ライフサイエンスコーパス: doxorubicin

1 ratio of encapsulated drugs (mertansine and doxorubicin).

2 o the DNA damage-inducing chemotherapy agent doxorubicin.

3 gical cancers, as are anthracyclines such as doxorubicin.

4 perturbation by hypoxia, ionophore (CCCP) or doxorubicin.

5 p21 that was synergistic with cisplatin and doxorubicin.

6 cal treatment modality to locally potentiate doxorubicin.

7 nd anticancer drugs such as erythromycin and doxorubicin.

8 tion, JAK-STAT and TNF-alpha signaling after doxorubicin.

9 mab regimen: carboplatin-pegylated liposomal doxorubicin.

10 1 cells to contribute to cross-resistance to doxorubicin.

11 ntainer to encapsulate chemotherapeutic drug doxorubicin.

12 ticipate to breast cancer cell resistance to doxorubicin.

13 to H(2)O(2)-induced oxidative stress and to doxorubicin.

14 ated pathways and gained cross-resistance to doxorubicin.

15 cancer cell model of acquired resistance to doxorubicin.

16 easing their resistance to the anthracycline doxorubicin.

17 al resistance to the topoisomerase II poison doxorubicin.

18 bling GACTZP nanotrain that carries the drug doxorubicin.

19 ntercalating drugs is then demonstrated with doxorubicin.

20 week after intraperitoneal administration of doxorubicin (1-25 mg/kg), revealing a dose-dependent dec

21 cin-induced cardiac atrophy, we administered doxorubicin 20 mg/kg to mice lacking MuRF1 (MuRF1(-/-))

22 g from 3.5 +/- 0.5 (control) to 1.8 +/- 0.1 (doxorubicin, 20 mg/kg).

23 E1-3 doxorubicin (3) could permeabilize an in vitro blood-bra

24 atin (AUC 5, day 1) plus pegylated liposomal doxorubicin (30 mg/m(2), day 1) every 4 weeks, both foll

25 intravenously on days 1-3 and five cycles of doxorubicin 37.5 mg/m(2) per dose intravenously on days

26 se intravenously on days 1-3 with mesna) and doxorubicin (37.5 mg/m(2) per dose intravenously on days

27 d reduction in cytotoxicity compared to free doxorubicin (5) in nontumor cells.

28 gated by conjugating E1-3 (1) or E1-7 (2) to doxorubicin (5).

29 sphamide 750 mg/m(2) on day 1 intravenously, doxorubicin 50 mg/m(2) on day 1 intravenously, and predn

30 ts received cyclophosphamide 750 mg/m(2) and doxorubicin 50 mg/m(2) on day 1 of each cycle intravenou

31 b 375 mg/m(2), cyclophosphamide 750 mg/m(2), doxorubicin 50 mg/m(2), and vincristine 1.4 mg/m(2) [to

32 (75 mg/m(2) every 3 weeks x 4 doses) or AC (doxorubicin 60 mg/m(2); cyclophosphamide 600 mg/m(2) eve

33 onsisted of pazopanib 800 mg once per day or doxorubicin 75 mg/m(2) once every 3 weeks (<= 6 cycles)

34 Doxorubicin, a brain-impermeable chemotherapeutic agent,

35 rected liposome that can selectively deliver doxorubicin, a standard-of-care chemotherapeutic agent,

36 ion in vitro and in vivo and synergized with doxorubicin, ABT-199 (a Bcl-2 antagonist), and dexametha

37 ationship of these drugs, we synthesized ten doxorubicin/aclarubicin hybrids varying in three distinc

38 diac dysfunction in a mouse model induced by doxorubicin administered in divided low doses as in the

39 es to cardiomyopathy pathogenesis induced by doxorubicin administered on a schedule simulating that i

40 modified liposomes that were formulated with doxorubicin against glioblastoma.

41 , (3) cyclophosphamide, (4) cisplatin or (5) doxorubicin, all followed by nivolumab.

