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1 rone, and the anthracyclines doxorubicin and epirubicin.
2 nge in HR or CO, compared to doxorubicin and epirubicin.
3 in the resistant counterparts in response to epirubicin.
4 tumors correlate with patients' response to epirubicin.
5 from patients who had complete responses to epirubicin.
6 breast cancer cells to paclitaxel but not to epirubicin.
7 to cisplatin, carboplatin, temozolomide, and epirubicin.
8 lls are highly resistant to mitoxantrone and epirubicin.
9 used such as daunorubicin, doxorubicin, and epirubicin.
10 ity in patients with breast cancer receiving epirubicin.
11 f the 1045 patients treated with accelerated epirubicin.
12 emical aptasensor for selective detection of epirubicin.
13 ctivation when compared with doxorubicin and epirubicin.
14 cycles of FEC (fluorouracil 500 mg/m(2) plus epirubicin 100 mg/m(2) plus cyclophosphamide 500 mg/m(2)
16 hose either FEC for eight cycles (n=1265) or epirubicin (100 mg/m(2) at 3-weekly intervals) for four
17 three cycles of fluorouracil (500 mg/m(2)), epirubicin (100 mg/m(2)), and cyclophosphamide (500 mg/m
18 treatment was 3 cycles of FEC (fluorouracil, epirubicin [100 mg/m(2) per dose], and cyclophosphamide)
19 receive three cycles of preoperative CT with epirubicin 120 mg/m(2) and ifosfamide 9 g/m(2) and granu
20 mly assigned to three preoperative cycles of epirubicin 120 mg/m(2) plus ifosfamide 9 g/m(2), and 160
21 t bypasses the low-yielding semisynthesis of epirubicin (4'-epidoxorubicin) and 4'-epidaunorubicin, i
22 s follows: ifosfamide 54 g/m(2) (both arms), epirubicin 450 mg/m(2), etoposide 1,350 mg/m(2) (six-dru
23 modified-dose EOC plus panitumumab (mEOC+P; epirubicin 50 mg/m(2) and oxaliplatin 100 mg/m(2) on day
24 up to eight 21-day cycles of open-label EOC (epirubicin 50 mg/m(2) and oxaliplatin 130 mg/m(2) on day
25 e 15 mg/kg intravenously on day 1) plus ECX (epirubicin 50 mg/m(2) intravenously on day 1, cisplatin
26 in combination with open-label chemotherapy (epirubicin 50 mg/m(2) intravenously; cisplatin 60 mg/m(2
28 dose de-escalation was made to EOC + P DL-1 (epirubicin 50 mg/m(2), oxaliplatin130 mg/m(2), capecitab
29 nd three postoperative cycles of intravenous epirubicin (50 mg per square meter of body-surface area)
30 d capecitabine (ECX; four 3-weekly cycles of epirubicin [50 mg/m(2)] and cisplatin [60 mg/m(2)] intra
31 on to receive FEC (fluorouracil 600 mg/m(2), epirubicin 60 mg/m(2), cyclophosphamide 600 mg/m(2) at 3
32 treatment received fluorouracil 500 mg/m(2), epirubicin 75 mg/m(2), and cyclophosphamide 500 mg/m(2)
33 in 75 mg/m2 and paclitaxel 200 mg/m2) or EC (epirubicin 75 mg/m2 and cyclophosphamide 600 mg/m2) admi
34 were randomly assigned to receive either EP (epirubicin 75 mg/m2 and paclitaxel 200 mg/m2) or EC (epi
35 concomitant with four cycles of neoadjuvant epirubicin (75 mg/m(2)) plus docetaxel (75 mg/m(2)) and
36 es 1-4) and FEC (fluorouracil [500 mg/m(2)], epirubicin [75 mg/m(2)], and cyclophosphamide [500 mg/m(
37 mg/m(2) followed in both arms by four times epirubicin 90 mg/m(2) plus cyclophosphamide 600 mg/m(2)
38 ree cycles of FEC (fluorouracil 600 mg/m(2), epirubicin 90 mg/m(2), and cyclophosphamide 600 mg/m(2))
39 /m(2)) every 3 weeks (DC) or three cycles of epirubicin (90 mg/m(2)) and cyclophosphamide (600 mg/m(2
40 eceive 3 cycles of fluorouracil (500 mg/m2), epirubicin (90 mg/m2), and cyclophosphamide (500 mg/m2),
43 ates were 72.7% (95% CI, 68.0% to 77.3%) for epirubicin alone and 79.5% (95% CI, 75.2% to 83.8%) for
44 n, and capecitabine chemotherapy: 50 mg/m(2) epirubicin and 60 mg/m(2) cisplatin on day 1 and 1250 mg
45 les of 90 mg/m(2) intravenously administered epirubicin and 600 mg/m(2) intravenously administered cy
