ライフサイエンスコーパス: doxorubicin

1 ination with MDR1, significantly transported doxorubicin.

2 eir single-cell counterparts when exposed to doxorubicin.

3 did the inhibition of A549 derived tumors by doxorubicin.

4 hemotherapy drugs: cisplatin, docetaxel, and doxorubicin.

5 toward chemotherapies such as paclitaxel or doxorubicin.

6 d or metastatic soft-tissue sarcoma has been doxorubicin.

7 damage induced by the chemotherapeutic drug doxorubicin.

8 ansporter-mediated uptake and disposition of doxorubicin.

9 re and after treatment with anti-cancer drug doxorubicin.

10 ased the susceptibility of cardiomyocytes to doxorubicin.

11 ardiotoxicity of the common anti-cancer drug doxorubicin.

12 of a critical intracellular concentration of doxorubicin.

13 ol shows synergistic anticancer effects with doxorubicin.

14 de (OATP) transporters to the disposition of doxorubicin.

15 and has an ability to load 7 +/- 0.3 wt% of doxorubicin.

16 isrupting agent, ICT-2552, and the cytotoxin doxorubicin.

17 ermore, CO sensitized breast cancer cells to doxorubicin.

18 tumor cell response to the chemotherapy drug doxorubicin.

19 heres alone (Bead Block [BB]) or loaded with doxorubicin 150 mg (LC Bead [LCB]).

20 75 mg/m(2)], cyclophosphamide [750 mg/m(2)], doxorubicin [50 mg/m(2)], and vincristine [1.4 mg/m(2),

21 ctedin 1.1 mg/m(2) in a 3-hour infusion plus doxorubicin 60 mg/m(2) as the experimental arm and doxor

22 bicin 60 mg/m(2) as the experimental arm and doxorubicin 75 mg/m(2) as the control arm were administe

23 ned 1:1 to receive six cycles of intravenous doxorubicin 75 mg/m(2) on day 1 every 3 weeks, or intrav

24 ctin patches, confers elevated resistance to doxorubicin (a toxic compound whose entry requires endoc

25 d form of Numb by Plk1 are more sensitive to doxorubicin, a classical chemotherapeutic drug.

26 Doxorubicin, a first-line chemotherapy drug, often cause

27 Compared to free doxorubicin, a single intravenous (IV) administration of

28 rapy, which included either cyclophosphamide/doxorubicin (AC) or cyclophosphamide/methotrexate/fluoro

29 Doxorubicin accumulated and penetrated similarly in both

30 oxorubicin, and passive transport of neutral doxorubicin across the lipid bilayer of the liposomes.

31 repair of DNA damage caused by cisplatin or doxorubicin, acting upstream of different repair pathway

32 nd four was stratified by extent of disease, doxorubicin administration method, and previous systemic

33 All patients received doxorubicin (Adriamycin), bleomycin, vinblastine, dacarb

34 ib-conjugating intermediate, and a dendritic doxorubicin-affinitive interior.

35 hanism, is more effective than cisplatin and doxorubicin against these cell lines and more potent tha

36 ents were randomly assigned (1:1) to receive doxorubicin alone (75 mg/m(2) via bolus injection admini

37 us doxorubicin did not show superiority over doxorubicin alone as first-line treatment of advanced ST

38 the combination group (45 [14%]) than in the doxorubicin alone group (four [1%]), as was grade 3-4 st

39 cause [n=1]) versus one (<1%) patient in the doxorubicin alone group (lactic acidosis [n=1]).

40 combination group and 99 (32%) of 308 in the doxorubicin alone group.

41 to doxorubicin plus evofosfamide and 323 to doxorubicin alone), all of whom were included in the int

42 osfamide versus 19.0 months (16.2-22.4) with doxorubicin alone.

43 ed 3 years after diagnosis were worse in the doxorubicin-alone group (n = 55 per group; P </= .01 for

44 assigned to the two treatment groups (129 to doxorubicin and 128 to gemcitabine and docetaxel).

45 ious adverse events in patients who received doxorubicin and 15 [12%] of 130 serious adverse events i

46 penia (32 [25%] of 128 patients who received doxorubicin and 25 [20%] of 126 patients who received ge

47 months (95% CI 4.1-8.3) with olaratumab plus doxorubicin and 4.1 months (2.8-5.4) with doxorubicin (s

48 OR) inhibition in combination with liposomal doxorubicin and bevacizumab in patients with advanced me

49 creening identified anthracyclines including doxorubicin and CDK9 inhibitors including dinaciclib tha

50 Intracellular doxorubicin and copper were 6-fold and 5-fold greater, r

51 el and cyclophosphamide (TC) was superior to doxorubicin and cyclophosphamide (AC) in a trial in earl

52 As doxorubicin and dinaciclib also reduced BCL-XL, the comb

53 vestigated under the treatment of two drugs (doxorubicin and etoposide).

