ライフサイエンスコーパス: epirubicin

1 tumors correlate with patients' response to epirubicin.

2 from patients who had complete responses to epirubicin.

3 breast cancer cells to paclitaxel but not to epirubicin.

4 to cisplatin, carboplatin, temozolomide, and epirubicin.

5 lls are highly resistant to mitoxantrone and epirubicin.

6 f the 1045 patients treated with accelerated epirubicin.

7 emical aptasensor for selective detection of epirubicin.

8 ctivation when compared with doxorubicin and epirubicin.

9 nge in HR or CO, compared to doxorubicin and epirubicin.

10 in the resistant counterparts in response to epirubicin.

11 cycles of FEC (fluorouracil 500 mg/m(2) plus epirubicin 100 mg/m(2) plus cyclophosphamide 500 mg/m(2)

12 was VPA 140 mg/kg/d for 48 hours followed by epirubicin 100 mg/m2.

13 hose either FEC for eight cycles (n=1265) or epirubicin (100 mg/m(2) at 3-weekly intervals) for four

14 three cycles of fluorouracil (500 mg/m(2)), epirubicin (100 mg/m(2)), and cyclophosphamide (500 mg/m

15 treatment was 3 cycles of FEC (fluorouracil, epirubicin [100 mg/m(2) per dose], and cyclophosphamide)

16 receive three cycles of preoperative CT with epirubicin 120 mg/m(2) and ifosfamide 9 g/m(2) and granu

17 mly assigned to three preoperative cycles of epirubicin 120 mg/m(2) plus ifosfamide 9 g/m(2), and 160

18 t bypasses the low-yielding semisynthesis of epirubicin (4'-epidoxorubicin) and 4'-epidaunorubicin, i

19 s follows: ifosfamide 54 g/m(2) (both arms), epirubicin 450 mg/m(2), etoposide 1,350 mg/m(2) (six-dru

20 modified-dose EOC plus panitumumab (mEOC+P; epirubicin 50 mg/m(2) and oxaliplatin 100 mg/m(2) on day

21 up to eight 21-day cycles of open-label EOC (epirubicin 50 mg/m(2) and oxaliplatin 130 mg/m(2) on day

22 e 15 mg/kg intravenously on day 1) plus ECX (epirubicin 50 mg/m(2) intravenously on day 1, cisplatin

23 in combination with open-label chemotherapy (epirubicin 50 mg/m(2) intravenously; cisplatin 60 mg/m(2

24 The recommended dose for EOC + P is epirubicin 50 mg/m(2), oxaliplatin 100 mg/m(2), capecita

25 dose de-escalation was made to EOC + P DL-1 (epirubicin 50 mg/m(2), oxaliplatin130 mg/m(2), capecitab

26 nd three postoperative cycles of intravenous epirubicin (50 mg per square meter of body-surface area)

27 d capecitabine (ECX; four 3-weekly cycles of epirubicin [50 mg/m(2)] and cisplatin [60 mg/m(2)] intra

28 on to receive FEC (fluorouracil 600 mg/m(2), epirubicin 60 mg/m(2), cyclophosphamide 600 mg/m(2) at 3

29 treatment received fluorouracil 500 mg/m(2), epirubicin 75 mg/m(2), and cyclophosphamide 500 mg/m(2)

30 in 75 mg/m2 and paclitaxel 200 mg/m2) or EC (epirubicin 75 mg/m2 and cyclophosphamide 600 mg/m2) admi

31 were randomly assigned to receive either EP (epirubicin 75 mg/m2 and paclitaxel 200 mg/m2) or EC (epi

32 concomitant with four cycles of neoadjuvant epirubicin (75 mg/m(2)) plus docetaxel (75 mg/m(2)) and

33 es 1-4) and FEC (fluorouracil [500 mg/m(2)], epirubicin [75 mg/m(2)], and cyclophosphamide [500 mg/m(

34 ree cycles of FEC (fluorouracil 600 mg/m(2), epirubicin 90 mg/m(2), and cyclophosphamide 600 mg/m(2))

35 /m(2)) every 3 weeks (DC) or three cycles of epirubicin (90 mg/m(2)) and cyclophosphamide (600 mg/m(2

36 The Docetaxel Epirubicin Adjuvant (DEVA) trial evaluated the efficacy

37 The National Epirubicin Adjuvant Trial (NEAT) and the BR9601 trial ex

38 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

39 n, and capecitabine chemotherapy: 50 mg/m(2) epirubicin and 60 mg/m(2) cisplatin on day 1 and 1250 mg

40 les of 90 mg/m(2) intravenously administered epirubicin and 600 mg/m(2) intravenously administered cy

41 CI 84.3-87.3) of patients receiving standard epirubicin and 87.1% (85.6-88.4) of those receiving acce

42 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

43 dvanced breast cancer, 3 months of high-dose epirubicin and cyclophosphamide (EC) administered every

44 axel with or without gemcitabine followed by epirubicin and cyclophosphamide achieved pCR compared wi

45 also the effect of sequencing the blocks of epirubicin and cyclophosphamide and paclitaxel (with or

46 gh addition of gemcitabine to paclitaxel and epirubicin and cyclophosphamide chemotherapy does not im

47 nadir-based tailored and dose-dense adjuvant epirubicin and cyclophosphamide every 2 weeks followed b

48 59 (15%, 11-18) of 406 patients who received epirubicin and cyclophosphamide first (p=0.03).

