ライフサイエンスコーパス: CDDP

1 CDDP (0.1-10 microg/ml) sensitized non-MART-1(27-35) pep

2 CDDP also induced apoptosis, as evidenced by induction o

3 CDDP and pyridoxine exhibited hyperadditive therapeutic

4 CDDP delivered with nanoparticles (NPs) exhibited signif

5 CDDP efficacy was enhanced by trastuzumab in cells expre

6 CDDP is initially sequestered in subcellular organelles

7 CDDP was first conjugated to polyglutamic acid (PGA) to

8 CDDP-exposed S cells experienced enhanced antioxidant pr

9 CDDP-induced activation of caspase-3-like proteases was

10 CDDP-induced PARC down-regulation is reversible by inhib

11 -resistant ovarian cancer cells than in 2008 CDDP-sensitive cells.

12 nd phospho-AKT levels are greater in 2008CI3 CDDP-resistant ovarian cancer cells than in 2008 CDDP-se

13 1 protein, and we determined that the SKOV-3 CDDP/R cell line is significantly more proficient at DNA

14 arcinoma cell lines, MCF-7 CDDP/R and SKOV-3 CDDP/R, we found increased levels of BRCA1 protein, and

15 overning 5-fluorouracil and cisplatin (5FU + CDDP) resistance remain elusive due to the paucity of ph

16 Here, we establish 5FU + CDDP resistant intestinal subtype GC patient-derived org

17 ant CVX-241 also showed promise in the EMT-6/CDDP murine breast cancer model, with or without an immu

18 east and ovarian carcinoma cell lines, MCF-7 CDDP/R and SKOV-3 CDDP/R, we found increased levels of B

19 A CDDP adduct at the very 5'-end of the tail was also clea

20 In contrast, a CDDP adduct just adjacent to the expected cleavage point

21 We then showed that a CDDP loaded BPN formulation (CDDP-BPN), composed of a bl

22 We found that a CDDP-sensitive sub-clone S16 isolated through limited di

23 cells from G0-G1 into S phase, and abrogates CDDP resistance.

24 8 levels enable them to re-proliferate after CDDP removal.

25 Retention of activity against CDDP-resistant cell lines and a different spectrum of ac

26 The synergistic effect of polymet alongside CDDP demonstrates that polymet-CDDP NPs can activate the

27 These results indicate that Cd and CDDP have a strong and specific inhibitory effect on hyp

28 protein production were suppressed by Cd and CDDP in a dose-dependent manner with no apparent cell da

29 HIF-1 binding in a manner similar to Cd and CDDP, whereas zinc chloride suppressed Co-induced EPO pr

30 re, the effects of cadmium chloride (Cd) and CDDP in the Hep3B human hepatoma cell line, which up-reg

31 d resistance to the toxicities of copper and CDDP treatments.

32 ms of hCtr1-mediated transport of copper and CDDP.

33 as a 30-minute infusion daily for 5 days and CDDP was given either before TPT on day 1 or after TPT o

34 e CD95/Fas receptor established that Dox and CDDP treatment sensitizes cells to CD95/Fas killing.

35 ing DN caspase-8, were resistant to Dox- and CDDP-induced apoptosis.

36 esistant cells, GSN was highly expressed and CDDP failed to abolish the I-GSN-FLIP-Itch interaction,

37 t hypoxia promoted mitochondrial fission and CDDP resistance in ovarian cancer cells.

38 nduced ROS trigger mitochondrial fission and CDDP resistance through downregulation of p-Drp1 (Ser637

39 ion, resulting in reduced rates of Cu(I) and CDDP transport and increased resistance to the toxicitie

40 ximal transport rates (V(max)) for Cu(I) and CDDP, reduction of K(m) only for Cu(I) but not for CDDP

41 co-load polymet, a polymeric metformin, and CDDP into the same nanoparticle for successful treatment

42 cally, alterations in apoptotic pathways and CDDP metabolism contributed to KiSS1-associated chemothe

43 CDDP-complete responders of CC patients and CDDP-insensitive CC cell lines with CDDP-sensitive group

44 ts confirmed the synergy between polymet and CDDP.

