ライフサイエンスコーパス: adriamycin

1 c and cardiomyopathic drug doxorubicin (Dox (adriamycin)).

2 p65 and in vitro resistance to doxorubicin (Adriamycin).

3 light) and DNA intercalators (oxaliplatin or adriamycin).

4 ndrial-mediated apoptosis in the presence of Adriamycin.

5 el association between Cas and resistance to Adriamycin.

6 rowth inhibitory and proapoptotic effects of Adriamycin.

7 ) (Cas) in resistance to the cytotoxic agent Adriamycin.

8 uction by MS275 alone or in combination with Adriamycin.

9 the HDAC inhibitor MS275 can be enhanced by Adriamycin.

10 A-MB-231 cell lines increases sensitivity to Adriamycin.

11 against the topoisomerase IIalpha inhibitor adriamycin.

12 g chemosensitivity of breast cancer cells to Adriamycin.

13 or are mildly repressed by either hypoxia or adriamycin.

14 have other resistance mechanisms selected by Adriamycin.

15 apoptosis induced by the DNA-damaging agent adriamycin.

16 us enhanced breast cancer cell resistance to Adriamycin.

17 activity of 5-fluorouridine, methotrexate or Adriamycin.

18 did not undergo G2 arrest in the presence of Adriamycin.

19 e) cells, using cytostatic concentrations of Adriamycin.

20 e, are repressed by p14ARF much more than by adriamycin.

21 n the IRF-1-infected cells are cultured with Adriamycin.

22 ed by treatment with the radiomimetic agent, adriamycin.

23 th p53 in response to the DNA-damaging agent adriamycin.

24 f transfected A9 cells treated with Taxol or Adriamycin.

25 challenging cells with the DNA-damaging drug adriamycin.

26 atment with gamma-irradiation, UV light, and adriamycin.

27 wild-type p53) but not after treatment with adriamycin.

28 bility to down-regulate BRCA1 in response to adriamycin.

29 duced BRCA1 protein levels after exposure to adriamycin.

30 2) arrest activated by ionizing radiation or adriamycin.

31 retinoic acid, versus DNA damage, caused by adriamycin.

32 a subset of chemotherapeutic agents, such as adriamycin.

33 and enhancing their sensitivity to VP-16 and ADRIAMYCIN:

34 P-16 (etoposide) was enhanced 18-fold and to Adriamycin 5-fold.

35 : cortisone acetate, vincristine, bleomycin, Adriamycin, 5-fluorouracil, cyclophosphamide, and etopos

36 , EPHB2, MX1 and WNT4) to protection against adriamycin (a DNA topoisomerase IIalpha inhibitor) using

37 ikely to have leukemia/lymphoma treated with adriamycin, a history of pneumonia before neutropenia, a

38 Adriamycin administration induced dramatically more albu

39 played minimal phenotypical changes prior to adriamycin administration.

40 protect cells against the DNA-damaging agent adriamycin (ADR) as a model for chemoresistance of SF/c-

41 Exposure of MCF10A cells to adriamycin (ADR) causes enhancement in the levels of RAD

42 hat exposure of MCF10A cells to cisplatin or adriamycin (ADR) induces recruitment of p14ARF into Rad6

43 Adriamycin (ADR) is a commonly used chemotherapeutic age

44 Adriamycin (ADR) is an anticancer agent that increases o

45 in activation and in glomerular podocytes in adriamycin (ADR) nephropathy, remnant kidney after 5/6 r

46 e injury, proteinuria, and renal fibrosis in adriamycin (ADR) nephropathy.

