ライフサイエンスコーパス: mitoxantrone

1 ed second-line drugs such as natalizumab and mitoxantrone.

2 ivity relative to the original screening hit mitoxantrone.

3 lude interferon, glatiramer, natalizumab and mitoxantrone.

4 as attenuated by doxorubicin, epirubicin, or mitoxantrone.

5 expression, and an increased sensitivity to mitoxantrone.

6 2007, all patients were allocated to receive mitoxantrone.

7 vantage of docetaxel-based chemotherapy over mitoxantrone.

8 rubicin or idarubicin or the anthracenedione mitoxantrone.

9 no effects on the BCRP-mediated transport of mitoxantrone.

10 mide, and a third course with diaziquone and mitoxantrone.

11 reatment with low doses of staurosporine and mitoxantrone.

12 WP631 showed 10-fold higher potency than mitoxantrone.

13 re 77% for cytarabine and 82% for cytarabine/mitoxantrone.

14 2; all three MXR/BCRP/ABCP forms transported mitoxantrone.

15 one (Dex), doxorubicin (Dox), melphalan, and mitoxantrone.

16 ine alone or a combination of cytarabine and mitoxantrone.

17 rugs such as VM-26, doxorubicin, m-AMSA, and mitoxantrone.

18 rouracil and 5-fluoro-2'-deoxyuridine and to mitoxantrone.

19 cluding strains resistant to doxorubicin and mitoxantrone.

20 azatoxin and the intercalators amsacrine and mitoxantrone.

21 rubicin and to a lesser extent for SN-38 and mitoxantrone.

22 presence of VP-16, azatoxin, amsacrine, and mitoxantrone.

23 ing doxorubicin, vincristine, etoposide, and mitoxantrone.

24 demonstrated that polyphenols can intercept mitoxantrone.

25 the stabilisation properties of analogues of mitoxantrone.

26 bitors that block efflux of rhodamine 123 or mitoxantrone.

27 rapeutics such as imatinib, doxorubicin, and mitoxantrone.

28 M, bodipy-verapamil, bodipy-vinblastine, and mitoxantrone.

29 courses were administered every 4 weeks with mitoxantrone 10 mg/m2 on day 1 and fludarabine 25 mg/m2

30 sly untreated AML were randomized to receive mitoxantrone (10 mg/m(2) per day x 5) and etoposide (100

31 igned to either idarubicin (109 analysed) or mitoxantrone (103 analysed).

32 The recommended phase II dose is mitoxantrone 12 mg/m2 and ixabepilone 35 mg/m2 every 21

33 Of 21 patients treated with mitoxantrone 12 mg/m2 plus ixabepilone > or = 30 mg/m2,

34 intensification 2 (high-dose cytarabine and mitoxantrone [12 mg/m(2)/dose daily; four total doses]),

35 tropenia (cabazitaxel, 303 [82%] patients vs mitoxantrone, 215 [58%]) and diarrhoea (23 [6%] vs one [

36 multiagent consolidation with two cycles of mitoxantrone (30 mg/m(2)) plus cytarabine (12 g/m(2)) an

37 men were allocated to treatment groups (377 mitoxantrone, 378 cabazitaxel) and were included in the

38 ere well tolerated at dose levels of 4 mg/m2 mitoxantrone, 40 mg/m2 etoposide, and 1 g/m2 C daily for

39 le sclerosis patients treated quarterly with mitoxantrone (48 mg/m(2) cumulative), with and without c

40 reated with WP631 (50 pm/ml to 500 nm/ml) or mitoxantrone (5-500 nm/ml).

41 clophosphamide 200 mg/m2 on days 1 to 3, and mitoxantrone 6 mg/m2 on day 1 (R-FCM), for 6 cycles, fol

42 hs) were randomly assigned to receive either mitoxantrone 8 mg/m(2), etoposide 80 mg/m(2), and cytara

43 of 28-day cycles); intravenous infusions of mitoxantrone (8 mg/m(2) per day), etoposide (100 mg/m(2)

44 which included daunorubicin 135 mg/m(2) and mitoxantrone 80 mg/m(2).

45 their inhibitory effect on the transport of mitoxantrone, a known ABCG2 substrate.