45 tains putative caspase-3 cleavage sites, and CDDP is known to induce the activation of caspases and c

46 To examine the interaction of TPT and CDDP in vitro, human A549 lung cancer cells were exposed

47 hibition of caspases specifically attenuates CDDP/MMR protein-dependent cytotoxicity, suggesting that

48 tic investigations revealed that AXL blocked CDDP-induced activation of endogenous p73beta (TP73), re

49 mminedichloroplatinum (II) (CDDP) or a bulky CDDP derivative was placed within or beyond the region p

50 inuclear region that could be dissociated by CDDP in sensitive cells, thereby inducing FLIP ubiquitin

51 caspase activation and apoptosis induced by CDDP.

52 ubclinical renal tubular toxicity induced by CDDP.

53 ic proteins, if and how PARC is regulated by CDDP in OVCA are unknown.

54 five groups of animals: control, DMSO, CDDP, CDDP + DMFM, and DMFM.

55 itant with inhibition of removal of cellular CDDP-induced DNA interstrand cross-links, which are pres

56 Cisplatin (CDDP) induces senescence characterized by senescence-ass

57 G3361/CP cells, a cisplatin (CDDP)-resistant subclone of the human melanoma cell line

58 0) after neoadjuvant single-agent cisplatin (CDDP) versus doxorubicin-cyclophosphamide (AC) in BRCA c

59 resistant to the alkylating agent cisplatin (CDDP), while trastuzumab coexposure completely reversed

60 Although cisplatin (CDDP) has been used as a first-line therapy in patients

61 response to doxorubicin (Dox) and cisplatin (CDDP) in S-type neuroblastoma cells.

62 s were treated with BCD, DOX, and cisplatin (CDDP).

63 um-based antitumor agents such as cisplatin (CDDP); however, the mechanisms that regulate hCtr1-media

64 adiotherapy (RT) with concomitant cisplatin (CDDP) versus concomitant cetuximab (CTX) as first-line t

65 ance to the chemotherapeutic drug cisplatin (CDDP) by suppression of CDDP-induced apoptosis.

66 cleoside synergistically enhanced cisplatin (CDDP)-induced cytotoxicity in vitro, and that the synerg

67 cis-diaminedichloroplatinum (II) cisplatin (CDDP) sensitizes MART-1/HLA A2.1(+) melanoma and melanom

68 CD40L in combination with 4 mg/kg cisplatin (CDDP) was increased over the effect of CDDP alone.

69 gimen consisted of two courses of cisplatin (CDDP) and doxorubicin (DOX) in addition to the usual pre

70 Clinically, combined therapy of cisplatin (CDDP) and metformin is an effective treatment for non-sm

71 The poor solubility of cisplatin (CDDP) often presents a major obstacle in the formulation

72 capacity in targeted delivery of Cisplatin (CDDP), a drug having physicochemical properties differen

73 AM) to the three-agent regimen of cisplatin (CDDP), dacarbazine (DTIC), and carmustine (BCNU) signifi

74 inoma (HNSCC), the integration of cisplatin (CDDP)-based therapy has led to improvements in local and

75 to potentiate the cytotoxicity of cisplatin (CDDP).

76 In contrast, A6 or cisplatin (CDDP) alone suppressed subcutaneous tumor growth in vivo

77 induction plus concurrent FU plus cisplatin (CDDP), but did not significantly impact disease-free sur

78 ble-strand breaks and potentiated cisplatin (CDDP)-induced DNA damage and death.

79 drial dynamics and sensitivity to cisplatin (CDDP) was examined in ovarian cancer cells.

80 Resistance to cisplatin (CDDP)-based therapy is a major hurdle to the successful

81 izes certain cancer cell types to cisplatin (CDDP).

82 gefitinib (250 or 500 mg), weekly cisplatin (CDDP; 30 mg/m2), and once-daily RT (cohort II).

83 eproductive system cancers, while cisplatin (CDDP) resistance is the one of main reasons for the leth

84 HIPEC with cisplatin (CDDP) 75 mg/m(2) for 60 minutes at 41.5 degrees C was ad

85 Combinatorial treatment with cisplatin (CDDP) and temozolomide (TMZ) induces an adaptive downreg

86 o cadmium and cancer therapy with cisplatin (CDDP) can induce anemia in patients owing to the insuffi

87 glycol (PEG) and are loaded with cisplatin (CDDP) could be delivered across both the blood-tumor and

88 potecan (TPT) in combination with cisplatin (CDDP) in minimally pretreated adults with solid tumors.

89 that treating cultured cells with cisplatin (CDDP) up-regulated the expression of glutathione (GSH) a

90 ients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses.