47 omoters was investigated in cells exposed to adriamycin (ADR) or ionizing radiation as well as in an

48 2-deoxy-D-glucose (2-DG) in combination with Adriamycin (ADR) or paclitaxel in nude mouse xenograft m

49 preincubated with HGF/SF and then exposed to Adriamycin (ADR), a DNA topoisomerase II inhibitor, exhi

50 rary for the compounds protecting cells from adriamycin (Adr), a series of small molecules was isolat

51 bunit p65/RelA by the chemotherapeutic agent adriamycin (ADR), but not NF-kappaB activation induced b

52 ucially controls disease in murine models of adriamycin (ADR)-induced focal and segmental glomerulosc

53 decreased podocyte number in the setting of Adriamycin (ADR)-induced nephropathy.

54 x pump for chemotherapeutic drugs, including Adriamycin (ADR).

55 maging agents such as ionizing radiation and adriamycin (ADR, a topoisomerase IIalpha inhibitor).

56 at protection against the DNA-damaging agent adriamycin (ADR; topoisomerase IIalpha inhibitor) requir

57 We hypothesized that adriamycin affects endothelial progenitor cells (EPCs),

58 1 as a key mediator of signaling by CD437 or adriamycin allows for delineation of pathways that, in t

59 nd mitochondrial apoptotic pathways, whereas Adriamycin alone activated only the mitochondrial pathwa

60 nd mitochondrial apoptotic pathways, whereas Adriamycin alone activated only the mitochondrial pathwa

61 significantly longer than rats treated with adriamycin alone.

62 on of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and marke

63 Adriamycin also markedly increased immunoreactive COX-2

64 Camptothecin and adriamycin also reduce the amount of chromatin-associate

65 of MDA-MB-453 human breast cancer cells with adriamycin (also known as doxorubicin, a DNA topoisomera

66 ce, which are susceptible to renal injury by Adriamycin, also increased podocyte COX-2 expression and

67 The clinical application of adriamycin, an exceptionally good chemotherapeutic agent

68 gM in the glomerulus after administration of adriamycin and attenuated the development of albuminuria

69 ypass arrest caused by the DNA-damaging drug adriamycin and become tetraploid.

70 ed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cell

71 Methotrexate, vincristine, adriamycin and cisplatin (M-VAC) chemotherapy has been t

72 Survivors of sequential treatment with Adriamycin and FUdR (MCF-7 A/F) release the most IL-8 an

73 Cells treated sequentially with Adriamycin and FUdR expressed a metastatic phenotype.

74 tosis signaling by diverse agents, including adriamycin and growth factors.

75 In this study, we show that adriamycin and mitomycin C, but not other DNA-damaging a

76 knockout mice, which were more sensitive to adriamycin and not protected by sildenafil.

77 Adriamycin and other DNA-damaging agents have been shown

78 ddition, we present evidence indicating that adriamycin and other DNA-damaging agents reduce BRCA2 mR

79 ffect is dependent on wild type p53 and that adriamycin and p53 mediate repression of the BRCA2 promo

80 lbuminuria were used in Sprague-Dawley rats: Adriamycin and passive Heymann nephritis (HN).

81 are more susceptible to glomerular injury by adriamycin and puromycin (PAN).

82 ng HER2/neu downregulation or treatment with Adriamycin and that Cerk is required for tumor cell surv

83 tency similar to that of the anticancer drug adriamycin and up to 1000 fold higher than that of the c

84 oma cells with the chemotherapeutic agents-, Adriamycin and/or 5-fluoro-2'-deoxyuridine (FUdR), induc

85 an p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole)

86 Examples include cisplatin, doxorubicin (adriamycin), and specific alkylating agents.

87 onse to injury by doxorubicin hydrochloride (Adriamycin), and we found that Myh9 podocyte-deleted mic

88 to neoadjuvant paclitaxel plus fluorouracil, adriamycin, and cyclophosphamide chemotherapy in both ER

89 amma- and UV irradiation, hydrogen peroxide, adriamycin, and cytokines.

90 fractionated cyclophosphamide, vincristine, adriamycin, and dexamethasone (hyper-CVAD) (4).