42 e cytotoxic chemotherapy drugs cisplatin and doxorubicin alter arginine and polyamine metabolites.

43 ed regimen M (vincristine, dactinomycin, and doxorubicin alternating with cyclophosphamide and etopos

44 Anthracycline anticancer drugs doxorubicin and aclarubicin have been used in the clinic

45 After doxorubicin and cisplatin induction, we detected an upre

46 data of this study indicate that short-term doxorubicin and cisplatin may induce a more favorable tu

47 ent for aggressive non-Hodgkin lymphoma, and doxorubicin and cyclophosphamide are both associated wit

48 the liposomes within a single tumor released doxorubicin and enhanced cross-presentation of a model a

49 poside, mitoxantrone, and the anthracyclines doxorubicin and epirubicin.

50 es demonstrated ~12 and 3.3 fold increase in doxorubicin and erlotinib accumulation in mice brain, re

51 We loaded doxorubicin and erlotinib into liposomes to enhance thei

52 such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamma-irradiation directly or indirectly

53 of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of proapoptotic g

54 red the sensitive detection of drugs such as doxorubicin and rifampicin (LOD = 18 nM/9.7 ppb and 202

55 Combined treatment with doxorubicin and unseeded non-inertial cavitation signifi

56 n this work, we show that sublethal doses of doxorubicin and vorinostat still increased cellular cera

57 imilar when mice are treated with commercial doxorubicin and with a 42-fold lower amount of the nanob

58 itumor activity of a chemotherapeutic agent (doxorubicin) and immune checkpoint inhibitor blocker (an

59 y assigned to cyclophosphamide, vincristine, doxorubicin, and dexamethasone (CVAD) induction had high

60 Patients received bortezomib, doxorubicin, and dexamethasone chemotherapy, and were th

61 rfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) on courses 1, 3, 5, and

62 with six courses of vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) and one course of vinc

63 xhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V.

64 rgroup metronomic trial of cyclophosphamide, doxorubicin, and paclitaxel were queried on their use of

65 uximab or obinutuzumab and cyclophosphamide, doxorubicin, and prednisone (CHP) in patients with previ

66 in vitro, resensitized PDX-derived cells to doxorubicin, and repressed lung metastasis in vivo.

67 , prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R) with standard ri

68 e, vincristine, dactinomycin with or without doxorubicin, and surgery or radiotherapy, or both) were

69 ne of these nanobodies to the cytotoxic drug doxorubicin, and we show that the conjugate internalizes

70 EC(50) = 15 nM) and was capable of restoring doxorubicin antiproliferative activity at nontoxic conce

71 ds (DEBs) carrying the chemotherapeutic drug doxorubicin are located at destroyed vascular locations,

72 und Anthracycline chemotherapeutics, such as doxorubicin, are used widely in the treatment of numerou

73 We used Doxorubicin as a therapeutic agent, TNFalpha as marker a

74 nd is being investigated in combination with doxorubicin as second-line therapy in a randomised phase

75 After the discontinuation PTX with doxorubicin as the substitute, there was no further prog

76 mg/m(2) every week for 12 weeks followed by doxorubicin at 60 mg/m(2) and cyclophosphamide at 600 mg

77 )methacrylamide (HPMA) with cytostatic agent doxorubicin attached via stimuli-sensitive hydrazone bon

78 fold lower amount of the nanobody-conjugated doxorubicin, attesting to the efficacy of the conjugated

79 d to receive carboplatin-pegylated liposomal doxorubicin-bevacizumab (experimental group) and 337 wer

80 Carboplatin-pegylated liposomal doxorubicin-bevacizumab is a new standard treatment opti

81 g from a single-site-and thus noncooperative-doxorubicin-binding aptamer.