46 MTX accumulation was greatly decreased by mitoxantrone, a known BCRP substrate, suggesting competi

47 nd a 7- to 12-fold increase in resistance to mitoxantrone, a known BCRP substrate.

48 hibitors, producing significant increases in mitoxantrone accumulation at concentrations of 0.5 or 1.

49 the tested flavonoids (50 microM) increased mitoxantrone accumulation in BCRP-overexpressing cells,

50 s demonstrated with the reduction in flux of mitoxantrone across PBMEC monolayers.

51 We show that anthracyclines and mitoxantrone act as topoisomerase II (TOP2) poisons at l

52 pite its favorable activity in cell culture, mitoxantrone administered intraperitoneally at the maxim

53 gnificantly improved with cabazitaxel versus mitoxantrone after prior docetaxel treatment.

54 gh-efficacy therapy (rituximab, ocrelizumab, mitoxantrone, alemtuzumab, or natalizumab) either 0-2 ye

55 studies showed selective protection against mitoxantrone among ABCG2-transduced rhesus PBPCs.

56 targeting chemotherapeutic drugs (etoposide, mitoxantrone, amsacrine, and ellipticine).

57 l line (MCF7/MX) selected in the presence of mitoxantrone, an anticancer agent associated with the mu

58 Using [(3)H]mitoxantrone, an established BCRP substrate, we observe

59 H]-paclitaxel in ABCB1 overexpressing cells; mitoxantrone and [(3)H]-mitoxantrone in ABCG2 overexpres

60 lts with AML, multiagent consolidation using mitoxantrone and amsacrine in combination with high-dose

61 d etoposide), plus a fourth course of MidAc (mitoxantrone and Ara-C) and following an amendment to on

62 in intracellular drug concentration of both mitoxantrone and BBR 3390 was reversed by a novel chemos

63 Two structurally related compounds, mitoxantrone and bisantrene, were tested in parallel as

64 cells and tested for their ability to efflux mitoxantrone and BODIPY-prazosin.

65 otoxic potency lower than that of DuP-941 or mitoxantrone and comparable to that of doxorubicin.

66 Mitoxantrone and cytarabine induction achieved a remissi

67 Mitoxantrone and cytarabine induction is effective with

68 e (VP-16) in patients who did not respond to mitoxantrone and cytarabine.

69 level of Pim-1L and BCRP was up-regulated in mitoxantrone and docetaxel-resistant prostate cancer cel

70 overexpressing cells are highly resistant to mitoxantrone and epirubicin.

71 s, combinations containing anthracyclines or mitoxantrone and etoposide may reduce the activity of et

72 analysis demonstrated that the clearances of mitoxantrone and etoposide were decreased by 59% and 50%

73 The doses of mitoxantrone and etoposide were substantially reduced to

74 Because of favorable phase 2 data using mitoxantrone and etoposide, we conducted a phase 3 study

75 sensitive to the topoisomerase II inhibitors mitoxantrone and etoposide.

76 or staurosporine and chemotherapeutic agents mitoxantrone and etoposide.

77 sly reported results using standard doses of mitoxantrone and etoposide.

78 his study was to demonstrate an advantage of mitoxantrone and hydrocortisone (M+H) over hydrocortison

79 ed the efflux of the known ABCG2 substrates, mitoxantrone and pheophorbide-a, from ABCG2-overexpressi

80 xel and estramustine than in the group given mitoxantrone and prednisone (17.5 months vs. 15.6 months

81 ated with docetaxel and estramustine (DE) or mitoxantrone and prednisone (MP).

82 tramustine and 3.2 months in the group given mitoxantrone and prednisone (P<0.001 by the log-rank tes

83 docetaxel and estramustine, as compared with mitoxantrone and prednisone, provides support for this a

84 and estramustine than among those receiving mitoxantrone and prednisone.

85 ocetaxel and estramustine and 336 to receive mitoxantrone and prednisone.

86 should be compared in a phase III trial with mitoxantrone and prednisone.

87 sults of a study on the interactions between mitoxantrone and some bioactive polyphenols.

88 hat ABCG2 expression conferred resistance to mitoxantrone and topotecan, but not to idarubicin.