91 rt, hypoxia, and ototoxins (e.g., cisplatin, CDDP), the role of calpain inhibitors under these condit

92 is-diammine-dichloroplatinum(II) (cisplatin, CDDP).

93 s cis-diaminedichloroplatinum II (cisplatin; CDDP).

94 In this study, we simultaneously compared CDDP-incomplete responders with CDDP-complete responders

95 cellular transport of melanosomes containing CDDP.

96 ce (KSR-/- MEF) is associated with decreased CDDP-induced ERK activation and increased resistance to

97 that p53 is not a mediator of MMR-dependent, CDDP-induced death.

98 lear understanding of MMR protein-dependent, CDDP-induced cell death is critical.

99 We developed CDDP-resistant A549 (A549/DDP) cells through prolonged i

100 ent cisplatin (cis-diamminedichloroplatinum, CDDP) is associated with changes in multiple signal tran

101 or by cis-platinum (II) diamine-dichloride (CDDP, or cisplatin), a cancer chemotherapy drug which pr

102 olves five groups of animals: control, DMSO, CDDP, CDDP + DMFM, and DMFM.

103 g/kg) such that it matched that of high-dose CDDP alone.

104 in U87MG.DeltaEGFR cells prior to and during CDDP treatment, whereas it decreased considerably in CDD

105 ly assigned in a 1:1 ratio to receive either CDDP 40 mg/m(2) once per week or CTX 400 mg/m(2) as load

106 026 (specific PRKDC inhibitor) could enhance CDDP sensitivity in vitro and in vivo, which was mediate

107 ually as effective as antisense and enhanced CDDP-vinorelbine in lung cancer xenografts.

108 GSN silencing also facilitated CDDP-induced apoptosis in chemoresistant cells.

109 novel supramolecular nanodrug LEE011-FFERGD/CDDP, which was validated in an OSCC orthotopic mouse mo

110 esulted in enhanced ERK activation following CDDP exposure and increased sensitivity to CDDP.

111 linked to changes in cell survival following CDDP treatment.

112 reduction of K(m) only for Cu(I) but not for CDDP was observed.

113 regimen, in particular in unfit patients for CDDP.At second-line, selective patients may benefit from

114 es higher than those reported previously for CDDP alone, or rhuMAb HER2 alone.

115 er (hCtr) 1, which is also a transporter for CDDP.

116 atinum (II), we have successfully formulated CDDP NPs with a controllable size (in the range of 12-75

117 n showed that a CDDP loaded BPN formulation (CDDP-BPN), composed of a blend of polyaspartic acid (PAA

118 antly increased tumor accumulation over free CDDP and suppressed tumor growth through apoptosis in NS

119 ected both KSR+/+ and KSR-/- MEFs cells from CDDP-induced apoptosis.

120 oxicity profile reflected that expected from CDDP alone with the most common toxicities being cytopen

121 tion of auditory hair cells and neurons from CDDP-induced damage (10 and 6 micrograms/ml, respectivel

122 S and OS versus induction plus concurrent FU/CDDP, and it has borderline significance for CFS, CF, an

123 ically better for RT + FU/MMC versus RT + FU/CDDP (5-year DFS, 67.8% v 57.8%; P = .006; 5-year OS, 78

124 Furthermore, CDDP up-regulated FasR expression and FasL-mediated kill

125 ophin-deprivation and ototoxic stress (e.g., CDDP) have been shown to be different.

126 Gemcitabine/Cisplatin (Gem/CDDP) combination has demonstrated a clear survival adva

127 and could be an alternative to standard Gem/CDDP regimen, in particular in unfit patients for CDDP.A

128 ed in 13% of patients given CTX and 0% given CDDP (P = .05).

129 tion occurred in 34% given CTX and 53% given CDDP (difference not significant).

130 h disrupted p21 genes also exhibited greater CDDP and HN2-sensitivity than parental HCT-116 cells.

131 tively hyperactivated in a majority of human CDDP-resistant cancer cells of distinct histologic origi

132 ventional cis-diamminedichloroplatinum (II) (CDDP) or a bulky CDDP derivative was placed within or be

133 tic drugs, cis-diamminedichloroplatinum(II) (CDDP) and etoposide, elicited increased expression of DR

134 iated with cis-diamminedichloroplatinum(II) (CDDP) resistance, and by differential display analysis,

135 cisplatin (cis-diamminedichloroplatinum(II) (CDDP)) is widely used in the treatment of human cancers.