54 or p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in ord

55 iac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac function.

56 Despite the known cardiotoxic effects of doxorubicin and other anthracyclines, no evidence-based

57 Encapsulated doxorubicin and paclitaxel exhibit cytotoxic effects on

58 uracil, carmustine, cisplatin, methotrexate, doxorubicin and paclitaxel.

59 We found that doxorubicin and related anthracycline agents (e.g., daun

60 ing of two model drugs: the chemotherapeutic doxorubicin and the antibiotic vancomycin.

61 art failure induced by the chemotherapy drug doxorubicin and their interaction with circular RNAs.

62 Doxorubicin and trastuzumab resulted in modest, persiste

63 ffects of commonly used therapies, including doxorubicin and trastuzumab, on cardiac remodeling and f

64 treated with temperature-sensitive liposomal doxorubicin and ultrasound hyperthermia.

65 in tumors treated with temperature-sensitive doxorubicin and ultrasound hyperthermia.

66 with or without topotecan, vincristine, and doxorubicin) and achieved an adequate disease response.

67 Regimen DD4A (vincristine, dactinomycin, and doxorubicin) and radiation therapy.

68 h (USOR) 06-090 compared TC6 with docetaxel, doxorubicin, and cyclophosphamide (TAC6).

69 % for dexamethasone and 50% for vincristine, doxorubicin, and cyclophosphamide, which shortened the t

70 domide in maintenance), and the vincristine, doxorubicin, and dexamethasone (VAD) group of the HOVON6

71 -damaging agents, cytarabine, 6-thioguanine, doxorubicin, and etoposide, but not to a non-DNA damagin

72 umor resistance to the most effective agent, doxorubicin, and further enabled assessment of a preclin

73 ) to receive either postoperative cisplatin, doxorubicin, and methotrexate (MAP) or MAP plus ifosfami

74 oadjuvant chemotherapy comprising cisplatin, doxorubicin, and methotrexate with intercalated surgery

75 ubicin, protonation/deprotonation of soluble doxorubicin, and passive transport of neutral doxorubici

76 therapeutic efficacy that is similar to free doxorubicin, and this efficacy can be enhanced by elevat

77 ERPRETATION: The addition of evofosfamide to doxorubicin as first-line therapy did not improve overal

78 assess the benefit of adding evofosfamide to doxorubicin as first-line therapy for advanced soft-tiss

79 dy compared gemcitabine and docetaxel versus doxorubicin as first-line treatment for advanced or meta

80 and temsirolimus (DAT) (N = 39) or liposomal doxorubicin, bevacizumab, and everolimus (DAE) (N = 13).

81 ge, 37-79 years) were treated with liposomal doxorubicin, bevacizumab, and temsirolimus (DAT) (N = 39

82 Liposomal doxorubicin, bevacizumab, and the mTOR inhibitors temsir

83 asis of early PET (ePET) after two cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (AB

84 been successfully treated with a regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine for

85 98 months), noninferiority of two cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD)

86 ng and response monitoring after 2 cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD)

87 We report that doxorubicin blocks cardiomyocyte autophagic flux in vivo

88 l (iPSC) derived cardiomyocytes treated with doxorubicin, both PLCE1 and ATP2B1 displayed anthracycli

89 The doxorubicin-breast cancer dose response was stronger in

90 cycles of cisplatin/fluorouracil/vincristine/doxorubicin (C5VD), and nonresponders received six cycle

91 Recently, it has become recognized that doxorubicin can contribute to re-establishing host antit

92 l formulations of chemotherapeutics, such as doxorubicin, can achieve locally high drug concentration

93 ify whether serial (18)F-FDG PET/CT predicts doxorubicin cardiotoxicity.

94 ytes is likely a critical mechanism by which doxorubicin causes cardiotoxicity.

95 Doxorubicin causes endothelial senescence but, surprisin

96 al (18)F-FDG uptake before the initiation of doxorubicin chemotherapy in HD patients may predict the

97 domized Phase II study, adding olaratumab to doxorubicin chemotherapy significantly improved overall

98 lines were created in response to prolonged doxorubicin chemotherapy.