89 ration-approved therapy) from prednisone and mitoxantrone and was predictive of overall survival in a

90 These data indicate that mitoxantrone and WP631 are very potent inhibitors of bas

91 nticancer drugs (etoposide, doxorubicin, and mitoxantrone) and also Top2 oxidation and DNA helical al

92 e TOP2 poisons (e.g. doxorubicin, etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-a

93 as p-hydroquinone, acetaminophen, anticancer mitoxantrone, and ametantrone, inhibit AR oxidation by c

94 cent substrates (rhodamine 123, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1 cel

95 n, mildly decreased cellular accumulation of mitoxantrone, and decreased nuclear accumulation of doxo

96 , including 4 who received only fludarabine, mitoxantrone, and dexamethasone (FND) for 6 to 8 courses

97 icin, 5-fluorouracil, cisplastin, melphalan, mitoxantrone, and dexamethasone.

98 red between study interventions (prednisone, mitoxantrone, and docetaxel) and off-treatment data when

99 te leukemia (e.g., doxorubicin, vincristine, mitoxantrone, and methotrexate), have been shown to be P

100 multiple sclerosis (MS): glatiramer acetate, mitoxantrone, and natalizumab.

101 These drugs include etoposide, mitoxantrone, and the anthracyclines doxorubicin and epi

102 platin, vinorelbine, doxorubicin, etoposide, mitoxantrone, and vincristine.

103 egrins resulted in a 40% to 60% reduction in mitoxantrone- and etoposide-induced DNA double-strand br

104 nfers resistance to anticancer drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.

105 no difference in sensitivity to doxorubicin, mitoxantrone, Ara-C, or etoposide, demonstrating that cr

106 ired drug resistance levels of resistance to mitoxantrone are 2- to 3-fold greater for cells adhered

107 Given that doxorubicin and mitoxantrone are effluxed by breast cancer resistance pr

108 reactions between the analysed compounds and mitoxantrone are large enough to generate an evident int

109 ncluding etoposide (VP-16), doxorubicin, and mitoxantrone, are among the most effective anticancer dr

110 for a reduction in relapse risk (RR) on the mitoxantrone arm, which was offset by increased myelosup

111 d then at 5 mg/m(2) on days 1-4 of course 2; mitoxantrone at 10 mg/m(2) on days 1-4 of course 3, and

112 Patients received mitoxantrone at 12 mg/m(2) daily for 3 days.

113 Mitoxantrone-based chemotherapy palliates pain without e

114 hat compared docetaxel-based chemotherapy to mitoxantrone-based therapy demonstrated that treatment w

115 reduction (35-50%) in the efflux activity of mitoxantrone, BODIPY-prazosin, and Hoechst 33342, P485A

116 toxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of gemcitabine, capecitabine,

117 ed cytotoxicity of SN-38, 5-fluorouracil and mitoxantrone, but not that of gemcitabine, capecitabine,

118 the sensitivity of ABCG2-expressing cells to mitoxantrone by 3-5-fold.

119 esistance to the anthracenes, doxorubicin or mitoxantrone, by continuous culture in the presence of e

120 f anticancer drugs effluxed by BCRP includes mitoxantrone, camptothecin-derived and indolocarbazole t

121 ance to several anticancer agents, including mitoxantrone, camptothecins, anthracyclines, and flavopi

122 Herein we describe how the drug mitoxantrone can bind, induce folding of and stabilise i

123 The anticancer drugs cisplatin, etoposide, mitoxantrone, chlorambucil, melphalan, and carmustine [1

124 e data (41, 39, and 41 patients in the three mitoxantrone comparator groups).

125 As compared with idarubicin, mitoxantrone conferred a significant benefit in progress

126 ionization mass spectrometry (ESI-MS) to the mitoxantrone conjugate was improved by an order of magni

127 The synthesized mitoxantrone conjugate was oil at physiological temperat

128 A novel mitoxantrone conjugate was synthesized by coupling mitox

129 omly assigned to induction chemotherapy with mitoxantrone, cytarabine, and etoposide preceded, or not

130 o amsacrine, cytarabine, etoposide, and then mitoxantrone/cytarabine (MACE-MidAC) or high-dose cytara

131 diate (cyclophosphamide alone) or intensive (mitoxantrone, cytosine arabinoside, cyclophosphamide) pr

132 t concentrations of 0.5 or 1.0 microM and in mitoxantrone cytotoxicity at a concentration of 2.5 micr

133 s the endpoint, compared docetaxel data with mitoxantrone data and showed that small sample sizes wer