49 thological complete response were 14.9% with epirubicin and cyclophosphamide followed by docetaxel an

50 phamide followed by docetaxel and 18.4% with epirubicin and cyclophosphamide followed by docetaxel pl

51 of 40 mm on palpation to receive neoadjuvant epirubicin and cyclophosphamide followed by docetaxel, w

52 hen epirubicin and cyclophosphamide; 208 had epirubicin and cyclophosphamide followed by paclitaxel a

53 ned via a central randomisation procedure to epirubicin and cyclophosphamide then paclitaxel (with or

54 0 (17%, 95% CI 14-21) of 404 patients in the epirubicin and cyclophosphamide then paclitaxel group ac

55 mly allocated 831 participants; 207 received epirubicin and cyclophosphamide then paclitaxel; 208 wer

56 f gemcitabine to accelerated paclitaxel with epirubicin and cyclophosphamide, and also the effect of

57 208 received paclitaxel and gemcitabine then epirubicin and cyclophosphamide.

58 aclitaxel (with or without gemcitabine) then epirubicin and cyclophosphamide.

59 n paclitaxel; 208 were given paclitaxel then epirubicin and cyclophosphamide; 208 had epirubicin and

60 ntegration of capecitabine into a regimen of epirubicin and docetaxel for node-positive early BC.

61 n, DNA damage and apoptosis in comparison to epirubicin and doxorubicin.

62 null cells are hypersensitive to DNA damage, epirubicin and gamma-irradiation.

63 2) inhibition by equimolar concentrations of epirubicin and idarubicin was significantly less than th

64 t cancer cells in response to treatment with epirubicin and mitotic inhibitors.

65 reat analysis of standard versus accelerated epirubicin and per-protocol analysis of CMF versus capec

66 al and resistant colon cancer cell lines for epirubicin and to a lesser extent for SN-38 and mitoxant

67 ollowed by three cycles of cyclophosphamide, epirubicin, and capecitabine (CEX; n = 753) or three cyc

68 ne followed by 3 cycles of cyclophosphamide, epirubicin, and capecitabine (TX+CEX).

69 bine and docetaxel followed by fluorouracil, epirubicin, and cyclophosphamide (FEC) or weekly paclita

70 weeks, followed by 3 cycles of fluorouracil, epirubicin, and cyclophosphamide after surgery.

71 weeks, followed by 3 cycles of fluorouracil, epirubicin, and cyclophosphamide after surgery.

72 weeks, followed by 3 cycles of fluorouracil, epirubicin, and cyclophosphamide after surgery.

73 bine into a regimen that contains docetaxel, epirubicin, and cyclophosphamide did not improve RFS sig

74 Capecitabine administration with docetaxel, epirubicin, and cyclophosphamide did not prolong RFS or

75 tabine to a regimen that contains docetaxel, epirubicin, and cyclophosphamide improves survival outco

76 xel followed by four cycles of fluorouracil, epirubicin, and cyclophosphamide or to the same chemothe

77 of paclitaxel or six cycles of fluorouracil, epirubicin, and cyclophosphamide.

78 six-drug combination (IVA plus carboplatin, epirubicin, and etoposide) both delivered over 27 weeks.

79 ) of the 1070 patients treated with standard epirubicin, and fatigue (63 [6%]) and infection (34 [3%]

80 PURPOSE Cyclophosphamide, epirubicin, and fluorouracil (CEF) and doxorubicin and c

81 ollowed by three cycles of cyclophosphamide, epirubicin, and fluorouracil (CEF; n = 747).

82 el followed by 3 cycles of cyclophosphamide, epirubicin, and fluorouracil (T+CEF), while the other ha

83 apsulated drugs, which included doxorubicin, epirubicin, and vinorelbine.

84 he treatment of pediatric malignancies, with epirubicin-based regimens, or with high-dose anthracycli

85 in, bleomycin, vinblastine, and dacarbazine; epirubicin, bleomycin, vinblastine, and prednisone).