91 d hyper-CVAD (cyclophosphamide, vincristine, Adriamycin, and dexamethasone) and imatinib mesylate fol

92 sone/vincristine, bischloroethylnitrosourea, adriamycin, and dexamethasone) followed by HDT/ASCT; n =

93 (fractionated cyclophosphamide, vincristine, Adriamycin, and dexamethasone) or modified hyper-CVAD us

94 fractionated cyclophosphamide, vincristine, adriamycin, and dexamethasone), RCHOP+HDT/ASCR (rituxima

95 ylated anthracyclines, including daunomycin, adriamycin, and idarubicin, to build alternate disacchar

96 ed from breast cancer cell line MCF7 against Adriamycin, and overexpression of ABCG2 was thought to c

97 aviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to supp

98 CDK7i response was altered in adriamycin- and mitoxantrone-resistant cell lines demons

99 atments with CD437 or chemotherapeutic agent adriamycin, as well as serum deprivation of HBC cells, s

100 Adriamycin-associated nephropathy (AAN) remains poorly u

101 h) of human monocyte-derived macrophages to adriamycin at concentrations as low as 1 microM promotes

102 al patients underwent repeated imaging after adriamycin-based chemotherapy.

103 All patients received doxorubicin (Adriamycin), bleomycin, vinblastine, dacarbazine chemoth

104 For the 412 patients treated with adriamycin, bleomycin, vinblastine, and dacarbazine (ABV

105 modality treatment with four cycles of ABVD (adriamycin, bleomycin, vinblastine, and dacarbazine) and

106 ept, based on limited numbers and follow-up, adriamycin, bleomycin, vinblastine, and dacarbazine.

107 atients, all scanned at baseline and after 2 adriamycin-bleomycin-vinblastine-dacarbazine (ABVD) cour

108 argeting anticancer drugs, such as VP-16 and Adriamycin, but not cisplatin.

109 no evidence for recognition of intercalated adriamycin by MutSalpha as if it were an insertion misma

110 blasts, DNA damage induced by agents such as adriamycin, campthothecin, and ionizing radiation induce

111 raviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and cis-Platinum(II)diammine d

112 In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six se

113 When compared to adriamycin, cisplatin, and the anti-CSC agent salinomyci

114 ath in a p53-dependent manner in response to adriamycin compared to that conferred by controls.

115 treated with BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, procarbazine,

116 of escalated BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, procarbazine,

117 e dose) followed by combined bevacizumab and adriamycin/cyclophosphamide/paclitaxel chemotherapy in H

118 ts obtained before and 1 week into a 3-month adriamycin/cytoxan neoadjuvant chemotherapy regimen can

119 prior to a 1-h incubation with paclitaxel or Adriamycin decreased the ED50 for inhibition of colony f

120 Mice receiving Adriamycin developed renal injury with loss of podocytes

121 rfractionated cyclophosphamide, vincristine, adriamycin, dexamethasone) plus imatinib/dasatinib or id

122 ent of senescent KCs with DNA damaging agent adriamycin did not result in activation of latent p53 or

123 cancer cells with the chemotherapeutic drug adriamycin (doxorubicin) induces A2B in a p73-dependent

124 with neoadjuvant methotrexate, vinblastine, Adriamycin (doxorubicin), and cisplatin, the 3-year over

125 cancer patients treated with 5-fluorouracil, Adriamycin (doxorubicin), and cyclophosphamide and ovari

126 roteasomal p53 degradation, are inhibited in Adriamycin (doxorubicin)-resistant MCF-7 cells (MCF-7/ad

127 roteinuria induced by lipopolysaccharide and Adriamycin (doxorubicin).

128 used paired cell lines that are resistant to Adriamycin due to either expression of MRP1 or lack of G

129 s (ED50 = 3.7 x 10(-3) microg/mL compared to adriamycin, ED50 = 1.0 x 10(-2) microg/mL).

130 We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 bind

131 Cells acutely exposed to adriamycin exhibited an increase in p53 activity, a decl

132 In vitro, podocyte injury induced by adriamycin exposure in cultured podocytes increased TRPC

133 e-6-specific Lamin A cleavage in response to Adriamycin exposure.

