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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 ) (Cas) in resistance to the cytotoxic agent Adriamycin.
5 uction by MS275 alone or in combination with Adriamycin.
6 the HDAC inhibitor MS275 can be enhanced by Adriamycin.
7 A-MB-231 cell lines increases sensitivity to Adriamycin.
8 against the topoisomerase IIalpha inhibitor adriamycin.
9 g chemosensitivity of breast cancer cells to Adriamycin.
10 or are mildly repressed by either hypoxia or adriamycin.
11 have other resistance mechanisms selected by Adriamycin.
12 apoptosis induced by the DNA-damaging agent adriamycin.
13 us enhanced breast cancer cell resistance to Adriamycin.
14 activity of 5-fluorouridine, methotrexate or Adriamycin.
15 did not undergo G2 arrest in the presence of Adriamycin.
16 e) cells, using cytostatic concentrations of Adriamycin.
17 e, are repressed by p14ARF much more than by adriamycin.
18 n the IRF-1-infected cells are cultured with Adriamycin.
19 ed by treatment with the radiomimetic agent, adriamycin.
20 th p53 in response to the DNA-damaging agent adriamycin.
21 f transfected A9 cells treated with Taxol or Adriamycin.
22 challenging cells with the DNA-damaging drug adriamycin.
23 atment with gamma-irradiation, UV light, and adriamycin.
24 retinoic acid, versus DNA damage, caused by adriamycin.
25 wild-type p53) but not after treatment with adriamycin.
26 bility to down-regulate BRCA1 in response to adriamycin.
27 duced BRCA1 protein levels after exposure to adriamycin.
28 2) arrest activated by ionizing radiation or adriamycin.
29 uding ethidium, propidium, daunorubicin, and adriamycin.
30 a subset of chemotherapeutic agents, such as adriamycin.
31 ndrial-mediated apoptosis in the presence of Adriamycin.
32 el association between Cas and resistance to Adriamycin.
33 rowth inhibitory and proapoptotic effects of Adriamycin.
34 and enhancing their sensitivity to VP-16 and ADRIAMYCIN:
36 : cortisone acetate, vincristine, bleomycin, Adriamycin, 5-fluorouracil, cyclophosphamide, and etopos
37 , EPHB2, MX1 and WNT4) to protection against adriamycin (a DNA topoisomerase IIalpha inhibitor) using
38 hed lung adenomas were treated with Taxol or Adriamycin, a decrease in tumor volume of approximately
39 ikely to have leukemia/lymphoma treated with adriamycin, a history of pneumonia before neutropenia, a
42 protect cells against the DNA-damaging agent adriamycin (ADR) as a model for chemoresistance of SF/c-
44 hat exposure of MCF10A cells to cisplatin or adriamycin (ADR) induces recruitment of p14ARF into Rad6
48 omoters was investigated in cells exposed to adriamycin (ADR) or ionizing radiation as well as in an
49 2-deoxy-D-glucose (2-DG) in combination with Adriamycin (ADR) or paclitaxel in nude mouse xenograft m
50 preincubated with HGF/SF and then exposed to Adriamycin (ADR), a DNA topoisomerase II inhibitor, exhi
51 rary for the compounds protecting cells from adriamycin (Adr), a series of small molecules was isolat
54 maging agents such as ionizing radiation and adriamycin (ADR, a topoisomerase IIalpha inhibitor).