99 The results indicated that honokiol and doxorubicin could be efficiently loaded into MPEG-PCL na

100 We report herein that Chimeric Polypeptide Doxorubicin (CP-Dox), a nanoparticle formulation of doxo

101 bronectin-targeting CREKA-modified liposomal doxorubicin (CREKA-Lipo-Dox) for the therapy of metastat

102 ibrosarcoma with a combination of F8-TNF and doxorubicin, curing the majority of treated animals (29/

103 thesis by administering cyclophosphamide and doxorubicin (Cyclo/Dox), a common treatment for breast c

104 She received neoadjuvant dose-dense doxorubicin, cyclophosphamide, and paclitaxel chemothera

105 ve been widely adopted in the United States: doxorubicin, cyclophosphamide, paclitaxel, and trastuzum

106 tched to two cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine

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

108 cles received BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine

109 onths), superiority of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine

110 evaluating the efficacy of either rituximab, doxorubicin, cyclophosphamide, vindesine, bleomycin, pre

111 ty and efficient intratumoral bortezomib and doxorubicin delivery by nanoformulation.

112 Further, doxorubicin delivery by temperature-sensitive liposomes

113 Finally, a combination of selinexor with doxorubicin demonstrated a synergistic decrease in the c

114 pression, and enhanced chemosensitization to doxorubicin, dexamethasone, and ibrutinib.

115 the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rituximab, and the Bruton ty

116 Trabectedin plus doxorubicin did not show superiority over doxorubicin al

117 In vivo doxorubicin disposition studies revealed that doxorubici

118 We show that crystalline doxorubicin dissolution can be described by a first orde

119 Doxorubicin dose-dependently increases LV MRGlu, particu

120 e concept is demonstrated by coencapsulating doxorubicin (DOX) (an anticancer drug) and IR780 iodide

121 latter, TSLs were prepared, coencapsulating doxorubicin (dox) and [Gd(HPDO3A)(H2O)], and injected in

122 the standard chemotherapeutic agents, i.e., doxorubicin (DOX) and cytarabine (Ara-C).

123 Anthracycline drugs such as doxorubicin (DOX) and daunorubicin remain some of the mo

124 aluated the effect of temporal scheduling of doxorubicin (DOX) and gemcitabine (GEM) on drug synergy.

125 Both doxorubicin (Dox) and irinotecan (Iri) elution kinetics

126 In this paper, honokiol (HK) and doxorubicin (Dox) co-loaded Methoxy poly(ethylene glycol

127 n permeability of the chemotherapeutic agent doxorubicin (DOX) in a xenograft model of prostate cance

128 Doxorubicin (Dox) is approved for use in liposomal form

129 MOP 5 can be fully loaded with doxorubicin (DOX) prodrug 2 via hetero-ternary complex f

130 d a reactive-oxygen-species (ROS)-responsive doxorubicin (DOX) prodrug, BDOX, in polymeric nanopartic

131 89 nanoreporter ((89)Zr-NRep) allows precise doxorubicin (DOX) quantification.

132 DHM markedly sensitized paclitaxel (PTX) and doxorubicin (DOX) resistant ovarian cancer cells to PTX

133 Here we demonstrated that doxorubicin (DOX) treatment of 4T1 breast tumor-bearing

134 LTSLs and NTSLs containing doxorubicin (Dox) were co-loaded with a nanobubble contr

135 Local drug delivery of Doxorubicin (Dox) with thermosensitive liposomes (TSL) a

136 Doxorubicin (DOX), a common chemotherapeutic agent, impa

137 Doxorubicin (DOX), a widely used clinical anticancer dru

138 that the main cytotoxic ingredient in CHOP, doxorubicin (Dox), has subtype-specific mechanisms of cy

139 of 277 breast cancer participants receiving doxorubicin (Dox), trastuzumab (Tras), or both (Dox+Tras

140 eneficial effects on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity via deacetylation of mi

141 umor-penetrating peptide and thermosensitive doxorubicin (DOX)-loaded nanoparticles in combination wi

142 The doxorubicin (DOX)-loaded SNP (SNP/DOX) shows significant

143 ct of IRE, used alone or in combination with doxorubicin (DOX)-loaded superparamagnetic iron oxide (S

144 dual-functional carriers for codelivery with doxorubicin (DOX).

145 ting concentration of the chemotherapy agent doxorubicin (DOX).

146 ic dye Nile Red (NR) and the anticancer drug doxorubicin (DOX).

147 e treated with paclitaxel (PTX, 2-1000nM) or doxorubicin (DOX, 20-1000nM) for 24-48h.