134 Similar results were found when the mitoxantrone data were compared with the prednisone data

135 el, etoposide, vinblastine, carboplatin, and mitoxantrone) demonstrated a marked increase in the sens

136 herapy), followed by IFN-alpha; fludarabine, mitoxantrone, dexamethasone (FND) followed by IFN-alpha;

137 ) followed by etoposide/cyclophosphamide and mitoxantrone/diaziquone (group I), three HDAC cycles (gr

138 by sequential cyclophosphamide/etoposide and mitoxantrone/diaziquone with or without filgrastim suppo

139 er of magnitude, in comparison with original mitoxantrone dihydrochloride.

140 a limit of detection of 2.9 x 10(-12) M for mitoxantrone dihydrochloride.

141 epting effect in the three-component system (mitoxantrone-DNA-polyphenol).

142 After the first mitoxantrone dose, gemcitabine was provided intravenousl

143 Ixabepilone and mitoxantrone doses were alternately escalated in a stand

144 -7 breast cancer cells confers resistance to mitoxantrone, doxorubicin, and daunorubicin, reduces dau

145 ed by the topoisomerase (topo) II inhibitors mitoxantrone, doxorubicin, and etoposide.

146 tremely effective in reversing resistance to mitoxantrone, doxorubicin, and topotecan in multidrug-se

147 in drug-sensitive cells confer resistance to mitoxantrone, doxorubicin, daunorubicin, and topotecan.

148 Corticosteroids and mitoxantrone each have been shown to be active agents in

149 ed to receive docetaxel in two schedules, or mitoxantrone, each with prednisone: 989 men provided dat

150 ity for ABCG2 and the complete inhibition of mitoxantrone efflux and coupled ATPase activity.

151 yindole are important for both inhibition of mitoxantrone efflux and inhibition of basal ATPase activ

152 ed and screened for their ability to inhibit mitoxantrone efflux from ABCG2-transfected HEK293 cells.

153 inducing inhibitors including m-AMSA, VP-16, mitoxantrone, ellipticine, and oxolinic acid.

154 o test the efficacy of the cyclophosphamide, mitoxantrone, etoposide regimen for high-dose chemothera

155 ent inhibitor of the MDR-1 efflux pump, plus mitoxantrone, etoposide, and cytarabine (PSC-MEC).

156 zed study was performed using valspodar plus mitoxantrone, etoposide, and cytarabine (PSC-MEC; n=66)

157 treated with plerixafor in combination with mitoxantrone, etoposide, and cytarabine.

158 ce to cytotoxic agents, including docetaxel, mitoxantrone, etoposide, vinblastine, and carboplatin.

159 3 times followed by cytosine arabinoside and mitoxantrone (FLAM) is active in adults with poor-risk a

160 Comparison of daunorubicin and mitoxantrone fluorescence emission profiles revealed sig

161 0 mg/m(2)/min for 12 hours with 12 mg/m(2)/d mitoxantrone for 3 days is a tolerable induction regimen

162 -3 cells was statistically identical (except mitoxantrone) for both "antisense" strategies, indicatin

163 itaxel group and 1.4 months (1.4-1.7) in the mitoxantrone group (HR 0.74, 0.64-0.86, p<0.0001).

164 ubicin group versus 64.6% (54.2-73.2) in the mitoxantrone group (p=0.0004), and 3-year overall surviv

165 n the cabazitaxel group and five (1%) in the mitoxantrone group had febrile neutropenia.

166 xel group and 12.7 months (11.6-13.7) in the mitoxantrone group.

167 In contrast, mitoxantrone had no significant effect on 5D3 binding.

168 In addition, mitoxantrone has been shown to inhibit the binding of hu

169 dies of 5q in camptothecin (CCRF-CEM/C2) and mitoxantrone (HL-60/MX2) resistant cancer cells highligh

170 e (OR, 3.58; 95% CI, 0.91-14.11) followed by mitoxantrone hydrochloride (OR, 2.73; 95% CI, 0.23-33.0)

171 y reversed SPF45-mediated drug resistance to mitoxantrone in A2780-SPF45 cells from 21-fold to 8- and

172 increased the accumulation of paclitaxel or mitoxantrone in ABCB1- or ABCG2-overexpressing cells.