136 cis-Diamminedichloroplatinum(II) (CDDP), which is mostly referred to as cisplatin, is a wi

137 actions of cis-diamminedichloroplatinum(II) (CDDP).

138 cis-Diammine dichloroplatinium (II) (CDDP)-induced GSN down-regulation is associated with its

139 isplatin (cis-dichlorodiammine platinum(II) (CDDP)).

140 G (IgG), cis-diammine-dichloroplatinum (II) [CDDP], and vinorelbine was examined in cell culture and

141 cisplatin (cis-diamminedichloroplatinum(II), CDDP), a cancer chemotherapeutic drug utilized clinicall

142 isplatin (cis-diamminedichloroplatinum (II); CDDP) resistance in A549 lung cancer (LC) cells by utili

143 rated that IPO4 and CEBPD knockdown improved CDDP-induced cytotoxicity in vitro and in vivo.

144 atment, whereas it decreased considerably in CDDP-treated parental cells.

145 poptosis by PARC as a contributing factor in CDDP resistance in OVCA cells and Ca(2+)/calpain in PARC

146 and up-regulated the expression of c-Jun in CDDP-resistant cells.

147 d ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells.

148 Genetic suppression of KiSS1 in CDDP-sensitive cell lines rendered them CR, an observati

149 y contributed to the GRP78 protein levels in CDDP-induces senescence.

150 whereas depletion of JNK2, c-Jun, or MDR1 in CDDP-resistant cancer cells promoted apoptosis upon CDDP

151 ication of a required signaling mechanism in CDDP-induced, MMR protein-dependent cytotoxicity, which

152 sceptibility gene BRCA1 was overexpressed in CDDP-resistant MCF-7 cells.

153 ssion in human EACs and examined its role in CDDP resistance in human EAC cells.

154 metastasis, as well as adverse survival, in CDDP-resistant (CR) tumors compared with sensitive tumor

155 treatment or si-Drp1 transfection increased CDDP sensitivity of ovarian cancer cells under hypoxia.

156 lls abrogated cellular migration and induced CDDP sensitivity.

157 educing its protein half-life, and inhibited CDDP-induced levels of p-c-ABL(Y412) and p-p73beta(Y99).

158 g protein delta (CEBPD), while intriguingly, CDDP treatment strengthened the transcriptional activity

159 It has also been shown that many CDDP-resistant cell lines exhibit high levels of GCLC/GC

160 Remarkably, the PGC-1beta-mediated CDDP resistance was independent of the mitochondrial eff

161 1 plays a role in DNA damage repair-mediated CDDP resistance.

162 neurotrophin-withdrawal and hypoxia, but not CDDP damage-induced apoptosis being calpain-dependent.

163 The melanosomal accumulation of CDDP remarkably modulates melanogenesis through a pronou

164 (D65A) suppressed CDDP-induced apoptosis of CDDP-sensitive cells, whereas depletion of JNK2, c-Jun,

165 b HER2 were unaltered by coadministration of CDDP.

166 K activity represents a novel determinant of CDDP sensitivity of cancer cells.

167 creased the efficacy of a suboptimal dose of CDDP (2mg/kg) such that it matched that of high-dose CDD

168 atin (CDDP) was increased over the effect of CDDP alone.

169 ore, we hypothesize that co-encapsulation of CDDP and metformin will avoid the prominent toxicity of

170 sents a major obstacle in the formulation of CDDP in nanoparticles (NPs) by traditional methods.

171 ated the putative synergistic interaction of CDDP with pyridoxine in the treatment of an orthotopic m

172 Thus, a majority of CDDP-resistant cancer cells appear to develop a dependen

173 HNSCC, we utilized an experimental model of CDDP resistance in this disease.

174 inhibits nucleotide excision repair (NER) of CDDP-induced DNA intrastrand adducts.

175 ative property of Cu(I) transport but not of CDDP transport.

176 aining KCl and a highly soluble precursor of CDDP, cis-diaminedihydroplatinum (II), we have successfu

177 N (I-GSN) was prosurvival in the presence of CDDP through a FLICE-like inhibitory protein (FLIP)-Itch

178 cured from NSCLC by the combined regimen of CDDP plus pyridoxine became resistant against subcutaneo

179 eveal a new role of GSH in the regulation of CDDP sensitivity.

180 up-regulation of hCtr1 and sensitization of CDDP transport and cell killing.