82 luded in survival analyses received standard doxorubicin, bleomycin, vinblastine and dacarbazone (ABV

83 8%]), followed by the combination regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine (19

84 atients treated with six to eight courses of doxorubicin, bleomycin, vinblastine, and dacarbazine (AB

85 Doxorubicin, bleomycin, vinblastine, and dacarbazine (AB

86 Patients received 2 cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (AB

87 ed in the United States by widespread use of doxorubicin, bleomycin, vinblastine, and dacarbazine and

88 tients (PET score, 3 to 5) received a fourth doxorubicin, bleomycin, vinblastine, and dacarbazine cyc

89 bined-modality treatment (CMT) with 2x ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) an

90 considered unsuitable for standard ABVD (ie, doxorubicin, bleomycin, vinblastine, and dacarbazine) th

91 derwent PET assessment after three cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine; 14

92 s them resistant to the cytotoxic effects of doxorubicin both in vitro and in vivo.

93 regimen DD4A (vincristine, dactinomycin and doxorubicin) but no radiation therapy.

94 tes which not only work synergistically with doxorubicin by producing reactive oxygen species but als

95 nd the drugs furosemide as well as furylated doxorubicin, by ultrasound-induced selective scission of

96 g the molecular and cellular determinants of doxorubicin cardiotoxicity, contributing to the developm

97 ting from TOP2 poisoning, may play a role in doxorubicin cardiotoxicity.

98 hat the organoids can model hypoxia-enhanced doxorubicin cardiotoxicity.

99 Conclusions Doxorubicin causes a subacute decrease in cardiac mass i

100 Targeted nanoparticle delivery of doxorubicin chemotherapy via the TRF1 receptor presents

101 heart failure (HF) is a known side effect of doxorubicin chemotherapy.

102 ptotic agents, such as staurosporine, taxol, doxorubicin, cisplatin and etoposide, utilized as contro

103 with the antineoplastic DNA-damaging agents doxorubicin, cisplatin, olaparib, and gamma-irradiation

104 mammary tumor cells, Cl66 cells resistant to doxorubicin (Cl66-Dox), or Cl66 cells resistant to pacli

105 Finally, doxorubicin combination with an oligonucleotide inhibiti

106 gimen versus carboplatin-pegylated liposomal doxorubicin combined with bevacizumab.

107 found that IL233 treatment even 2-weeks post-doxorubicin completely restored kidney function accompan

108 erapy with doxorubicin resulted in increased doxorubicin concentration in the tumor and dramatic inhi

109 oprinting allows to deposit large amounts of doxorubicin-containing liposomes to the outer cell layer

110 CTx was predominantly bleomycin, etoposide, doxorubicin cyclophosphamide, vincristine, procarbazine,

111 al Wilms Tumor Study 5 (NWTS-5; vincristine, doxorubicin, cyclophosphamide, and etoposide plus radiot

112 Doses of doxorubicin, cyclophosphamide, and etoposide were reduce

113 e hypothesized that dose-adjusted etoposide, doxorubicin, cyclophosphamide, vincristine, prednisone,

114 ix to eight courses of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine

115 switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine

116 and the other half with R-ACVBP (rituximab, doxorubicin, cyclophosphamide, vindesine, bleomycin, and

117 djuvant single-agent cisplatin (CDDP) versus doxorubicin-cyclophosphamide (AC) in BRCA carriers with

118 of age who completed 4 cycles of dose-dense doxorubicin-cyclophosphamide for stage I-III breast canc

119 ing the paclitaxel portion of the dose-dense doxorubicin-cyclophosphamide-paclitaxel regimen.

120 In vivo, treatment with the chemotherapeutic doxorubicin decreased [(18)F]FSPG tumor uptake in a mous

121 Mice received a clinically relevant dose of doxorubicin delivered systemically and were euthanized 7

122 .004), drug-eluting embolic TACE (P = .03), doxorubicin dose (P = .003), history of PES (P < .001) a

123 m week 10 (2 weeks after the fifth and final doxorubicin dose).

124 f these, 5 received 5 biweekly intracoronary doxorubicin doses (0.45 mg/kg/injection) and were follow

125 eased response to the chemotherapeutic agent doxorubicin (DOX) (P < 0.01).