134 egimen consisted of neoadjuvant doxorubicin (Adriamycin), followed by operation (BCT if sufficient cl

135 The adriamycin group was divided into minimal albumin excret

136 Doxorubicin (Dox, Adriamycin) has been widely used in breast cancer treatm

137 Also, in the presence of Adriamycin, HCT116-p21-/- cancer cells with a defective

138 generation and activation of caspase-9 with adriamycin in a hydroxyproline-dependent manner.

139 to 2 logs for paclitaxel and up to 1 log for Adriamycin in all three cell lines but had no effect on

140 s taxol and considerably more effective than adriamycin in induction of tumor cell apoptosis and enha

141 liorated the albuminuria that was induced by Adriamycin in the transgenic mice.

142 periments involving the drug (daunomycin and adriamycin) in water, the drug-DNA complexes, the comple

143 ng rats treated with the chemotherapy agent, adriamycin, in combination with vardenafil survived sign

144 Adriamycin, in contrast, caused dramatic changes at or n

145 ar pretreatment levels by 72 h; UV light and adriamycin induced a less rapid but more robust and prol

146 Administration of adriamycin induced rapid generation of RAGE ligands, and

147 Treatment with adriamycin induced Wnt and activated beta-catenin in mou

148 e, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor

149 itro findings were confirmed in doxorubicin (Adriamycin)-induced nephropathy.

150 usceptibility of a resistant mouse strain to adriamycin-induced (ADR-induced) focal segmental glomeru

151 In contrast, in animals subjected to either adriamycin-induced acute chemical injury or genetic dele

152 otecting MDA-MB-231 breast cancer cells from adriamycin-induced apoptosis, whereas two mutants of Sta

153 ression of Survivin protects BaF3 cells from Adriamycin-induced apoptosis, while dominant-negative (T

154 -3 tau or E2F1, but not E2F2 or E2F3, blocks adriamycin-induced apoptosis.

155 e mice by its inhibitor, U73122, exacerbated adriamycin-induced cardiac dysfunction.

156 7.7%), postpartum cardiomyopathy (4.4%), and adriamycin-induced cardiomyopathy (4.1%) had highest rat

157 receptor signaling in the protection against adriamycin-induced cardiotoxicity.

158 ng RNA silencing decreased TNFalpha-mediated Adriamycin-induced caspase activation and apoptosis, and

159 ering RNA silencing decreased MS275-mediated Adriamycin-induced caspase activation and apoptosis, thu

160 e RNA silencing decreased 5-aza-CdR-mediated Adriamycin-induced caspase activation and apoptosis, thu

161 increases Siva-1 protein levels and augments adriamycin-induced caspase-3 cleavage and apoptosis.

162 n redox cycling and ROS generation, mediates adriamycin-induced cell damage.

163 crucial role in protecting macrophages from adriamycin-induced cell injury.

164 is critical for Cas-mediated protection from Adriamycin-induced death.

165 SC58236 also reduced Adriamycin-induced foot process effacement in both the C

166 -3-3tau inducer, decreases p21 and abrogates adriamycin-induced G(1)/S arrest.

167 Second, we evaluated adriamycin-induced glomerulosclerosis in Jh mice, a stra

168 ling in transgenic mice and BALB/c mice with Adriamycin-induced glomerulosclerosis is associated with

169 ceptor-positive kidney ILC2s and ameliorated adriamycin-induced glomerulosclerosis.

170 cells, using three different strategies, on adriamycin-induced glomerulosclerosis.

171 In RARE-LacZ mice, Adriamycin-induced heavy albuminuria was associated with

172 ) did not alter the increased sensitivity to adriamycin-induced injury observed in mice overexpressin

173 F receptor-mediated cardioprotection against adriamycin-induced injury was evaluated by measuring cha

174 netic deletion of TP in these mice prevented adriamycin-induced injury, with attenuated albuminuria a

175 dicating that thiol oxidation is involved in adriamycin-induced macrophage death.