46 CI 84.3-87.3) of patients receiving standard epirubicin and 87.1% (85.6-88.4) of those receiving acce
47 ates were 81.8% (95% CI, 77.7% to 85.9%) for epirubicin and 88.9% (95% CI, 85.5% to 92.2%) for epirub
49 dvanced breast cancer, 3 months of high-dose epirubicin and cyclophosphamide (EC) administered every
50 axel with or without gemcitabine followed by epirubicin and cyclophosphamide achieved pCR compared wi
51 also the effect of sequencing the blocks of epirubicin and cyclophosphamide and paclitaxel (with or
52 gh addition of gemcitabine to paclitaxel and epirubicin and cyclophosphamide chemotherapy does not im
53 nadir-based tailored and dose-dense adjuvant epirubicin and cyclophosphamide every 2 weeks followed b
55 he intention-to-treat population assigned to epirubicin and cyclophosphamide followed by docetaxel (E
56 thological complete response were 14.9% with epirubicin and cyclophosphamide followed by docetaxel an
57 phamide followed by docetaxel and 18.4% with epirubicin and cyclophosphamide followed by docetaxel pl
58 of 40 mm on palpation to receive neoadjuvant epirubicin and cyclophosphamide followed by docetaxel, w
59 hen epirubicin and cyclophosphamide; 208 had epirubicin and cyclophosphamide followed by paclitaxel a
60 ned via a central randomisation procedure to epirubicin and cyclophosphamide then paclitaxel (with or
61 0 (17%, 95% CI 14-21) of 404 patients in the epirubicin and cyclophosphamide then paclitaxel group ac
62 mly allocated 831 participants; 207 received epirubicin and cyclophosphamide then paclitaxel; 208 wer
63 f gemcitabine to accelerated paclitaxel with epirubicin and cyclophosphamide, and also the effect of
67 n paclitaxel; 208 were given paclitaxel then epirubicin and cyclophosphamide; 208 had epirubicin and
69 ntegration of capecitabine into a regimen of epirubicin and docetaxel for node-positive early BC.
73 2) inhibition by equimolar concentrations of epirubicin and idarubicin was significantly less than th
75 reat analysis of standard versus accelerated epirubicin and per-protocol analysis of CMF versus capec
76 al and resistant colon cancer cell lines for epirubicin and to a lesser extent for SN-38 and mitoxant
78 ollowed by three cycles of cyclophosphamide, epirubicin, and capecitabine (CEX, 753 patients), or to
79 ollowed by three cycles of cyclophosphamide, epirubicin, and capecitabine (CEX; n = 753) or three cyc
81 bine and docetaxel followed by fluorouracil, epirubicin, and cyclophosphamide (FEC) or weekly paclita
85 ervals followed by 3 cycles of fluorouracil, epirubicin, and cyclophosphamide at 3-week intervals.
86 bine into a regimen that contains docetaxel, epirubicin, and cyclophosphamide did not improve RFS sig
87 Capecitabine administration with docetaxel, epirubicin, and cyclophosphamide did not prolong RFS or
88 chemotherapy with 3 cycles of fluorouracil, epirubicin, and cyclophosphamide followed by 3 cycles of
89 tabine to a regimen that contains docetaxel, epirubicin, and cyclophosphamide improves survival outco
90 xel followed by four cycles of fluorouracil, epirubicin, and cyclophosphamide or to the same chemothe
91 emotherapy regimen that contained docetaxel, epirubicin, and cyclophosphamide prolonged the survival
93 six-drug combination (IVA plus carboplatin, epirubicin, and etoposide) both delivered over 27 weeks.
94 ) of the 1070 patients treated with standard epirubicin, and fatigue (63 [6%]) and infection (34 [3%]
98 el followed by 3 cycles of cyclophosphamide, epirubicin, and fluorouracil (T+CEF), while the other ha
101 he treatment of pediatric malignancies, with epirubicin-based regimens, or with high-dose anthracycli
102 in, bleomycin, vinblastine, and dacarbazine; epirubicin, bleomycin, vinblastine, and prednisone).