86 trial evaluated the combination of CIS plus epirubicin (CIS-EPI) in patients with metastatic germ ce

87 harmacokinetics of rilotumumab combined with epirubicin, cisplatin, and capecitabine (ECX) in patient

88 ntravenously on days 1-4]) or four cycles of epirubicin, cisplatin, and capecitabine (ECX; four 3-wee

89 e (rilotumumab group; n=304) or placebo plus epirubicin, cisplatin, and capecitabine (placebo group;

90 s were randomly assigned to rilotumumab plus epirubicin, cisplatin, and capecitabine (rilotumumab gro

91 igned patients 1:1 to receive peri-operative epirubicin, cisplatin, and capecitabine chemotherapy or

92 operative and three post-operative cycles of epirubicin, cisplatin, and capecitabine chemotherapy: 50

93 harmacokinetics of rilotumumab combined with epirubicin, cisplatin, and capecitabine, and to assess p

94 mly assigned at a one-to-one-to-one ratio to epirubicin, cisplatin, and continuous-infusion fluoroura

95 rapy (MAGIC) trial established perioperative epirubicin, cisplatin, and fluorouracil chemotherapy as

96 randomized to surgery alone or perioperative epirubicin, cisplatin, and fluorouracil chemotherapy in

97 whose tumor did not respond to preoperative epirubicin, cisplatin, and fluorouracil may be appropria

98 A regimen of epirubicin, cisplatin, and infused fluorouracil (ECF) im

99 diotherapy (FU plus LV arm) or postoperative epirubicin, cisplatin, and infusional FU (ECF) before an

100 uracil, leucovorin, and irinotecan) and ECX (epirubicin, cisplatin,and capecitabine) for AGC from the

101 vival rates were significantly higher in the epirubicin-CMF groups than in the CMF-alone groups (2-ye

102 nthracycline (Anthra) -based (doxorubicin or epirubicin combinations [doxorubicin/cyclophosphamide, e

103 tamer conformation and formation of aptamer- epirubicin complex instead of aptamer on the modified el

104 pirubicin increased linearly with increasing epirubicin concentration, due to the switching in the ap

105 tensified, dose-dense concomitant regimen of epirubicin + cyclophosphamide (historically called SIM)

106 TNBC patients, 23 received EC-D (4 cycles of epirubicin + cyclophosphamide followed by 4 cycles of do

107 emcitabine (gemcitabine group; n=1576) or to epirubicin, cyclophosphamide, and paclitaxel (control gr

108 gned (1:1) to one of two treatment regimens: epirubicin, cyclophosphamide, and paclitaxel (four cycle

109 as a 3 h infusion on day 1 every 3 weeks) or epirubicin, cyclophosphamide, and paclitaxel plus gemcit

110 ients were enrolled and randomly assigned to epirubicin, cyclophosphamide, paclitaxel, and gemcitabin

111 emotherapy with 3 cycles of fluorouracil and epirubicin-cyclophosphamide every 3 weeks followed by 3

112 combinations [doxorubicin/cyclophosphamide, epirubicin/cyclophosphamide, fluorouracil/epirubicin/cyc

113 e, epirubicin/cyclophosphamide, fluorouracil/epirubicin/cyclophosphamide, or fluorouracil/doxorubicin

114 doses of VPA (days 1 through 3) followed by epirubicin (day 3) in 3-week cycles.

115 treatment was stopped after reaching maximal epirubicin doses rather than progression in 13 (32%) of

116 signed to receive four cycles of 100 mg/m(2) epirubicin either every 3 weeks (standard epirubicin) or

117 For example, 2nd generation HPMA copolymer-epirubicin (EPI) conjugates (2P-EPI) demonstrated comple

118 ydroxypropyl)methacrylamide (HPMA) copolymer-epirubicin (EPI) conjugates.

119 Indocyanine green (ICG) and epirubicin (EPI) could co-self-assemble into small molec

120 Epirubicin (EPI) is less cardiotoxic compared with other

121 e, methotrexate, and fluorouracil (CMF) with epirubicin followed by CMF (epi-CMF), were analyzed for

122 bicin and 88.9% (95% CI, 85.5% to 92.2%) for epirubicin followed by docetaxel.

123 alone and 79.5% (95% CI, 75.2% to 83.8%) for epirubicin followed by docetaxel; evidence of improvemen

124 the BR9601 trial, we compared four cycles of epirubicin followed by four cycles of CMF, with eight cy

125 In NEAT, we compared four cycles of epirubicin followed by four cycles of cyclophosphamide,

126 lgrastim on day 2 of each cycle (accelerated epirubicin), followed by four 4-week cycles of either cl

127 ll trial, that substitution of docetaxel for epirubicin for the last three cycles of chemotherapy res

128 : doxorubicin, daunorubicin, idarubicin, and epirubicin for their ability to inhibit iPLA(2).