126 elivery and showed that co-delivery of 3 muM doxorubicin (DOX) + MB + US reduced spheroid viability t

127 ptide scaffolds laden with precise ratios of doxorubicin (DOX) and camptothecin (CPT).

128 In vitro, linking doxorubicin (Dox) and transferrin (TF) to CND (CND-Dox-T

129 e diselenide bonds for controlled release of doxorubicin (DOX) at tumor sites are developed.

130 rted activation in failing human hearts with doxorubicin (DOX) cardiomyopathy, and its activation acu

131 d, AP1-DEVD-S-DOX was able to exert improved doxorubicin (DOX) delivery to the tumor and anticancer e

132 h-throughput promoter-dependent drug screen, doxorubicin (dox) exhibited this ability, acting on DNA

133 Doxorubicin (Dox) is a highly effective anticancer drug

134 Doxorubicin (Dox) is a widely used antineoplastic agent

135 Although doxorubicin (DOX) is an effective anti-cancer drug with

136 Doxorubicin (DOX) is one of the most effective anticance

137 Planar obelisk-like apomorphine and doxorubicin (DOX) molecules intercalated well within the

138 ation with widely used chemotherapeutic drug doxorubicin (Dox) proved effective in killing of HeLa ca

139 In our investigations, we considered doxorubicin (DOX) spiked in homogenized tissue matrix at

140 sterically-stabilized liposomes loaded with doxorubicin (Dox) stably incorporate small amounts of a

141 ith anti-cancer drugs temozolomide (TMZ) and doxorubicin (DOX) were investigated.

142 The anticancer drug (doxorubicin (DOX))-treated cells show slow increases of

143 ) were first loaded with the anticancer drug Doxorubicin (Dox), coated with magnetic iron oxide nanop

144 e previously reported that an anthracycline, doxorubicin (DOX), induces apoptotic death of cardiomyoc

145 g and immunogenic cell death inducing agent, doxorubicin (DOX), we sought to determine the in vitro p

146 istance by co-delivering a chemotherapeutic, Doxorubicin (Dox), with a Pgp inhibitor, either Pluronic

147 Doxorubicin (DOX)-loaded lysolipid temperature-sensitive

148 g delivery systems (DDSs) in the delivery of doxorubicin (DOX).

149 fying concentrations of the anticancer drug, doxorubicin (DOX).

150 of 92 kDa was synthesized to conjugate with doxorubicin (DOX).

151 some and commercial liposomal formulation of doxorubicin (DOXIL).

152 High-throughput screening identified doxorubicin (DXR) as an inhibitor of the Akt-beta-cateni

153 Doxorubicin (DXR) enhanced tumor cell sEV secretion to a

154 eria and/or their products are necessary for doxorubicin (DXR)-induced small intestine mucosal damage

155 oordinated interaction of TFs to explain the Doxorubicin, E2 and TNFalpha induced repression mechanis

156 resence of cavitation as required to enhance doxorubicin efficacy, but ruled out the influence of cha

157 derived protein corona formed onto PEGylated doxorubicin-encapsulated liposomes (Caelyx) is thoroughl

158 de-stabilized DNA cleavage was attenuated by doxorubicin, epirubicin, or mitoxantrone.

159 according to IGHG-defined risk groups (low [doxorubicin-equivalent anthracycline dose of 1-99 mg/m(2

160 specific for the combination treatment with Doxorubicin + Estradiol + TNFalpha in comparison with si

161 ESR1 network regulation based on analysis of Doxorubicin, Estradiol, and TNFalpha combination treatme

162 ion than clinically representative liposomal doxorubicin for breast cancer treatment and presents a n

163 usly showed that an intravenous injection of doxorubicin-free Doxil-like PEGylated nano-liposomes (Do

164 from 22.8 +/- 2.5% ID to -3.5 +/- 3.1%, and doxorubicin from 23.0 +/- 2.2% ID to 17.8 +/- 0.7, p < 0

165 therapy with vincristine, actinomycin-D, and doxorubicin given singly or in combination.