104 trial evaluated the combination of CIS plus epirubicin (CIS-EPI) in patients with metastatic germ ce
105 harmacokinetics of rilotumumab combined with epirubicin, cisplatin, and capecitabine (ECX) in patient
106 ntravenously on days 1-4]) or four cycles of epirubicin, cisplatin, and capecitabine (ECX; four 3-wee
107 e (rilotumumab group; n=304) or placebo plus epirubicin, cisplatin, and capecitabine (placebo group;
108 s were randomly assigned to rilotumumab plus epirubicin, cisplatin, and capecitabine (rilotumumab gro
109 igned patients 1:1 to receive peri-operative epirubicin, cisplatin, and capecitabine chemotherapy or
110 operative and three post-operative cycles of epirubicin, cisplatin, and capecitabine chemotherapy: 50
111 harmacokinetics of rilotumumab combined with epirubicin, cisplatin, and capecitabine, and to assess p
112 mly assigned at a one-to-one-to-one ratio to epirubicin, cisplatin, and continuous-infusion fluoroura
113 rapy (MAGIC) trial established perioperative epirubicin, cisplatin, and fluorouracil chemotherapy as
114 randomized to surgery alone or perioperative epirubicin, cisplatin, and fluorouracil chemotherapy in
115 whose tumor did not respond to preoperative epirubicin, cisplatin, and fluorouracil may be appropria
116 In both groups, patients received either epirubicin, cisplatin, and fluorouracil or fluorouracil,
118 diotherapy (FU plus LV arm) or postoperative epirubicin, cisplatin, and infusional FU (ECF) before an
119 uracil, leucovorin, and irinotecan) and ECX (epirubicin, cisplatin,and capecitabine) for AGC from the
120 vival rates were significantly higher in the epirubicin-CMF groups than in the CMF-alone groups (2-ye
121 nthracycline (Anthra) -based (doxorubicin or epirubicin combinations [doxorubicin/cyclophosphamide, e
122 tamer conformation and formation of aptamer- epirubicin complex instead of aptamer on the modified el
123 pirubicin increased linearly with increasing epirubicin concentration, due to the switching in the ap
124 ydroxypropyl)methacrylamide (HPMA) copolymer-epirubicin conjugate that induces immunogenic cell death
125 b-paclitaxel 125 mg/m(2) q1w, followed by 4x epirubicin + cyclophosphamide (90 mg + 600 mg) q2w; incl
126 tensified, dose-dense concomitant regimen of epirubicin + cyclophosphamide (historically called SIM)
127 TNBC patients, 23 received EC-D (4 cycles of epirubicin + cyclophosphamide followed by 4 cycles of do
129 emcitabine (gemcitabine group; n=1576) or to epirubicin, cyclophosphamide, and paclitaxel (control gr
130 gned (1:1) to one of two treatment regimens: epirubicin, cyclophosphamide, and paclitaxel (four cycle
131 as a 3 h infusion on day 1 every 3 weeks) or epirubicin, cyclophosphamide, and paclitaxel plus gemcit
132 ients were enrolled and randomly assigned to epirubicin, cyclophosphamide, paclitaxel, and gemcitabin
133 emotherapy with 3 cycles of fluorouracil and epirubicin-cyclophosphamide every 3 weeks followed by 3
134 al phase III trial which compared sequential epirubicin/cyclophosphamide and docetaxel administered e
135 4 cycles (8 doses), followed by 4 cycles of epirubicin/cyclophosphamide, 90/600 mg/m2 (every 2 weeks
136 combinations [doxorubicin/cyclophosphamide, epirubicin/cyclophosphamide, fluorouracil/epirubicin/cyc
137 e, epirubicin/cyclophosphamide, fluorouracil/epirubicin/cyclophosphamide, or fluorouracil/doxorubicin
139 nthracyclines Doxorubicin, Daunorubicin, and Epirubicin decrease the transcription of nuclear factor
140 ancer (median age, 53 years) received a mean epirubicin dose of 304 mg/m(2), and 25 age/sex-matched c
141 treatment was stopped after reaching maximal epirubicin doses rather than progression in 13 (32%) of
142 al function (p=0.36), compared with standard epirubicin during treatment, but the effect did not pers
143 nts were randomly assigned to four cycles of epirubicin (E)(90)/cyclophoshamide (C)(600) followed by
144 gned (1:1:1:1) to four cycles of 100 mg/m(2) epirubicin either every 3 weeks (standard epirubicin) or
145 signed to receive four cycles of 100 mg/m(2) epirubicin either every 3 weeks (standard epirubicin) or
146 how that two anthracyclines, doxorubicin and epirubicin, elicit distinct primary metabolic vulnerabil
147 at baseline, end of standard or accelerated epirubicin, end of CMF or capecitabine, and at 12 and 24
148 For example, 2nd generation HPMA copolymer-epirubicin (EPI) conjugates (2P-EPI) demonstrated comple
149 ydroxypropyl)methacrylamide (HPMA) copolymer-epirubicin (EPI) conjugates (ST-P-EPI); the latter is at
150 cessful design of polymer enhanced rituximab-epirubicin (EPI) conjugates targeted to non-Hodgkin lymp
154 ons; four Anthracyclines: Doxorubicin (DOX), Epirubicin (EPI), Idarubicin (IDA) and Daunorubicin (DAU