148 outcomes than clinically approved liposomal doxorubicin (Doxil) in HER2-overexpressing BT474 tumor x

149 ll populations were produced by performing a doxorubicin drug challenge on two parental cell lines (e

150 f cancer cells to the chemotherapeutic agent doxorubicin (DXR) and growth factors (EGF and IGF-1).

151 e cardiomyocytes and mice to the cancer drug doxorubicin (DXR).

152 age range, 23-72 years) underwent TACE with doxorubicin-eluting microspheres (DEB) (hereafter, DEB-T

153 We engineered ICAM-1 antibody conjugated, doxorubicin encapsulating immunoliposomes (ICAM-Dox-LPs)

154 This study evaluates the penetration of doxorubicin-encased liposomes into three-dimensional cel

155 icin (CP-Dox), a nanoparticle formulation of doxorubicin, enhances antitumor immunity.

156 The maximum concentration level of delivered doxorubicin exceeded levels previously shown (using unco

157 Conclusion The results strongly suggest that doxorubicin exposure in CCSs increases the risk of subse

158 Total cellular doxorubicin fluorescence was similar following CuDox and

159 ld zebrafish injected intraperitoneally with doxorubicin followed by LSFI at 3, 30, and 60 days post-

160 revious chemotherapy for sarcoma or previous doxorubicin for any cancer.

161 chemotherapy (vincristine, dactinomycin, and doxorubicin) for 6 or 12 weeks based on radiographic res

162 Doxorubicin forms the basis of chemotherapy regimens for

163 and mitigates toxicity compared to standard doxorubicin formulations.

164 Spheroids were dosed with liposomal doxorubicin, free doxorubicin, or media control to asses

165 every 21-day cycle for up to six cycles) or doxorubicin (given via the same dose procedure) plus evo

166 population: 74 (57%) of 129 patients in the doxorubicin group and 80 (63%) of 128 in the gemcitabine

167 es of treatment, patients in the single-drug doxorubicin group were followed up expectantly whereas p

168 evofosfamide group vs 65 [21%] of 308 in the doxorubicin group), neutropenia (47 [15%] vs 92 [30%]),

169 higher drug resistance than Hep-G2 cells and doxorubicin had a higher efficacy than etoposide for tre

170 further enhance the immunological effects of doxorubicin has not been adequately examined.

171 esting Oatp1b transporters are important for doxorubicin hepatic uptake.

172 ce treated with PLD compared to conventional doxorubicin (HR 0.39; 95% CI 0.27-0.56).

173 In addition, a small molecule drug (i.e., doxorubicin hydrochloride) was loaded into the nanoparti

174 profiling from murine myocardium exposed to doxorubicin identified 5 differentially expressed RBPs.

175 Doxil liposomes are designed to retain doxorubicin in circulation, minimize clearance by the mo

176 This study of olaratumab with doxorubicin in patients with advanced soft-tissue sarcom

177 e overall survival compared with single-drug doxorubicin in patients with locally advanced, unresecta

178 es by assessing the delivery and efficacy of doxorubicin in small molecular form versus hyaluronic ac

179 edly resistant to the dysfunction induced by doxorubicin in WTs.

180 escence was similar following CuDox and free doxorubicin incubation.

181 I-IMS is able to detect three metabolites of doxorubicin, indicating that cells actively metabolize t

182 Doxorubicin-induced acute cardiotoxicity did not increas

183 ediated overexpression of Qki5 inhibited the doxorubicin-induced apoptosis in cardiomyocytes.

184 rts, among which TCONS_00009015 responded to doxorubicin-induced cardiac stress.

185 E5 inhibitor tadalafil on the development of doxorubicin-induced cardiomyopathy in WT and KI mice was

186 o predict which patients will be affected by doxorubicin-induced cardiotoxicity (DIC).

187 rom iPSC and nt-ESCs could both recapitulate doxorubicin-induced cardiotoxicity and exhibited insigni

188 The mechanisms of doxorubicin-induced cardiotoxicity remain incompletely u

189 us, an interesting target molecule to combat doxorubicin-induced cardiotoxicity.

190 ated in vivo, this FOXO4 peptide neutralized doxorubicin-induced chemotoxicity.

191 Here we investigated doxorubicin-induced cytotoxicity in human induced plurip

192 is further confirmed increased resistance to doxorubicin-induced cytotoxicity in these cells.