166 After pooling the doxorubicin groups for the efficacy analysis, median ove

167 Doxorubicin-GSH adduct formation kinetics are thermodyna

168 NAsomes are loaded with the hydrophilic drug doxorubicin hydrochloride and anti-P-glycoprotein siRNA,

169 ding hydrophilic small molecule drugs (e.g., doxorubicin hydrochloride), nucleic acids (e.g., DNA and

170 Doxorubicin impaired muscle performance, which was indic

171 bution, and retention of the anticancer drug doxorubicin in both cancerous and normal tissues.

172 pazopanib has efficacy comparable to that of doxorubicin in elderly patients with STS and offers supe

173 A phase 1b/3 trial of tazemetostat plus doxorubicin in the front-line setting is currently under

174 on reorganization and altered sensitivity to doxorubicin-induced apoptosis.

175 In mice, doxorubicin-induced cardiac atrophy is dependent on MuRF

176 To investigate the determinants of doxorubicin-induced cardiac atrophy, we administered dox

177 Doxorubicin-induced cardiomyocyte death is mediated by u

178 nderstanding the key role of mitochondria in doxorubicin-induced cardiomyopathy is essential to reduc

179 ll-derived cardiomyocytes from patients with doxorubicin-induced cardiomyopathy.

180 purpose of this study was to identify early doxorubicin-induced cardiotoxicity by serial multiparame

181 and anatomical properties all play a role in doxorubicin-induced cardiotoxicity phenotypes.

182 henylphosphonium and their response to acute doxorubicin-induced cardiotoxicity were assessed in rats

183 ial RNA binding protein, in replication- and doxorubicin-induced cellular senescence.

184 is an efficient sensitizer of radiation- and doxorubicin-induced DNA damage, with combinations in xen

185 miR-221 network and P-glycoprotein (P-gp) in doxorubicin-induced drug resistance of leukemia cells.

186 Collectively, doxorubicin-induced lesions likely span mitochondrial co

187 corroborated these findings, indicating that doxorubicin-induced mitochondrial impairments are locate

188 We focus on the involvement of doxorubicin-induced mitochondrial oxidative stress, disr

189 Studies investigating doxorubicin-induced myotoxicity have reported disrupted

190 Here, using doxorubicin-induced nephrotoxic renal injury model, we i

191 covalent complexes, but we could not detect doxorubicin-induced TOP2-DNA complexes, and doxorubicin

192 double hit: immunoproteasome inhibition and doxorubicin-induced toxicity.

193 TMT-based multiplexing and demonstrate that doxorubicin induces MHC-I peptide ligands that are large

194 to an in vivo rat model, 2 weeks after bolus doxorubicin injection, there was a dose-dependent loss o

195 cilitated penetration and/or accumulation of doxorubicin into spheroids, and displayed low toxicity a

196 e selectivity of the aptamer binding directs doxorubicin into the aptamer-targeted cells.

197 tic cells (DCs), CpG oligonucleotides, and a doxorubicin-iRGD conjugate enhance the immunogenic death

198 When loaded with doxorubicin, irradiated NP-[CPP] significantly reduces n

199 Doxorubicin is a standard of care in patients with advan

200 Doxorubicin is a widely used chemotherapeutic agent that

201 Doxorubicin is already a frontline chemotherapy in a var

202 Doxorubicin is an anthracycline-based chemotherapeutic t

203 The model predicts that HF in the absence of doxorubicin is characterized by a 2- to 3-fold stiffness

204 Doxorubicin is one of the most highly prescribed anthrac

205 ular uptake and immunoproteasome inhibition, doxorubicin is released from the immunoproteasome inhibi

206 gh ROS-induced cleavage of thioketal linker, doxorubicin is released from the polyprodrug.

