se (5 muM) of the topoisomerase II inhibitor etoposide.
7 ier function following exposure to high-dose etoposide.
8 ange enhanced the effects of camptothecin or etoposide.
9 ction of apoptosis by the DNA-damaging agent etoposide.
10 e highly resistant to ATRA, doxorubicin, and etoposide.
11 inst cell death induced by dexamethasone and etoposide.
12 d with the DNA-damaging agents cisplatin and etoposide.
13 to topoisomerase II (topo II) inhibition by etoposide.
14 -strand breaks in response to doxorubicin or etoposide.
15 n, paclitaxel, vinblastine, vincristine, and etoposide.
16 n response to tumor necrosis factor (TNF) or etoposide.
17 following exposure to the DNA-damaging agent etoposide.
18 n Top2beta-DNA covalent complexes induced by etoposide.
19 nced response to the topoisomerase-II poison etoposide.
20 ll sensitivity to the Topo II-targeting drug etoposide.
21 LC) are carboplatin-paclitaxel and cisplatin-etoposide.
22 or the expression of ZNF281 and treated with etoposide.
23 ders cells sensitive to the anticancer agent etoposide.
24 by treatment with the chemotherapeutic agent etoposide.
25 hemotherapeutic drugs, that is, cisplatin or etoposide.
28 s of high-dose carboplatin 1,500 mg/m(2) and etoposide 1,500 mg/m(2) (CE, arm A) or three cycles of V
29 ycle of high-dose carboplatin 2,200 mg/m(2), etoposide 1,800 mg/m(2), and cyclophosphamide 6,400 mg/m
31 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
32 rum concentration-time curve 5 on day 1 plus etoposide 100 mg/m(2) per day on days 1 to 3 every 21 da
34 rum concentration-time curve 4 on day 1 plus etoposide 100 mg/m(2) per day plus palifosfamide 130 mg/
35 n day -12), carmustine 300 mg/m(2) (day -6), etoposide 100 mg/m(2) twice daily (days -5 to -2), cytar
36 eceive mitotane plus either a combination of etoposide (100 mg per square meter of body-surface area
37 s cisplatin [20 mg/m(2) per day for 5 days], etoposide [100 mg/m(2) per day for 5 days], and intramus
38 cycles (cisplatin 33 mg/m(2) on days 1 to 3, etoposide 167 mg/m(2) on days 1 to 3, bleomycin 15 U/m(2
40 of carboplatin AUC 5, day 3; three doses of etoposide 200 mg/m(2) every 12 h, day 1) before consider
43 h either one cycle of cisplatin 100 mg/m(2), etoposide 375 mg/m(2), and ifosfamide 6 g/m(2) (VIP) plu
44 m2) alternating with ifosfamide (9 g/m2) and etoposide (500 mg/m2) for 14 cycles, with filgrastim (5
45 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
46 ith cytarabine 100 mg/m(2) daily for 5 days, etoposide 75 mg/m(2) daily for 5 days, and idarubicin 9
48 s reduced by lowering the cumulative dose of etoposide (950 to 450 mg/m(2)) and intrathecal central n
49 did not occur when ABT-737 was combined with etoposide, a gold-standard cytotoxic for SCLC therapy.
50 The moderate and temporally limited use of etoposide, a topoisomerase inhibitor, to eliminate encep
52 orubicin and cytarabine (DA) with or without etoposide (ADE; n = 1983) or ADE versus fludarabine, cyt
53 nts with HL treated with BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, pr
54 two cycles of escalated BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, pr
56 y to (-)-4'-desmethylepipodophyllotoxin (the etoposide aglycone), a naturally occurring lignan that i
58 B patients were treated with carboplatin and etoposide, alternating with cyclophosphamide, idarubicin
59 iological evaluation of a focused library of etoposide analogues, with the identification of two nove
60 totic agents tumor necrosis factor alpha and etoposide and are the first to confirm ks-vFLIP as a tra
62 to high-dose chemotherapy with thiotepa and etoposide and autologous peripheral blood stem-cell resc
63 NF-kappaB activation by BRCA1 in response to etoposide and camptothecin is demonstrated by the signif
64 ng agents mitomycin C and Irofulven, but not etoposide and camptothecin, suggesting a role in nucleot
65 fference in response rates between cisplatin-etoposide and carboplatin-paclitaxel (58% vs 56%; P = .2
66 outcomes and toxic effects between cisplatin-etoposide and carboplatin-paclitaxel in patients with no
68 current chemotherapy consisting of cisplatin/etoposide and chest radiotherapy, resulting in a marked
69 cancer survivors (TCSs) after four cycles of etoposide and cisplatin (EPX4) or three or four cycles o
70 une 2010, he was treated with four cycles of etoposide and cisplatin for pulmonary and thoracic lymph