173 verexpressing cells; mitoxantrone and [(3)H]-mitoxantrone in ABCG2 overexpressing cells, respectively

174 ent partial efficacy for the anthrecenedione mitoxantrone in active and progressive MS.

175 he cellular accumulation and cytotoxicity of mitoxantrone in both BCRP-overexpressing and BCRP-negati

176 c cells were significantly more sensitive to mitoxantrone in drug-treated transplanted mice.

177 re allocated to receive either idarubicin or mitoxantrone in induction by stratified concealed random

178 re allocated to receive either idarubicin or mitoxantrone in induction by stratified concealed random

179 We validate mitoxantrone in orthogonal mammalian cell-based assays,

180 taxel improve overall survival compared with mitoxantrone in patients with metastatic castration-resi

181 01) and a 1.8-fold longer beta half-life for mitoxantrone in plasma (P <.05).

182 docetaxel, prednisone/hydrocortisone, and/or mitoxantrone in specific settings.

183 IIalpha was observed in cells selected with mitoxantrone in suspension culture.

184 Increasing the degree of resistance to mitoxantrone in the 8226 cell line from 10 to 37 times (

185 was associated with a 10-fold resistance to mitoxantrone in the 8226/MR4 cell line.

186 sms of drug resistance during selection with mitoxantrone in the human myeloma cell line 8226.

187 ows the highest affinity for complexing with mitoxantrone, in contrast to resveratrol, which shows th

188 Before SWOG 9921, there were no cases of mitoxantrone-induced AML reported in patients treated fo

189 rotection of tumor cells from melphalan- and mitoxantrone-induced apoptosis.

190 s to elevated accumulation of etoposide- and mitoxantrone-induced TOP2A and TOP2B-DNA covalent comple

191 d in vivo treatment with either etoposide or mitoxantrone induces DNA damage, elevates expression (60

192 say data showed that GC-binding drugs (e.g., mitoxantrone) inhibited the DNA binding of both E2F1 and

193 ndomly assigned to receive either 12 mg/m(2) mitoxantrone intravenously over 15-30 min or 25 mg/m(2)

194 esistance to chemotherapeutic agents such as mitoxantrone, irinotecan, and flavopiridol.

195 Mitoxantrone is a drug that acts on nucleic acids primar

196 gest that the combination of ixabepilone and mitoxantrone is feasible and active in CRPC and requires

197 this electrochemical chip, the metabolism of mitoxantrone is studied by microchip electrospray ioniza

198 The anticancer drug mitoxantrone is unique among the inhibitors identified i

199 Cell exposure to mitoxantrone leads to HuR detachment and the subsequent

200 Mitoxantrone may be offered, accompanied by discussion o

201 Increased resistance to mitoxantrone may result from reduced intracellular drug

202 ts of cancer chemotherapeutic agents such as mitoxantrone (MIT) in multiple sclerosis (MS) patients j

203 locker SDZ PSC-833 (PSC) in combination with mitoxantrone (MITO) and etoposide (VP) was performed.

204 of idarubicin (IDR), daunorubicin (DNR), or mitoxantrone (MTA) gave the same percentages of apoptoti

205 A series of mitoxantrone (MTX) analogues have been designed, synthes

206 ds (MSNR) on hemolysis, colloidal stability, mitoxantrone (MTX) loading, in vitro MTX release, and ce

207 Using human leukemia (HL) 60/mitoxantrone (MX) 2 cell line as the model, we demonstra

208 protein (MRP) 1 (ABCC1) in the emergence of mitoxantrone (MX) cross-resistance in a MCF7 breast canc

209 y target MDR cancer cells and synergize with mitoxantrone (MX) in HL60/MX2 MDR cells.

210 BCC1) expression and cellular sensitivity to mitoxantrone (MX) toxicity can be ascertained; thus, the

211 essing R482T transported daunorubicin (DNR), mitoxantrone (MX), rhodamine 123, and flavopiridol (FLV)

212 we have reported that a multidrug-resistant, mitoxantrone (MX)-selected cell line, MCF7/MX, is highly

213 d with the chemotherapeutic agents SN-38 and mitoxantrone (MX).

214 the MDR cells to the chemotherapeutic agent mitoxantrone (MX); combination treatment with MX and caf

215 se IIbeta confers resistance specifically to mitoxantrone, not to other topoisomerase II inhibitors.