207 However, the therapeutic index of doxorubicin is undermined by dose-dependent cardiotoxici

208 Doxorubicin is widely used in breast cancer chemotherapy

209 ednisone, vincristine, cyclophosphamide, and doxorubicin) is a preferred regimen for HIV-non-Hodgkin

210 s (including 25.8% rosmarinic acid and 9.04% doxorubicin), keep stable in a high concentration of ani

211 Using doxorubicin-liposome-loaded microbubbles, we show that s

212 ong-term survival study and compared against doxorubicin liposomes and gemcitabine liposomes.

213 The model was tested on DOXIL(R) (doxorubicin liposomes), and an excellent agreement was f

214 nanoparticles (30 mg/m(2) group), 20 mg/m(2) doxorubicin-loaded nanoparticles (20 mg/m(2) group), or

215 were randomly assigned to receive 30 mg/m(2) doxorubicin-loaded nanoparticles (30 mg/m(2) group), 20

216 227 (94%) of 242 patients who received doxorubicin-loaded nanoparticles and 100 (75%) of 134 pa

217 s occurred in 74 (31%) patients who received doxorubicin-loaded nanoparticles and 48 (36%) in the con

218 re neutropenia (25 [10%] of 242 treated with doxorubicin-loaded nanoparticles and eight [6%] of 134 i

219 s 9.1 months (95% CI 8.1-10.4) in the pooled doxorubicin-loaded nanoparticles group and 9.0 months (7

220 We assessed the intravenous perfusion of doxorubicin-loaded nanoparticles in patients with hepato

221 ntial for imaging cardiotoxicity in an acute doxorubicin model.

222 Following IV administration of doxorubicin, MRgFUS-treated animals exhibited a 4-fold h

223 providing potential targets for alleviating doxorubicin myotoxicity.

224 onally engineered peptide-targeted liposomal doxorubicin nanoparticles that have an enhanced selectiv

225 ticancer efficacy than free rosmarinic acid, doxorubicin, non-crosslinked Rososome and commercial lip

226 icacious combination of these compounds with doxorubicin on MCF7 cells was demonstrated after 72 h of

227 r DNA double-strand breaks induced by either doxorubicin or ionizing radiation.

228 bserved when combined with inducers of DSBs (doxorubicin or irradiation) or PARP inhibition (olaparib

229 emical induction of glomerular disease (with Doxorubicin or LPS).

230 te, and fluorouracil or cyclophosphamide and doxorubicin) or capecitabine.

231 peroxide, human serum, potassium iodide and doxorubicin/ oxaliplatin for both ex vivo and in vitro e

232 ition, including drugs such as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its i

233 ssessed in rats in vivo (10, 15, or 20 mg of doxorubicin per kilogram, intravenously, 48 h beforehand

234 ebo combined with nab-paclitaxel followed by doxorubicin plus cyclophosphamide as neoadjuvant treatme

235 y, Pep8 alone or together with a low dose of doxorubicin potently induced p53 expression and suppress

236 matrix metalloproteinase 9 (MMP9)-activated doxorubicin prodrug (MMP9-DOX-NPs) is developed.

237 etargeting strategy, we have shown selective doxorubicin prodrug activation and instantaneous fluores

238 avable linkers, yielding peptide epoxyketone-doxorubicin prodrugs that remained selective and active

239 er cell layers of the spheroids, followed by doxorubicin release into the deeper layers of the sphero

240 erase inhibitor, it enhanced the activity of doxorubicin released locally in liver tumor xenografts w

241 Pazopanib was noninferior to doxorubicin, rendering pazopanib a putative therapeutic

242 doxorubicin, suggesting that MAF1 regulates doxorubicin resistance in HCC by controlling RNA pol III

243 rs and CTCF binding sites that are linked to doxorubicin resistance.

244 and SYF2, whose depletion partially reversed doxorubicin resistance.