181 The sequence of CDDP before TPT at doses of 50 and 0.75 mg/m2, respectiv

182 The sequence of CDDP before TPT induced significantly worse neutropenia

183 utic drug cisplatin (CDDP) by suppression of CDDP-induced apoptosis.

184 tformin will avoid the prominent toxicity of CDDP while maintaining the synergy between the regimens.

185 portant clinical implications for the use of CDDP in the treatment of those malignant gliomas express

186 f hCtr1 oligomerization induced by copper or CDDP, suggesting a distinct structural requirement betwe

187 Sequential dose escalation of TPT or CDDP resulted in three dosage permutation of TPT/CDDP (m

188 cytopenia resulted after the doses of TPT or CDDP were increased to greater than 0.75 and 50 mg/m2, r

189 otoxicity, which can be uncoupled from other CDDP response pathways, and defines a critical contribut

190 polyglutamic acid (PGA) to form anionic PGA-CDDP which was electrostatically complexed with the cati

191 more strikingly, the combination of A6 plus CDDP inhibited tumor growth by 92%.

192 atient population for which trastuzumab plus CDDP or taxol are extremely efficient without Her-2 over

193 met alongside CDDP demonstrates that polymet-CDDP NPs can activate the AMP-activated protein kinase a

194 rs reduced Bcl-XL expression and potentiated CDDP-induced apoptosis in U87MG.DeltaEGFR cells.

195 ancer were randomly assigned to preoperative CDDP (75 mg/m(2) every 3 weeks x 4 doses) or AC (doxorub

196 coexposure completely reversed HRG-promoted CDDP resistance.

197 her, our results establish that AXL promotes CDDP resistance in esophageal adenocarcinoma and argue t

198 The pure CDDP NPs were first stabilized for dispersion in an orga

199 s cisplatin (COLO-704(r)CDDP(1000), EFO-21(r)CDDP(2000), EFO-27(r)CDDP(2000)) or oxaliplatin (UKF-NB-

200 (r)CDDP(1000), EFO-21(r)CDDP(2000), EFO-27(r)CDDP(2000)) or oxaliplatin (UKF-NB-3(r)OXALI(2000)), hen

201 the anti-cancer drugs cisplatin (COLO-704(r)CDDP(1000), EFO-21(r)CDDP(2000), EFO-27(r)CDDP(2000)) or

202 Patients received CDDP (75 mg/m2) on days 1, 29, and 57.

203 Because mammalian cells remove CDDP-induced DNA adducts through the nucleotide excision

204 53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.

205 H levels in these transfected cells reversed CDDP sensitivity with concomitant reduction of hCtr1 exp

206 ated nanoparticles loaded with cisplatin (SQ-CDDP NP).

207 In cell culture, SQ-CDDP NP exhibited at least 10-fold greater cytotoxic pot

208 nal tumorigenesis, oral administration of SQ-CDDP NP curtailed spontaneous tumor formation and azoxym

209 Cytotoxic effects of SQ-CDDP NP were assessed in human colonic cells and in mous

210 Mechanistic investigations showed that SQ-CDDP NP stimulated ROS production, expression of heavy m

211 age-resistant c-Jun mutant (D65A) suppressed CDDP-induced apoptosis of CDDP-sensitive cells, whereas

212 ve developed a novel method for synthesizing CDDP NPs taking advantage of its poor solubility.

213 Here, we present evidence that CDDP promotes calpain-mediated PARC down-regulation, mit

214 marginal survival improvement suggests that CDDP resistance is an innate characteristic of HNSCC.

215 g AXL in nonoverexpressing cells doubled the CDDP IC(50) and increased cell survival three-fold, whil

216 ession of mitochondrial fission enhanced the CDDP sensitivity of hypoxic ovarian cancer cells.

217 ed levels of GCL/GSH are responsible for the CDDP resistance.

218 enal, and GI toxicities more frequent in the CDDP arm, and cutaneous toxicity and the need for nutrit

219 lude that eIF3a has an important role in the CDDP response and in NER activity of NPCs by suppressing

220 which were significantly upregulated in the CDDP-resistant cells.

221 cer, pretreatment with Mdivi-1 increased the CDDP sensitivity.