129 etoposide, pegylated liposomal doxorubicin, epirubicin, gemcitabine, altretamine, oxali platin, and

130 events between the accelerated and standard epirubicin groups (overall hazard ratio [HR] 0.94, 95% C

131 as successfully assessed by determination of epirubicin in a human blood serum sample.

132 gylated liposomal-delivered doxorubicin, and epirubicin in HL-1 adult cardiomyocytes in culture as we

133 its expression level is low but inducible by epirubicin in MCF-7 cells.

134 inhibitor (HDACi), valproic acid (VPA), and epirubicin in solid tumor malignancies and to define the

135 hracycline were treated with doxorubicin (or epirubicin in the case of 36 women) and cyclophosphamide

136 th this idea, the loss of P-ATM induction by epirubicin in the NBS1-deficient NBS1-LBI fibroblasts ca

137 er optimized conditions, the peak current of epirubicin increased linearly with increasing epirubicin

138 FOXM1 depletion reduced NBS1 expression and epirubicin-induced ataxia-telangiectasia mutated (ATM)ph

139 CF-7 and MCF-7Epi(R) cells more sensitive to epirubicin-induced cellular senescence.

140 FOXM1 regulates BRIP1 expression to modulate epirubicin-induced DNA damage repair and drug resistance

141 FOXM1 regulates BRIP1 expression to modulate epirubicin-induced DNA damage repair and drug resistance

142 e embryonic fibroblasts (MEFs) into entering epirubicin-induced senescence, with the loss of long-ter

143 ovel regimen IVE/MTX (ifosfamide, etoposide, epirubicin/methotrexate)-ASCT [corrected] was piloted fr

144 10% to 20% of patients include doxorubicin, epirubicin, mitomycin, cyclophosphamide, ifosfamide, cis

145 ly breast cancer compared with six cycles of epirubicin monotherapy.

146 of 6 weeks of vincristine, dactinomycin, and epirubicin or doxorubicin.

147 CF-1 mice (10/group) received doxorubicin, epirubicin or non-pegylated liposomal-doxorubicin (10 mg

148 h in PARG null-TS cells after treatment with epirubicin or sub-IC(50) doses of cisplatin and cyclopho

149 2) epirubicin either every 3 weeks (standard epirubicin) or every 2 weeks with 6 mg pegfilgrastim on

150 gate DSBs sustained by MCF-7 cells following epirubicin, owing to an enhancement in repair efficiency

151 ion of the anti-EGFR antibody panitumumab to epirubicin, oxaliplatin, and capecitabine (EOC) in patie

152 Epirubicin, oxaliplatin, and capecitabine (EOC) is a sta

153 Epirubicin plus CMF is superior to CMF alone as adjuvant

154 0.67; 95% CI, 0.55 to 0.82; P<0.001) favored epirubicin plus CMF over CMF alone.

155 dverse effects was significantly higher with epirubicin plus CMF than with CMF alone but did not sign

156 ot significantly interact with the effect of epirubicin plus CMF.

157 4 patients were randomly assigned to receive epirubicin plus cyclophosphamide (EC; 90 and 600 mg/m(2)

158 The NAC regimen consisted of 4 cycles of epirubicin plus cyclophosphamide, followed by 4 courses

159 cetaxel (100 mg/m(2) x four cycles; EC-T) or epirubicin plus docetaxel (ET; 90 and 75 mg/m(2), respec

160 axel (75 mg/m(2)) and two cycles of adjuvant epirubicin plus docetaxel.

161 No exacerbation of epirubicin-related toxicities was observed.

162 OTUB1 can enhance the proliferative rate and epirubicin resistance through targeting FOXM1, as OTUB1

163 the protein and mRNA levels in MCF-7 and the epirubicin-resistant MCF-7 Epi(R) cells.

164 Like FOXM1, NBS1 is overexpressed in the epirubicin-resistant MCF-7Epi(R) cells and its expressio

165 ind that FOXM1 expression is associated with epirubicin sensitivity and DSB repair.

166 agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of

167 tumors did not benefit from the addition of epirubicin to CMF.

168 nd toxicity of incorporating docetaxel after epirubicin to create a sequential anthracycline-taxane r

169 ote tumor retention of ND-complexes, prevent epirubicin toxicities and mediate regression of triple n

170 % (85.6-88.4) of those receiving accelerated epirubicin were free from TTR events.

171 s absent in combinations of formaldehyde and epirubicin, which cannot form stable oxazolidines.

172 ) cells exposed to the chemotherapeutic drug epirubicin, which suggests a feed-forward loop to enrich

173 The interactions of epirubicin with aptamer on the AuNPs/Fe3O4@SiO2/DABCO/SP

174 t two hypotheses: whether use of accelerated epirubicin would improve time to tumour recurrence (TTR)