193 Furthermore, TRAIL potentiated doxorubicin-induced decrease in beating rate and amplitu

194 Mechanistically, doxorubicin-induced DNA damage in c-kit(+) cells resulte

195 ebrafish cardiac architecture in response to doxorubicin-induced injury and repair.

196 ments and protected mice from cisplatin- and doxorubicin-induced nephrotoxic injury.

197 d with p53-mutant tumors protected them from doxorubicin-induced neutropenia and anemia while retaini

198 redistribution of NuMA upon actinomycin D or doxorubicin-induced nucleolar stress.

199 f HSP90beta, where it may play a role in the doxorubicin-induced resistance of ES.

200 rogen repression of LNCaP or C4-2 cells from doxorubicin induction of gammaH2ax, a DNA damage marker.

201 ied at baseline, 1 month, and 2 months after doxorubicin initiation.

202 Doxorubicin-injected fish developed ventricular diastoli

203 ount of the chemotherapeutic drug (liposomal doxorubicin) into the brain.

204 Doxorubicin is a highly effective anticancer agent but c

205 Doxorubicin is a highly efficacious and well-established

206 Although doxorubicin is a known substrate for efflux transporters

207 Doxorubicin is encapsulated within the hydrophilic core

208 mal formulation of the chemotherapeutic drug doxorubicin, is FDA-approved for multiple indications.

209 levels can sensitize breast cancer cells to doxorubicin leading to apoptotic cell death.

210 Doxorubicin leakage can be described by first order rate

211 is to quantitatively assess the kinetics of doxorubicin leakage from Doxil liposomes.

212 droplets containing a paramagnetic salt and doxorubicin (leukemia drug) are magnetically actuated an

213 In addition, honokiol and doxorubicin loaded in MPEG-PCL nanoparticles could effic

214 ng a glioma mouse model, we demonstrate that doxorubicin-loaded (D)CDX-RBCNPs have superior therapeut

215 Additionally, treatments with doxorubicin-loaded BLNs displaying Affibody ligands exhi

216 Herein, a radionuclide-(64) Cu-labeled doxorubicin-loaded polydopamine (PDA)-gadolinium-metallo

217 We aimed to identify key RBPs involved in doxorubicin-mediated heart failure and to elucidate thei

218 oxidase-11, MP-11; CdSe/ZnS quantum dots; or doxorubicin-modified dextran, DOX-D) is described.

219 for cellular metabolism show in response to doxorubicin, NAD(P)H mean fluorescence lifetime (taum) a

220 Neither doxorubicin nor mitomycin C potentiated the cytotoxic ef

221 of BCL-2 inhibitor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic

222 uced DNA double-strand breaks in response to doxorubicin or etoposide.

223 diated downregulation of MDM2 in response to doxorubicin or nutlin-3 results in continuing and consti

224 overactivation, mice were given carboplatin, doxorubicin, or cyclophosphamide and were cotreated with

225 were dosed with liposomal doxorubicin, free doxorubicin, or media control to assess drug distributio

226 l lines, and (2) cell population response to doxorubicin over 30 days.

227 ough distinct in their mechanisms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and r

228 y with saline (n = 5) or with 5 or 7.5 mg of doxorubicin per kilogram (n = 5 each) and underwent dyna

229 that a three compartment model can describe doxorubicin pharmacokinetics, and pharmacokinetic parame

230 oxorubicin disposition studies revealed that doxorubicin plasma area under the curve was significantl

231 She received neoadjuvant chemotherapy with doxorubicin plus cyclophosphamide, followed by paclitaxe

232 ndomly assigned to a treatment group (317 to doxorubicin plus evofosfamide and 323 to doxorubicin alo

233 ng anaemia (150 [48%] of 313 patients in the doxorubicin plus evofosfamide group vs 65 [21%] of 308 i

234 vival of 18.4 months (95% CI 15.6-22.1) with doxorubicin plus evofosfamide versus 19.0 months (16.2-2

235 nsider three processes: dissolution of solid doxorubicin, protonation/deprotonation of soluble doxoru

236 We found dose-dependent doxorubicin-related increased risks of all solid cancers

237 Doxorubicin resistance conferred by loss of the SMARCB1

238 monstrate that the miR-221 zipper attenuates doxorubicin resistance with higher efficiency than anti-

239 cal autophagy inhibitor, PS-1001, to reverse doxorubicin resistance.