216 Fludarabine, mitoxantrone (Novantrone), and dexamethasone (FND) were

217 rospectively the effects of three courses of mitoxantrone (Novantrone), vincristine (Oncovin), vinbla

218 Because the effects of mitoxantrone on human male fertility were unknown, we de

219 mitremorgin C had no effect on resistance to mitoxantrone or BBR 3390 in the P-glycoprotein-positive

220 ated that high drug concentrations of either mitoxantrone or distamycin completely blocked transcript

221 nhibition of transcription was observed when mitoxantrone or distamycin was added either before or af

222 er ethylmethanesulfonate (EMS), mitomycin C, mitoxantrone or doxorubicin, at therapeutic concentratio

223 the effective intracellular concentration of mitoxantrone or the fluorescent compound BODIPY-prazosin

224 ytotoxicity or inhibition of stem cells from mitoxantrone or the other drugs.

225 Although known substrates of ABCG2 such as mitoxantrone or topotecan were not identified, we charac

226 , granulocyte colony-stimulating factor, and mitoxantrone), or reduced-dose CLAG-M, 197 (30%) met at

227 istic fashion with cytarabine, daunorubicin, mitoxantrone, or etoposide if used simultaneously or imm

228 relbine, oxaliplatin, ifosfamide, etoposide, mitoxantrone, or gemcitabine) given at prespecified stan

229 munosuppression, such as cyclophosphamide or mitoxantrone, or with autologous haematopoeitic stem cel

230 y minimizes false-positive hits, we identify mitoxantrone out of more than 600 clinically approved dr

231 divided doses before docetaxel, or 12 mg of mitoxantrone per square meter on day 1 plus 5 mg of pred

232 ost transport for rhodamine 123 and impaired mitoxantrone, pheophorbide a, and BODIPY-prazosin transp

233 ntions, including high-dose corticosteroids, mitoxantrone, plasma exchange (PE), rituximab (anti-CD20

234 hance the release of various drugs including mitoxantrone, plasmid DNA, and a chemokine from the scaf

235 plus granulocyte colony-stimulating factor, mitoxantrone plus cytarabine, or high-dose cytarabine).

236 Mitoxantrone plus prednisone and ixabepilone each have m

237 of cabazitaxel plus prednisone with those of mitoxantrone plus prednisone in men with metastatic cast

238 We compared docetaxel plus estramustine with mitoxantrone plus prednisone in men with metastatic, hor

239 ed to cabazitaxel plus prednisone (C + P) or mitoxantrone plus prednisone were used.

240 Using this method, we found that cancer drug mitoxantrone possesses significant DPP-4 inhibitory acti

241 ) and high toxicity risk are associated with mitoxantrone/prednisone after docetaxel.

242 ituximab, fludarabine, cyclophosphamide, and mitoxantrone (R-FCM).

243 ne) and R-FM (rituximab plus fludarabine and mitoxantrone) regimens without rituximab maintenance as

244 ors using established in vitro assays (e.g., mitoxantrone resensitization and BODIPY-prazosin assays)

245 The mitoxantrone resistance (MXR) gene encodes a recently ch

246 G2 (breast cancer resistance protein [BCRP], mitoxantrone resistance [MXR]) is associated with drug r

247 his question, we compared the acquisition of mitoxantrone resistance in U937 cells adhered to fibrone

248 These data demonstrate that low-level mitoxantrone resistance is due to the presence of a nove

249 r 2 (ABCG2; breast cancer resistance protein/mitoxantrone resistance protein)-mediated multidrug resi

250 ollowed by breast cancer resistance protein (mitoxantrone resistance protein, ABCG2) in 1999.

251 TP-binding cassette G2 (ABCG2, also known as mitoxantrone resistance protein, breast cancer-resistanc

252 P-overexpressing cells, completely reversing mitoxantrone resistance, with no effect on the correspon

253 overexpressed in MCF7/MX cells and to confer mitoxantrone resistance-were not MTX resistant, which su

254 omerase IIbeta downregulation is specific to mitoxantrone resistance.

255 DK7i response was altered in adriamycin- and mitoxantrone-resistant cell lines demonstrating ABC-tran

256 sette transporter, which is overexpressed in mitoxantrone-resistant cells.