176 against GR or glutaredoxin (Grx) potentiated adriamycin-induced macrophage injury.

177 rs mediated cytoprotective signaling against adriamycin-induced mitochondrial injury and cardiomyocyt

178 the increased TRPC6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycem

179 Adriamycin-induced nephropathy increased TRPC6 mRNA and

180 the mTOR inhibitor rapamycin developed worse adriamycin-induced nephropathy than WT mice, consistent

181 dent mouse models, diabetic nephropathy, and adriamycin-induced nephropathy.

182 to measure kidney function in SCID mice with adriamycin-induced nephropathy.

183 s of superoxide and peroxyl radicals blocked adriamycin-induced oxidation of dichlorodihydrofluoresce

184 gene silencing of YAP in podocytes increases adriamycin-induced podocyte apoptosis.

185 In the adriamycin-induced proteinuria model, C3aR-deficient mic

186 of a high-fat diet were more susceptible to Adriamycin-induced proteinuria than were animals on stan

187 We have examined a model of adriamycin-induced proteinuria to determine the effect o

188 arboring podocyte-specific deletion of Klf4, adriamycin-induced proteinuria was substantially exacerb

189 f integrin alpha2beta1 significantly reduced adriamycin-induced proteinuria, glomerular injury, and c

190 e first to demonstrate that the mechanism of adriamycin-induced senescence is dependent on both funct

191 As a result, adriamycin-induced Siva-1 protein stabilization is atten

192 beta-catenin and aggravated albuminuria and adriamycin-induced suppression of nephrin expression, wh

193 These findings suggest a new mechanism for adriamycin-induced tissue injury whereby thiol oxidation

194 ocytes with 1,25-D3 dose dependently reduced adriamycin-induced TRPC6 expression.

195 Here, we show that adriamycin induces DNA damage and podocyte lysis in mice

196 he cardiotoxic anticancer agent doxorubicin (adriamycin) induces the phosphorylation of p300 in prima

197 ot kill adriamycin-resistant BC cells, while adriamycin inhibited SM-164-resistant BC cell growth, si

198 Adriamycin injections were used to challenge the mice, a

199 Using a zebrafish in vivo PAN and adriamycin injury models, we further demonstrated the ab

200 These data suggest that adriamycin interacts with the mismatch repair pathway th

201 Adriamycin is a widely used antitumor antibiotic, but it

202 f total and phospho-Ser15-p53 in response to Adriamycin is blocked by Survivin and enhanced by Surviv

203 IL by the combined treatments with MS275 and Adriamycin is mediated by Sp1 and suggest that transcrip

204 showing an altered telomere state induced by adriamycin is probably a causal factor leading to the se

205 etween EPCs and endothelial cells exposed to adriamycin, leading to the multiple rounds of exchange b

206 E2F-1 and low concentrations of etoposide or Adriamycin markedly sensitized melanoma cells to apoptot

207 the relationship between p53 and HDM2 in the adriamycin-mediated stabilization of p53 in NB.

208 n normal kidneys and in those from mice with Adriamycin nephropathy (AN).

209 sfunction, proteinuria, and kidney injury in adriamycin nephropathy by inhibiting Wnt/beta-catenin si

210 n enhanced sensitivity to the development of Adriamycin nephropathy was examined.

211 athy and focal segmental glomerulosclerosis (adriamycin nephropathy), we observed upregulation of MMP

212 In mice with Adriamycin nephropathy, a model of human FSGS, blocking

213 nistering IL-2/IL-2Ab complexes in mice with adriamycin nephropathy, a model of proteinuric kidney di

214 In Adriamycin nephropathy, injections with either IFN-alpha

215 r, Synpo (-/-) mice were more susceptible to Adriamycin nephropathy.

216 he susceptibility gene for doxorubicin (DOX; Adriamycin) nephropathy, a Mendelian form of selective p

217 , such as the nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role

218 he link between these processes in rats with adriamycin nephrosis.