72 The median cumulative doses of doxorubicin-etoposide and cyclophosphamide administered in the SC-EP
73 and thalidomide with alternating periods of etoposide and cyclophosphamide, whereas the other arm re
75 ss the treatment response to the neoadjuvant etoposide and found a consistent and reliable improvemen
76 ine key structural elements of merbarone and etoposide and generated new type II topoisomerase (topoI
80 n-ATP-competitive inhibitors of TopoIIalpha, etoposide and merbarone, were ineffective at preventing
81 ansforms the topoisomerase II (TOP2) poisons etoposide and mitoxantrone to chemical forms that have a
82 and cisplatin (VIPx4) instead of bleomycin, etoposide and platinum (BEPx4) to prevent pulmonary comp
85 of TDP2 sensitizes mtp53-expressing cells to etoposide and that mtp53 and TDP2 are frequently overexp
86 P2ccs can be trapped by cancer drugs such as etoposide and then converted into DNA double-strand brea
89 ng lignan that is the immediate precursor of etoposide and, unlike podophyllotoxin, a potent topoisom
91 s (MGCT) if the administration of cisplatin, etoposide, and bleomycin (PEb) is reduced from four to t
92 chemotherapy with compressed PEB (cisplatin, etoposide, and bleomycin) was initiated every 3 weeks fo
93 up A patients were treated with vincristine, etoposide, and carboplatin (VEC) and group B patients we
94 temic chemotherapy with vincristine sulfate, etoposide, and carboplatin had failed in 10 patients (91
95 motherapy with a combination of vincristine, etoposide, and carboplatin in patients with focal vitreo
98 etroperitoneal radiotherapy (RT); bleomycin, etoposide, and cisplatin (BEP); or more than 1 line of t
101 , vincristine, cyclophosphamide, ifosfamide, etoposide, and dactinomycin and identified prognostic fa
102 and doxorubicin or vincristine, prednisone, etoposide, and doxorubicin chemotherapy; additional two
103 including neocarzinostatin, gamma rays, and etoposide, and found that H3K36me3 and H4K16ac were both
104 orubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M/IVAC) for H
106 to busulfan and melphalan or to carboplatin, etoposide, and melphalan by minimisation, balancing age
107 lan group and 188 of 302 in the carboplatin, etoposide, and melphalan group had an event; 3-year even
108 d melphalan group and 11 in the carboplatin, etoposide, and melphalan group had died without relapse
109 roup vs 103 [38%] of 270 in the carboplatin, etoposide, and melphalan group), infection (55 [19%] of
117 ubicin, vinblastine, vincristine, bleomycin, etoposide, and prednisone (Stanford V) in G studies.
119 (cyclophosphamide, doxorubicin, vincristine, etoposide, and prednisone) was administered (in patients
120 da; n = 1268), and to amsacrine, cytarabine, etoposide, and then mitoxantrone/cytarabine (MACE-MidAC)
122 ese data demonstrate for the first time that etoposide- and cisplatin-induced apoptosis in medullobla
123 e activity leads to elevated accumulation of etoposide- and mitoxantrone-induced TOP2A and TOP2B-DNA
124 ng in an increased Bcl-2 level and decreased etoposide- and UV/gamma radiation-mediated DNA fragmenta
125 targeting poisons such as anthracyclines and etoposide are commonly used for cancer chemotherapy and
126 erase poisons such as the epipodophyllotoxin etoposide are widely used effective cytotoxic anticancer
127 ly assigned to receive either cisplatin plus etoposide (arm A) or the same regimen with bevacizumab (
129 ) and augmented ifosfamide, carboplatin, and etoposide (augICE), we assessed clinical factors, quanti
130 nced ABCB5 positivity after carboplatin- and etoposide-based chemotherapy, pointing to clinical signi
131 rapy entailing three cycles of cisplatin and etoposide before radiation (chemotherapy first [CT1]) or
133 initially highly responsive to cisplatin and etoposide but in almost every case becomes rapidly chemo
134 kt signaling synergized with camptothecin or etoposide, but higher A-443654 or MK-2206 concentrations
135 cytarabine, 6-thioguanine, doxorubicin, and etoposide, but not to a non-DNA damaging agent, l-aspara
136 erapy to 60 Gy in 6 wk with either cisplatin/etoposide (C/E, n = 28) weeks 1 and 5 or weekly carbopla
137 Topoisomerase II (Topo II) poisons such as etoposide can induce abortive DNA strand breaks in which
139 tarting on day 22 after commencing cisplatin-etoposide chemotherapy (given as four to six cycles ever
144 e Veterans Health Administration with either etoposide-cisplatin (EP) or carboplatin-paclitaxel (CP).