55 at protection against the DNA-damaging agent adriamycin (ADR; topoisomerase IIalpha inhibitor) requir
57 1 as a key mediator of signaling by CD437 or adriamycin allows for delineation of pathways that, in t
58 nd mitochondrial apoptotic pathways, whereas Adriamycin alone activated only the mitochondrial pathwa
59 nd mitochondrial apoptotic pathways, whereas Adriamycin alone activated only the mitochondrial pathwa
61 on of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and marke
64 of MDA-MB-453 human breast cancer cells with adriamycin (also known as doxorubicin, a DNA topoisomera
65 ce, which are susceptible to renal injury by Adriamycin, also increased podocyte COX-2 expression and
67 gM in the glomerulus after administration of adriamycin and attenuated the development of albuminuria
69 ed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cell
77 ddition, we present evidence indicating that adriamycin and other DNA-damaging agents reduce BRCA2 mR
78 ffect is dependent on wild type p53 and that adriamycin and p53 mediate repression of the BRCA2 promo
81 ng HER2/neu downregulation or treatment with Adriamycin and that Cerk is required for tumor cell surv
82 tency similar to that of the anticancer drug adriamycin and up to 1000 fold higher than that of the c
83 oma cells with the chemotherapeutic agents-, Adriamycin and/or 5-fluoro-2'-deoxyuridine (FUdR), induc
84 an p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole)
86 onse to injury by doxorubicin hydrochloride (Adriamycin), and we found that Myh9 podocyte-deleted mic
87 to neoadjuvant paclitaxel plus fluorouracil, adriamycin, and cyclophosphamide chemotherapy in both ER
90 d hyper-CVAD (cyclophosphamide, vincristine, Adriamycin, and dexamethasone) and imatinib mesylate fol
91 sone/vincristine, bischloroethylnitrosourea, adriamycin, and dexamethasone) followed by HDT/ASCT; n =
92 (fractionated cyclophosphamide, vincristine, Adriamycin, and dexamethasone) or modified hyper-CVAD us
93 fractionated cyclophosphamide, vincristine, adriamycin, and dexamethasone), RCHOP+HDT/ASCR (rituxima
94 ylated anthracyclines, including daunomycin, adriamycin, and idarubicin, to build alternate disacchar
95 ed from breast cancer cell line MCF7 against Adriamycin, and overexpression of ABCG2 was thought to c
96 aviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to supp
98 tly inhibit PCD as induced by either Co60 or adriamycin, and the dose-dependent nature of this effect
99 atments with CD437 or chemotherapeutic agent adriamycin, as well as serum deprivation of HBC cells, s
101 h) of human monocyte-derived macrophages to adriamycin at concentrations as low as 1 microM promotes
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
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
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
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
128 used paired cell lines that are resistant to Adriamycin due to either expression of MRP1 or lack of G
129 < 0.001) and were 28-fold more sensitive to adriamycin (EC(50), 0.44 +/- 0.01 versus 12.4 +/- 0.7 mi
135 egimen consisted of neoadjuvant doxorubicin (Adriamycin), followed by operation (BCT if sufficient cl
140 to 2 logs for paclitaxel and up to 1 log for Adriamycin in all three cell lines but had no effect on
141 s taxol and considerably more effective than adriamycin in induction of tumor cell apoptosis and enha
143 periments involving the drug (daunomycin and adriamycin) in water, the drug-DNA complexes, the comple
144 ng rats treated with the chemotherapy agent, adriamycin, in combination with vardenafil survived sign
146 ar pretreatment levels by 72 h; UV light and adriamycin induced a less rapid but more robust and prol
149 e, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor
151 usceptibility of a resistant mouse strain to adriamycin-induced (ADR-induced) focal segmental glomeru
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
156 7.7%), postpartum cardiomyopathy (4.4%), and adriamycin-induced cardiomyopathy (4.1%) had highest rat
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.