155 e, methotrexate, and fluorouracil (CMF) with epirubicin followed by CMF (epi-CMF), were analyzed for
157 alone and 79.5% (95% CI, 75.2% to 83.8%) for epirubicin followed by docetaxel; evidence of improvemen
158 the BR9601 trial, we compared four cycles of epirubicin followed by four cycles of CMF, with eight cy
160 lgrastim on day 2 of each cycle (accelerated epirubicin), followed by four 4-week cycles of either cl
161 lgrastim on day 2 of each cycle (accelerated epirubicin), followed by four 4-week cycles of either CM
163 ll trial, that substitution of docetaxel for epirubicin for the last three cycles of chemotherapy res
165 etoposide, pegylated liposomal doxorubicin, epirubicin, gemcitabine, altretamine, oxali platin, and
166 events between the accelerated and standard epirubicin groups (overall hazard ratio [HR] 0.94, 95% C
167 ested by applying them for the extraction of epirubicin hydrochloride (EPI) from plasma samples, foll
168 TACT2 trial investigated whether accelerated epirubicin improves time to recurrence and if oral capec
170 gylated liposomal-delivered doxorubicin, and epirubicin in HL-1 adult cardiomyocytes in culture as we
172 inhibitor (HDACi), valproic acid (VPA), and epirubicin in solid tumor malignancies and to define the
173 hracycline were treated with doxorubicin (or epirubicin in the case of 36 women) and cyclophosphamide
174 th this idea, the loss of P-ATM induction by epirubicin in the NBS1-deficient NBS1-LBI fibroblasts ca
175 er optimized conditions, the peak current of epirubicin increased linearly with increasing epirubicin
176 FOXM1 depletion reduced NBS1 expression and epirubicin-induced ataxia-telangiectasia mutated (ATM)ph
178 FOXM1 regulates BRIP1 expression to modulate epirubicin-induced DNA damage repair and drug resistance
179 FOXM1 regulates BRIP1 expression to modulate epirubicin-induced DNA damage repair and drug resistance
180 e embryonic fibroblasts (MEFs) into entering epirubicin-induced senescence, with the loss of long-ter
181 jugated with anthracycline anticancer agent, epirubicin, integrates the advantages of both chemosensi
184 ovel regimen IVE/MTX (ifosfamide, etoposide, epirubicin/methotrexate)-ASCT [corrected] was piloted fr
185 10% to 20% of patients include doxorubicin, epirubicin, mitomycin, cyclophosphamide, ifosfamide, cis
188 CF-1 mice (10/group) received doxorubicin, epirubicin or non-pegylated liposomal-doxorubicin (10 mg
189 h in PARG null-TS cells after treatment with epirubicin or sub-IC(50) doses of cisplatin and cyclopho
190 2) epirubicin either every 3 weeks (standard epirubicin) or every 2 weeks with 6 mg pegfilgrastim on
191 2) epirubicin either every 3 weeks (standard epirubicin) or every 2 weeks with 6 mg pegfilgrastim on
193 gate DSBs sustained by MCF-7 cells following epirubicin, owing to an enhancement in repair efficiency
195 ion of the anti-EGFR antibody panitumumab to epirubicin, oxaliplatin, and capecitabine (EOC) in patie
199 dverse effects was significantly higher with epirubicin plus CMF than with CMF alone but did not sign
201 4 patients were randomly assigned to receive epirubicin plus cyclophosphamide (EC; 90 and 600 mg/m(2)
202 ly solvent-based (sb) paclitaxel followed by epirubicin plus cyclophosphamide as neoadjuvant treatmen
203 Patients were treated by sequential NAC (epirubicin plus cyclophosphamide followed by docetaxel w
205 The NAC regimen consisted of 4 cycles of epirubicin plus cyclophosphamide, followed by 4 courses
206 cetaxel (100 mg/m(2) x four cycles; EC-T) or epirubicin plus docetaxel (ET; 90 and 75 mg/m(2), respec
209 OTUB1 can enhance the proliferative rate and epirubicin resistance through targeting FOXM1, as OTUB1
210 ion and de novo glutathione synthesis, while epirubicin-resistant cells display markedly increased bi
211 es with glutathione synthesis, compared with epirubicin-resistant counterparts that are more sensitiv
213 Like FOXM1, NBS1 is overexpressed in the epirubicin-resistant MCF-7Epi(R) cells and its expressio
215 agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of
216 sicles were loaded with the chemotherapeutic epirubicin, superior inhibition of triple negative breas
218 nd toxicity of incorporating docetaxel after epirubicin to create a sequential anthracycline-taxane r
219 ote tumor retention of ND-complexes, prevent epirubicin toxicities and mediate regression of triple n
220 -naive patients with breast cancer receiving epirubicin versus sex- and age-matched healthy controls.
225 ) cells exposed to the chemotherapeutic drug epirubicin, which suggests a feed-forward loop to enrich
227 t two hypotheses: whether use of accelerated epirubicin would improve time to tumour recurrence (TTR)