145 group 1 epipodophyllotoxins (teniposide and etoposide) consistently produced the greatest transducti
146 The topoisomerase II poisons doxorubicin and etoposide constitute longstanding cornerstones of chemot
147 curve 4.1 mg/mL per min per day for 4 days, etoposide continuous infusion of 338 mg/m(2) per day for
148 Patients were prepared using carmustine, etoposide, cytarabine, and melphalan and received consis
149 eceived high-dose treatment with carmustine, etoposide, cytarabine, and melphalan as well as rabbit a
150 igh-dose BEAM/C (bis-chloroethylnitrosourea, etoposide, cytarabine, and melphalan or cyclophosphamide
154 rospective study of infusional dose-adjusted etoposide, doxorubicin, and cyclophosphamide with vincri
155 rospective study of infusional dose-adjusted etoposide, doxorubicin, and cyclophosphamide with vincri
156 ow-intensity treatment consisting of infused etoposide, doxorubicin, and cyclophosphamide with vincri
158 s two standard cycles of BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
159 w-up, 106 months), superiority of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
160 EACOPP(escalated) (escalated-dose bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
161 After six to eight cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
162 atients switched to two cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
163 nfavorable HIV-HL, four cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
164 to 5) were switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
165 fter two cycles received BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, p
166 strate that the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rituximab, and th
169 g of 700 mg/m(2) carboplatin and 750 mg/m(2) etoposide, each for 3 consecutive days, and each followe
170 h as the topoisomerase II (TopoII) inhibitor etoposide effectively reduce disease in a minority of pa
171 tment with the conventional chemotherapeutic etoposide equivalently enhanced the survival of both str
174 duced by topoisomerase inhibitors, including etoposide (ETO), results in a potent block to HIV-1 infe
176 terial gyrase, GSK299423, ciprofloxacin, and etoposide exhibited 15-, 57-, and 3-fold selectivity for
177 icacy of HDCT, consisting of carboplatin and etoposide followed by stem cell reinfusion, for the salv
178 -line recommendations or using platinum plus etoposide for those with large-cell neuroendocrine carci
180 mice, to study the activity and mechanism of etoposide for treating HLH and found that it substantial
181 ing bevacizumab to first-line cisplatin plus etoposide for treatment of extensive-disease (ED) small-
182 re included from 31 studies in the cisplatin-etoposide groups (median age, 61 years; 65% male; 40% sq
183 y metastases, age, or doses of cisplatin and etoposide had no influence on follow-up PFT, and renal f
185 sing cells recovered from cytotoxic doses of etoposide; however, LMP1 expression was sufficient for t
186 therapy, either ifosfamide, carboplatin, and etoposide (ICE) or dexamethasone, cytarabine, and cispla
188 for the DNA topoisomerase II (TOP2A) poison etoposide identified TOP2A, as expected, and also cyclin
190 Seventy-six patients were treated with EIA (etoposide, ifosfamide, doxorubicin)+RHT (>/=5 cycles: 69
191 dose cytosine arabinoside, cyclophosphamide, etoposide, ifosphamide, corticosteroids, and triple intr
193 at inhibition of TOP2 religation activity by etoposide in AIRE-expressing cells had a synergistic eff
195 addition of palifosfamide to carboplatin and etoposide in extensive stage (ES) small-cell lung cancer
196 eased the apoptosis induced by cisplatin and etoposide in medulloblastoma and glioblastoma cell lines
197 The addition of bevacizumab to cisplatin and etoposide in the first-line treatment of ED-SCLC had an
198 We found that the therapeutic mechanism of etoposide in this model system involved potent deletion
199 ally survived treatment with carboplatin and etoposide in vitro and in human MCC xenograft-bearing mi
200 nd find that cisplatin, cyclophosphamide and etoposide induce extra base substitutions with distinct
201 ethylbenz(a)anthracene (DMBA), cisplatin and etoposide induce nuclear DNA leakage into the cytosol th
202 ased NFkappaB promoter reporter activity and etoposide induced nuclear translocation of NFkappaB.
203 sion in SS was associated with resistance to etoposide-induced apoptosis and cell migration toward ch
204 Nrf2-activated tumor cells led to increased etoposide-induced apoptosis and decreased cell survival
205 ons, protecting up to 80% of neurons against etoposide-induced apoptosis at concentrations as low as
206 Moreover, although Trim39 loss inhibited etoposide-induced apoptosis in p53-negative cells, apopt
207 c-Src with shRNA decreased irradiation- and etoposide-induced apoptosis, suggesting that inhibitors
210 aC were less sensitive to staurosporine- and etoposide-induced cell death, and silencing of VDAC1-Del
211 ion of miR-23a and miR-27a mimics attenuated etoposide-induced changes in Noxa, Puma, and Bax, reduce
212 ated with leukemic transformation, including etoposide-induced chromosomal breaks at the MLL and RUNX
213 We demonstrated that 2DG synergized with etoposide-induced cytotoxicity and significantly increas
214 Consistent with this, isoeugenol exacerbated etoposide-induced cytotoxicity, which generates TOP2-med
216 hairpin RNA (shRNA) increases sensitivity to etoposide-induced DNA damage and neuronal cell death.