245 RNA, and ECT2-Ex5+ isoform depletion reduced doxorubicin resistance.

246 eotide inhibiting ECT2-Ex5 inclusion reduced doxorubicin-resistant tumor growth in mouse xenografts,

247 exposure of tumor cells to hyperthermia and doxorubicin resulted in immunogenic cell death and the l

248 Combination therapy with doxorubicin resulted in increased doxorubicin concentrat

249 The aptamer-nanotrain assembly, charged with doxorubicin, selectively kills liver cancer cells in cul

250 In this study, a doxorubicin-specific in silico quinone redox metabolism

251 ell growth and re-sensitizes T-DM1R cells to doxorubicin, suggesting that dual targeting EGFR and MRP

252 unit (BRF1) enhanced HCC cell sensitivity to doxorubicin, suggesting that MAF1 regulates doxorubicin

253 doxorubicin-induced TOP2-DNA complexes, and doxorubicin suppressed etoposide-induced TOP2-DNA comple

254 ombinatorial therapy of a WNT inhibitor with doxorubicin synergistically activated apoptosis in vitro

255 Stopping doxorubicin therapy upon detection of T(2) prolongation

256 induced by (N = 22) or unrelated to (N = 25) doxorubicin therapy.

257 oaded with a chemotherapeutic payload (i.e., doxorubicin), these cellular vectors (CELVEC) were shown

258 chemoradiotherapy by selectively delivering doxorubicin to the tumor with less systemic cytotoxicity

259 For effective delivery of free doxorubicin to tumors with minimal toxicity, we stabiliz

260 breaks induced by several agents (bleomycin, doxorubicin, topotecan, hydrogen peroxide, UV, photosens

261 A61603 did not protect mutant myocytes from doxorubicin toxicity in vitro.

262 dels (nephrotoxic serum nephritis, diabetes, doxorubicin toxicity, and CD2AP deficiency).

263 en a similar mtDNA protection role of p53 in doxorubicin-treated human induced pluripotent stem cell

264 gnificant dose response of cardiac uptake to doxorubicin treatment was observed before detectable bio

265 Following doxorubicin treatment, resistant cells accumulated in S

266 retention of (18)F-MitoPhos was observed on doxorubicin treatment, with average cardiac SUV from 30

267 vation of LV function and mitochondria after doxorubicin treatment.

268 ventricular (LV) systolic dysfunction after doxorubicin treatment.

269 e and cell death mediated by oxaliplatin and doxorubicin treatments.

270 y, but ruled out the influence of changes in doxorubicin uptake, temperature increase, hydroxyl radic

271 n relapsed HL and was recently approved with doxorubicin, vinblastine, and dacarbazine (AVD) for prev

272 apy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the major

273 Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)-based

274 cle of standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP; ritu

275 tion of rituximab (R) into cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) by Coiff

276 uximab or obinutuzumab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-/G-CHOP) che

277 is abbreviated rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and ra

278 ly treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and th

279 ) with standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) as fro

280 herapy with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has be

281 h frontline rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP; or var

282 comes after rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone immunochemother

283 reated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone therapy or the

284 -CHOP biweekly (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) and the other

285 ed with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show t

286 use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome

287 er diseases, such as CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) for diffuse la

288 to R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) into maintenan

289 ne; n = 45, rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), with the latt

290 A regimen of cyclophosphamide, doxorubicin, vincristine, and prednisone, with (R-CHOP)

291 prognostic for rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone or salvage immunoch

292 Doxorubicin was conjugated to an immunoproteasome-select

293 Doxorubicin was selected from a drug screen consisting o

294 HF due to doxorubicin was similar but showed stronger bias toward

295 Objective response rates for pazopanib and doxorubicin were 12.3% and 15.4%, respectively.

296 Pazopanib and doxorubicin were given to 81 and 39 patients, respective

297 lied this approach to measuring responses to doxorubicin, which is known to promote antitumor CD8(+)

298 ious redox cyclers, present in drugs such as doxorubicin, which is used to treat a host of human canc

299 tumors with minimal toxicity, we stabilized doxorubicin with copper in temperature-sensitive liposom

300 ified infusional etoposide, vincristine, and doxorubicin with cyclophosphamide and prednisone (EPOCH)