219 important cause of loss of renal function in adriamycin nephrosis.

220 Adriamycin nephrotoxicity and subtotal nephrectomy (SNx)

221 docytes and attenuated glomerular disease in adriamycin nephrotoxicity, SNx, and diabetes.

222 We found that adriamycin, nogalamycin, and actinomycin D comprise a cl

223 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such chang

224 When combined with Adriamycin or etoposide, E2F-1 adenovirus therapy result

225 short-term exposure of MCF-7 cells to either Adriamycin or FUdR rapidly increases, in a dose-dependen

226 s indistinguishable following treatment with adriamycin or induction of p14ARF.

227 In vivo, AdMnSOD, BCNU, and Adriamycin or ionizing radiation inhibited tumor growth

228 p53-dependent gene expression in response to adriamycin or p14ARF, we found that most genes were regu

229 and integrin alpha2-null mice to injury with adriamycin or partial renal ablation.

230 The cytotoxic effects of Adriamycin or radiation, agents known to produce O(2)(*-

231 BCNU sensitized cells to the cytotoxicity of Adriamycin or radiation.

232 Macrophages treated with either adriamycin or the thiol oxidant diamide showed elevated

233 xposure of mice to CO followed by genotoxin (Adriamycin) or radiation-induced injury led to diminishe

234 rding to assigned groups with four cycles of adriamycin plus cyclophosphamide alone or followed by fo

235 ng melanoma B16 syngeneic tumor treated with Adriamycin plus DCs.

236 ized to receive rituximab, cyclophosphamide, adriamycin, prednisone, and either vincristine (R-CHOP)

237 ting parental cells in G2, 20 to 40 ng/mL of Adriamycin prevented cell death caused by Taxotere.

238 Also, Adriamycin prevented the effects of Taxotere in normal h

239 Treatment of MCF-7-hTERT cells with adriamycin produced an identical senescence response as

240 Finally, 20 ng/mL of Adriamycin protected normal FDC-P1 hematopoietic cells f

241 ministration of the anthracycline antibiotic adriamycin provokes severe podocyte stress and glomerulo

242 minemia in the puromycin aminonucleoside and adriamycin rat models of nephrotic syndrome.

243 se activation and apoptosis, thus conferring Adriamycin resistance.

244 se activation and apoptosis, thus conferring Adriamycin resistance.

245 owth arrest, and in multidrug-resistant MCF7/adriamycin-resistant (ADR) human breast carcinoma cells,

246 SM-164 did not kill adriamycin-resistant BC cells, while adriamycin inhibite

247 lycosylated form of ceramide, accumulates in adriamycin-resistant breast carcinoma cells, in vinblast

248 The goal was to selectively kill Adriamycin-resistant cancer cells with Docetaxel (Taxote

249 ies showed activity against solid tumors and Adriamycin-resistant leukemia.

250 In adriamycin-resistant MCF-7-AdrR cells, transfection of G

251 (Ab), on two human breast cancer cell lines: Adriamycin-resistant MCF-7/Adr and wild-type MCF-7/wt.

252 TRAIL induces apoptosis in Adriamycin-resistant MCF7 cells already expressing high

253 ulated with B16 melanoma, P388 leukemia, and Adriamycin-resistant P388.

254 doxorubicin micelles in Bcl-2 overexpressing adriamycin-resistant spheroids.

255 of this notion, p53 stabilization following adriamycin resulted in an inhibition of both p53 ubiquit

256 However, we found that exposure to adriamycin resulted in an overrepresentation of cytogene

257 K-MEL-2, were treated with drugs (etoposide, Adriamycin, roscovitine, cisplatin, 5-fluorouracil, or c

258 While adriamycin's ability to redox cycle via one-electron tra

259 taxel (Taxotere), while protecting parental (Adriamycin-sensitive) cells, using cytostatic concentrat

260 ith disturbance of this apoptotic pattern in Adriamycin, Shh and Nkx2.1 models.