220 n contrast, miRs hairpin inhibitors enhanced etoposide-induced neuronal apoptosis and caspase activat
222 he defects in Mre11 compromise the repair of etoposide-induced Top2-DNA covalent complexes, and MRE11
225 y used chemotherapeutic drugs, docetaxel and etoposide, judging from significantly reduced IC50 value
226 n chemotherapeutics (such as doxorubicin and etoposide), leading to the accumulation of cytotoxic enz
228 ethotrexate (MAP) or MAP plus ifosfamide and etoposide (MAPIE) using concealed permuted blocks with t
229 hoblastic neoplasia (GTN) frequently receive etoposide, methotrexate, and dactinomycin alternating we
230 5 to 1.1) and also for patients treated with etoposide, methotrexate, and dactinomycin followed by cy
231 r high-dose cytarabine plus daunorubicin and etoposide; of these, 18 showed association (P < .05) wit
232 onstrate that DSBs induced in pre-B cells by etoposide or bleomycin inhibit recombination of Igkappa
233 wing treatment with the DNA-damaging agents, etoposide or camptothecin, BRCA1 is required for the act
234 Cellular responses to DNA damage induced by etoposide or doxorubicin include down-regulation of endo
235 preparations of mammalian cells treated with etoposide or electrochemically induced DNA damage condit
236 accumulate in normal human cells exposed to etoposide or infected by an E1B 55-kDa protein-null muta
239 n stimulated with apoptotic triggers such as etoposide or vesicular stomatitis virus infection, but d
240 how that DSBs induced by ionizing radiation, etoposide, or bleomycin suppress Rag1 and Rag2 mRNA leve
241 autophagy induced by amino acid starvation, etoposide, or interleukin-3 withdrawal did not affect ce
242 is was induced by exposure to actinomycin D, etoposide, or tunicamycin, with each agent triggering a
244 se (GR) received four cycles of platinum and etoposide (PE), for total doses of platinum 420 mg/m(2)
246 r placebo, combined with up to six cycles of etoposide plus cisplatin or carboplatin every 3 weeks, u
247 approach using high-dose consolidation with etoposide plus cytarabine (EA); three, progression-free
248 motherapy with mitoxantrone, cytarabine, and etoposide preceded, or not, by a course of GO (6 mg/m(2)
250 received six cycles of dose-adjusted EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, an
251 n, vincristine, and prednisone or rituximab, etoposide, prednisone, vincristine, cyclophosphamide, an
252 ilized by antitopoisomerase II drugs such as etoposide, providing the opportunity for illegitimate en
253 we have found several possible indicators of etoposide resistance operating in MCF7VP cells, includin
258 the death response to other stimuli such as etoposide, staurosporine, or UV remained fully intact.
259 hibitor NSC23766 attenuated doxorubicin- and etoposide-stimulated H2AX phosphorylation, induction of
260 d reduce tumor growth and sensitize cells to etoposide, suggesting a clinical application of miRNAs a
261 by R-HDS (cyclophosphamide, cytarabine, and etoposide) supported by autologous stem-cell transplanta
265 rmal cells, and it acts synergistically with etoposide to kill cancer cells in vitro and slow tumor g
266 o not support the addition of ifosfamide and etoposide to postoperative chemotherapy in patients with
268 evated in SI stem/progenitor cells of fasted etoposide-treated mice, which importantly correlated wit
270 served when p53 was activated in response to etoposide treatment and remained lower than those measur
273 uction of endogenous Ei24 expression through etoposide treatment similarly inhibited nuclear import i
274 ments responded in a heterogeneous manner to etoposide treatment, which could be determined only by t
283 t not with anti-EGFR antibody (Cetuximab) or etoposide, triggers a burst in emission of exosome-like
284 etespib synergized with both doxorubicin and etoposide, two topoisomerase II inhibitors commonly used
285 ng vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) in standard-risk localized disease (NCT
288 , GSK2830371 enhanced doxorubicin- (Dox) and etoposide- (VP-16) induced cytotoxicity in a subset of N
291 apoptosis induction in neuroblastoma cells, etoposide was ineffective for glioblastoma cell lines.
293 RT) with carboplatin-paclitaxel or cisplatin-etoposide were identified using electronic databases (ME
297 boplatin, cyclophosphamide, vincristine, and etoposide with or without topotecan, vincristine, and do
298 antibacterial QPT-1 and the anticancer drug etoposide with Staphylococcus aureus DNA gyrase, showing
299 pathway and suppressed senescence caused by etoposide without affecting DNA damage response, p53/p21
300 al product precursor of the chemotherapeutic etoposide, yet only part of its biosynthetic pathway is
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