240 In a CIVO-identified subset of doxorubicin-resistant tumors, PS-1001 resulted in enhanc

241 ts of mice with MN-anti-miR-10b and low-dose doxorubicin resulted in complete regression of pre-exist

242 Doxorubicin selectively and dose-dependently increased t

243 mib-conjugated telodendrimers, together with doxorubicin, self-assembled into monodispersed micelles

244 INTERPRETATION: Doxorubicin should remain the standard first-line treatm

245 In addition, doxorubicin significantly inhibited XBP1 activation in C

246 us doxorubicin and 4.1 months (2.8-5.4) with doxorubicin (stratified hazard ratio [HR] 0.67; 0.44-1.0

247 l line (SUM-149PT) treated for 12 hours with doxorubicin, the mean percent errors of the best-fit and

248 scribe how the concentration and duration of doxorubicin therapy shape subsequent cell population dyn

249 ting the efficacy of combining selinexor and doxorubicin therapy to improve the outcome of ATC patien

250 In breast cancer patients undergoing doxorubicin therapy, early alterations in arginine-NO me

251 is able to identify both free and liposomal doxorubicin throughout the spheroid after just 12 hours

252 IN-6 beta-cells revealed that treatment with doxorubicin to directly induce DNA damage mimicked our o

253 argeted PEGylated liposome that encapsulates doxorubicin to facilitate its delivery to HER2-overexpre

254 ox-LPs) to selectively recognize and deliver doxorubicin to MM cells and simultaneously neutralize IC

255 noparticles for codelivery of bortezomib and doxorubicin to synchronize their pharmacokinetic profile

256 were associated with significantly impaired doxorubicin transport in vitro.

257 phorylated at Thr(507) (which accumulates in doxorubicin-treated cardiomyocytes) displays decreased C

258 Doxorubicin treatment in a xenograft model using A549 lu

259 LV SUV showed a progressive increase during doxorubicin treatment that persisted at follow-up.

260 toxic capacity were increased by F8-TNF plus doxorubicin treatment, arguing that cognate CD8(+) T cel

261 cantly increased mitochondrial ROS following doxorubicin treatment, showing the critical role of TRPM

262 that can be generally boosted by F8-TNF and doxorubicin treatment.

263 with experimental imaging data, to describe doxorubicin uptake and predict subsequent population dyn

264 microscopy experiments that characterize (1) doxorubicin uptake dynamics in a panel of TNBC cell line

265 ortholog Oatp1a4 were capable of significant doxorubicin uptake.

266 ks did not differ between those who received doxorubicin versus those who received gemcitabine and do

267 of a recombinant polypeptide conjugated with doxorubicin via an acid-labile hydrazone linker as a fun

268 Qki5 strongly attenuates the toxic effect of doxorubicin via regulating a set of circular RNAs.

269 395 patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) +/- ritu

270 followed by four cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemothe

271 ontaining regimens, namely cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), nowaday

272 esized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could

273 reated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in the

274 f bortezomib to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) on out

275 with either rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) or int

276 first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) or R-C

277 to compare rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)-14 (ei

278 of RT after rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).

279 uximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).

280 py (six-to-eight cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone [CHOP] or eight

281 therapy (14 rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone and 6 cyclophos

282 ith R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) and R-FM (ritu

283 ed with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) at the British

284 tine, and prednisone and 6 cyclophosphamide, doxorubicin, vincristine, and prednisone) for DLBCL.

285 ont-line chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone, with or withou

286 reated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.

287 ression-free survival over cyclophosphamide, doxorubicin, vincristine, and prednisone.

288 ne (R-ACVBP) or rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP14) inductio

289 s collected under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy

290 ecurrences were treated with three cycles of doxorubicin/vincristine/prednisone/cyclophosphamide (AV-

291 t efflux activity on the cytotoxic effect of doxorubicin was investigated by counting viable cell num

292 The liver-to-plasma ratio of doxorubicin was significantly decreased (2.3-fold) in Sl

293 sion of the RBP QKI (Quaking) in response to doxorubicin was strongly downregulated in rodent cardiom

294 DNA-damaging stimuli such as treatment with doxorubicin, was also significantly inhibited by FKBP12.

295 nticancer effects of combined bortezomib and doxorubicin were observed in vitro against both multiple

296 lass near-infrared fluorescent dye, Cy7, and doxorubicin were synthetically attached to polyfluorinat

297 d apoptosis and atrophy after treatment with doxorubicin, whereas lentiviral mediated overexpression

298 cardiomyocyte differentiation in response to doxorubicin, whereas stabilization of p53 was sufficient

299 ncer cells improved the therapeutic index of doxorubicin with C646 cotreatment.

300 t of 170 breast cancer patients treated with doxorubicin with or without trastuzumab.