257 ike ABCG2 (breast cancer resistance protein, mitoxantrone-resistant protein), MRP1-mediated MX transp

258 In the present study, a cDNA library from mitoxantrone-resistant S1-M1-80 human colon carcinoma ce

259 Reports of multiple distinct mitoxantrone-resistant sublines without overexpression o

260 The isolation of mitoxantrone-resistant vaccinia strains underscores that

261 Whole-genome sequencing of mitoxantrone-resistant viruses pinpointed missense mutat

262 those randomized to cytarabine or cytarabine/mitoxantrone, respectively.

263 r capacity to expel cytotoxic drugs, such as mitoxantrone, resulting in better survival.

264 esistance to the anthracenes, doxorubicin or mitoxantrone, results in coselection for resistance to C

265 inished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expres

266 was recently found to be overexpressed in a mitoxantrone-selected human colon cell line, S1-M1-3.2,

267 tively, but did not significantly affect the mitoxantrone sensitivity of vector control cells.

268 n MCF-7/MX100 cells resulted in an increased mitoxantrone sensitivity, as manifested by a significant

269 y with corticosteroids, plasma exchange, and mitoxantrone, severe cognitive impairment persisted and

270 wing characteristics: profound resistance to mitoxantrone; significant cross-resistance to doxorubici

271 creased their sensitivity to doxorubicin and mitoxantrone significantly but not to taxol.

272 ve shown that the anticancer drugs VM-26 and mitoxantrone stabilize preferentially the binding of top

273 lines and another intercalating TOP2 poison, mitoxantrone, stabilize TOP2-DNA covalent complexes less

274 t BFM 93 trial with high-dose cytarabine and mitoxantrone suggest that there may be some benefit to i

275 the LLC-MDR1-3H cells are more resistant to mitoxantrone than the LLC-MDR1-WT cells after being trea

276 ent in cell lines selected for resistance to mitoxantrone that do not overexpress P-glycoprotein or m

277 opoisomerase II (TOP2) poisons etoposide and mitoxantrone to chemical forms that have altered DNA dam

278 ma cell line in increasing concentrations of mitoxantrone to obtain a resistant subline, S1-M1-3.2, w

279 Finally, we exposed cells to mitoxantrone to promote folding and processing of the mu

280 Time from the start of mitoxantrone to the detection of AML was 13, 48, and 72

281 erexpressing cells studied; all demonstrated mitoxantrone transport, whereas only two effluxed rhodam

282 a cardioprotective effect of dexrazoxane in mitoxantrone treated multiple sclerosis patients.

283 e reported of a total of 487 patients in the mitoxantrone treatment arm.

284 thal CXL146 exposure regained sensitivity to mitoxantrone treatment.

285 HOP-rituximab (CHOP-R); or cyclophosphamide, mitoxantrone, vincristine, and prednisone (CNOP).

286 these cell lines to paclitaxel, doxorubicin, mitoxantrone, vincristine, and trabectedin with no effec

287 respectively, for 181 patients treated with mitoxantrone, vincristine, vinblastine, and prednisone a

288 with cabazitaxel compared with those taking mitoxantrone was 0.70 (95% CI 0.59-0.83, p<0.0001).

289 for GMTZ in combination with cytarabine and mitoxantrone was 3 mg/m(2) while the MTD in combination

290 Additionally, mitoxantrone was found to bind i-motif forming sequences

291 The pharmacophore of mitoxantrone was further investigated by testing a varie

292 Because cytarabine/mitoxantrone was more toxic and no more effective than c

293 Mitoxantrone was mutagenic to S. typhimurium TA1538 and

294 Day 4 mitoxantrone was omitted and a cardiology consult obtain

295 the fluorescent substrates rhodamine 123 and mitoxantrone, we showed that cyclosporin A inhibits P-gp

296 he cellular accumulation and cytotoxicity of mitoxantrone were flavonoid concentration dependent, and

297 Mitoxantrone, which was a stronger inhibitor of transcri

298 ntrone conjugate was synthesized by coupling mitoxantrone with ionic liquid tags, and cytotoxic behav

299 cokinetic (PK) interactions of etoposide and mitoxantrone with PSC were anticipated, measured in comp

300 ely 1000-fold weaker than the interaction of mitoxantrone with the DNA, which implies that the presen