168 ling in transgenic mice and BALB/c mice with Adriamycin-induced glomerulosclerosis is associated with
171 ) did not alter the increased sensitivity to adriamycin-induced injury observed in mice overexpressin
172 F receptor-mediated cardioprotection against adriamycin-induced injury was evaluated by measuring cha
173 netic deletion of TP in these mice prevented adriamycin-induced injury, with attenuated albuminuria a
176 rs mediated cytoprotective signaling against adriamycin-induced mitochondrial injury and cardiomyocyt
177 the increased TRPC6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycem
179 the mTOR inhibitor rapamycin developed worse adriamycin-induced nephropathy than WT mice, consistent
182 s of superoxide and peroxyl radicals blocked adriamycin-induced oxidation of dichlorodihydrofluoresce
185 of a high-fat diet were more susceptible to Adriamycin-induced proteinuria than were animals on stan
187 arboring podocyte-specific deletion of Klf4, adriamycin-induced proteinuria was substantially exacerb
188 f integrin alpha2beta1 significantly reduced adriamycin-induced proteinuria, glomerular injury, and c
189 e first to demonstrate that the mechanism of adriamycin-induced senescence is dependent on both funct
191 beta-catenin and aggravated albuminuria and adriamycin-induced suppression of nephrin expression, wh
192 These findings suggest a new mechanism for adriamycin-induced tissue injury whereby thiol oxidation
195 he cardiotoxic anticancer agent doxorubicin (adriamycin) induces the phosphorylation of p300 in prima
199 f total and phospho-Ser15-p53 in response to Adriamycin is blocked by Survivin and enhanced by Surviv
200 IL by the combined treatments with MS275 and Adriamycin is mediated by Sp1 and suggest that transcrip
201 showing an altered telomere state induced by adriamycin is probably a causal factor leading to the se
202 etween EPCs and endothelial cells exposed to adriamycin, leading to the multiple rounds of exchange b
203 E2F-1 and low concentrations of etoposide or Adriamycin markedly sensitized melanoma cells to apoptot
206 sfunction, proteinuria, and kidney injury in adriamycin nephropathy by inhibiting Wnt/beta-catenin si
208 athy and focal segmental glomerulosclerosis (adriamycin nephropathy), we observed upregulation of MMP
210 nistering IL-2/IL-2Ab complexes in mice with adriamycin nephropathy, a model of proteinuric kidney di
212 he susceptibility gene for doxorubicin (DOX; Adriamycin) nephropathy, a Mendelian form of selective p
213 , such as the nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role
219 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such chang
221 short-term exposure of MCF-7 cells to either Adriamycin or FUdR rapidly increases, in a dose-dependen
224 p53-dependent gene expression in response to adriamycin or p14ARF, we found that most genes were regu
229 xposure of mice to CO followed by genotoxin (Adriamycin) or radiation-induced injury led to diminishe
231 rding to assigned groups with four cycles of adriamycin plus cyclophosphamide alone or followed by fo
233 ized to receive rituximab, cyclophosphamide, adriamycin, prednisone, and either vincristine (R-CHOP)
234 ting parental cells in G2, 20 to 40 ng/mL of Adriamycin prevented cell death caused by Taxotere.
238 ministration of the anthracycline antibiotic adriamycin provokes severe podocyte stress and glomerulo
240 competence to glycosylate ceramide conferred adriamycin resistance in MCF-7 breast cancer cells.
244 owth arrest, and in multidrug-resistant MCF7/adriamycin-resistant (ADR) human breast carcinoma cells,
245 lycosylated form of ceramide, accumulates in adriamycin-resistant breast carcinoma cells, in vinblast
249 (Ab), on two human breast cancer cell lines: Adriamycin-resistant MCF-7/Adr and wild-type MCF-7/wt.
254 of this notion, p53 stabilization following adriamycin resulted in an inhibition of both p53 ubiquit
256 K-MEL-2, were treated with drugs (etoposide, Adriamycin, roscovitine, cisplatin, 5-fluorouracil, or c
258 taxel (Taxotere), while protecting parental (Adriamycin-sensitive) cells, using cytostatic concentrat
260 atment of breast cancer cells with MS275 and Adriamycin significantly increases apoptotic cell death
261 nt of breast cancer cells with 5-aza-CdR and Adriamycin significantly increases apoptotic cell death
262 ent of breast cancer cells with TNFalpha and Adriamycin significantly increases cell death compared w
263 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
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 ad minimal phenotype, lipopolysaccharide- or adriamycin-treated KLF15(-/-) mice had a significant inc
279 in a transition of the cellular response to adriamycin treatment from replicative senescence to dela
280 substrate DNA was not covalently modified by adriamycin treatment in a way that prevents repair, and
286 ll killing effects of paclitaxel (Taxol) and Adriamycin, two chemotherapeutic agents commonly used in
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 non-Hodgkin lymphoma (eg cyclo-phosphamide, adriamycin, vincristine, and prednisone) are ineffective
291 tant with cisplatin, and cross-resistance to Adriamycin was circumvented by replacing XY=en with 1,2-
292 nd the chemotherapeutic efficacy of Taxol or Adriamycin was examined in wt mice or mice with a mutati
293 n of the effects of paclitaxel than those of Adriamycin, we determined the effects of preincubation o
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
300 In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and gene
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