261 atment of breast cancer cells with MS275 and Adriamycin significantly increases apoptotic cell death

262 nt of breast cancer cells with 5-aza-CdR and Adriamycin significantly increases apoptotic cell death

263 ent of breast cancer cells with TNFalpha and Adriamycin significantly increases cell death compared w

264 ion of RAGE-expressing murine podocytes with adriamycin stimulated AGE formation, and treatment with

265 a HeLa cells to anticancer agents, including Adriamycin, Taxol, or UVB resulted in a 4-5-fold increas

266 a few genes exhibit classical induction with adriamycin, the majority of the genes are unchanged or a

267 Whereas parental cells were protected by Adriamycin, the mitogen-activated protein/extracellular

268 Using Adriamycin to initiate p53-dependent apoptosis, we showe

269 d on defining the molecular events that link adriamycin to mismatch repair-dependent drug resistance

270 camptothecin (topoisomerase I inhibitor) or adriamycin (topoisomerase II inhibitor) were not equival

271 than WT mice, consistent with the fact that adriamycin toxicity is augmented by mTOR inhibition.

272 sed levels were similar to those observed in adriamycin-treated double TNF receptor-deficient mice.

273 ng of Nkx2.1 and Sox2 expression occurred in Adriamycin-treated embryos with defective foregut separa

274 failure of tracheo-oesophageal separation in Adriamycin-treated embryos, whereas active septation was

275 in vivo significantly reduced albuminuria in adriamycin-treated glomerulosclerotic mice.

276 ad minimal phenotype, lipopolysaccharide- or adriamycin-treated KLF15(-/-) mice had a significant inc

277 Furthermore, in Adriamycin-treated MCF7 cells, ectopic Survivin decrease

278 Infusion of EPCs to adriamycin-treated mice reduced plasma levels of interle

279 In contrast to wild-type animals, adriamycin-treated RAGE-null mice were significantly pro

280 in a transition of the cellular response to adriamycin treatment from replicative senescence to dela

281 substrate DNA was not covalently modified by adriamycin treatment in a way that prevents repair, and

282 e the molecular and cellular consequences of adriamycin treatment in breast tumor cells.

283 Microarray analysis revealed that adriamycin treatment induced the down-regulation of seve

284 out cells, in response to PUMA induction and adriamycin treatment.

285 produce more ROS both at baseline and after adriamycin treatment.

286 WT p53 and intact G(1) cell cycle arrest on Adriamycin treatment.

287 tch repair-dependent drug resistance because adriamycin, unlike drugs that covalently modify DNA, can

288 fficacy of brentuximab vedotin (BV) and AVD (adriamycin, vinblastine, and dacarbazine) followed by 30

289 LBCL patients who received cyclophosphamide, adriamycin, vincristine and prednisone (CHOP)-based chem

290 rease the response rate to cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) chemother

291 non-Hodgkin lymphoma (eg cyclo-phosphamide, adriamycin, vincristine, and prednisone) are ineffective

292 tant with cisplatin, and cross-resistance to Adriamycin was circumvented by replacing XY=en with 1,2-

293 nd the chemotherapeutic efficacy of Taxol or Adriamycin was examined in wt mice or mice with a mutati

294 ker (V2X) from 4 to 16 wk after injection of adriamycin, whereas a second group received no treatment

295 ted in Cas-overexpressing cells treated with Adriamycin, whereas expression of the proapoptotic prote

296 esult in inhibition of apoptosis by CD437 or adriamycin, whereas increased expression of CARP-1 cause

297 rapeutics such as cisplatin and doxorubicin (Adriamycin), which was detected in vitro in cell culture

298 Using a model of glomerular injury by adriamycin, which induces reactive oxygen species (ROS)

299 Moreover, unlike the DNA-damaging agent adriamycin, which induces strong phosphorylation of p53

300 In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and gene