222 These CDDP-BPN were delivered from the systemic circulation in

223 Thus, CDDP precipitate serves as the major material for assemb

224 R proteins have been demonstrated to bind to CDDP-DNA adducts and initiate MMR protein-dependent cell

225 Sensitization of HCT-116/p21-/- cells to CDDP and HN2 was not limited to the HCT-116 cell backgro

226 equired to sensitize chemoresistant cells to CDDP in a p53-dependent manner, an effect enhanced by PA

227 t (C-GSN) sensitized chemoresistant cells to CDDP, intact GSN and its N-terminal fragment (N-GSN) att

228 R1 expression on the sensitivity of cells to CDDP-induced apoptosis.

229 stablished the sensitivity of these cells to CDDP-induced apoptosis.

230 chemical inhibitors sensitized the cells to CDDP-mediated apoptosis.

231 a different spectrum of activity compared to CDDP and also within different classes of polynuclear pl

232 A549 non-small-cell lung cancer cell line to CDDP is associated with the hetero- to homoplasmic shift

233 ntified that DNA-PKcs (PRKDC) was related to CDDP sensitivity after overlapping in CC sample tissues

234 ism underlying intrinsic tumor resistance to CDDP remains elusive.

235 n S16 cells increased cellular resistance to CDDP, NER activity and synthesis of the NER proteins XPA

236 d ERK activation and increased resistance to CDDP-induced apoptosis compared with wild-type MEFs (KSR

237 cells and that increases their resistance to CDDP-mediated apoptosis, implying novel regulatory funct

238 tumor cell lines sensitive and resistant to CDDP (cisplatin, cis-[Pt(NH(3))(2)Cl(2)]) is described a

239 ession also changed the cellular response to CDDP and UV treatment in other NPC cell lines.

240 lear factor kappaB activation in response to CDDP.

241 DC-mediated DNA damage repair in response to CDDP.

242 ted to be important in clinical responses to CDDP, a clear understanding of MMR protein-dependent, CD

243 gen in JNK2(-/-) mice were more sensitive to CDDP compared with those in JNK2(+/+) mice.

244 line resulted in an increased sensitivity to CDDP, a decreased proficiency of DNA repair, and an enha

245 y, thereby eliciting vascular sensitivity to CDDP-mediated toxicity.

246 g CDDP exposure and increased sensitivity to CDDP.

247 ion, thus resulting in cell sensitization to CDDP and TRAIL.

248 ing the GCLC cDNA conferred sensitization to CDDP through up-regulation of human copper transporter (

249 more sensitive than control transfectants to CDDP and another DNA crosslinking agent, nitrogen mustar

250 resulted in three dosage permutation of TPT/CDDP (mg/m2): 0.75/50, 1/50, and 0.75/75.

251 idate the biological mechanisms underpinning CDDP resistance in HNSCC, we utilized an experimental mo

252 sistant cancer cells promoted apoptosis upon CDDP treatment.

253 In vitro, CDDP and pyridoxine did not only cause synergistic killi

254 major ingredient of the DOPA-coated NPs was CDDP.

255 The dose schedule was CDDP 25 mg/m(2) given intravenously (IV) for 30 to 45 mi

256 or concurrent chemoradiotherapy with weekly CDDP.

257 rt, to lower TPT clearance and exposure when CDDP preceeds TPT, possibly due to subclinical renal tub

258 The pCR rate was 18% with CDDP and 26% with AC, yielding a risk ratio (RR) of 0.70

259 he risk of RCB 0 or 1 (RCB 0/1) was 33% with CDDP and 46% with AC (RR, 0.73; 90% CI, 0.50 to 1.1).

260 ose) polymerase upon treatment of cells with CDDP.

261 HER2 was unaffected by coadministration with CDDP.

262 tion between trastuzumab in combination with CDDP (paclitaxel or vincristine) was obtained in MCF-7/H

263 The use of rhuMAb HER2 in combination with CDDP in patients with HER2/neu-overexpressing metastatic

264 o to soluble human TRAIL in combination with CDDP or etoposide resulted in synergistic cell death tha

265 bitor) or targeting IPO4 in combination with CDDP.

266 of tumor-bearing animals when compared with CDDP or A6 alone.

267 determine whether pCR was >= 20% higher with CDDP than AC.

268 or RCB 0/1 is not significantly higher with CDDP than with AC in BRCA carriers with stage I-III HER2

269 ents and CDDP-insensitive CC cell lines with CDDP-sensitive group.

270 sly compared CDDP-incomplete responders with CDDP-complete responders of CC patients and CDDP-insensi

271 ystemic in vivo administration of TRAIL with CDDP synergistically suppressed both tumor formation and

272 dvanced malignant melanoma were treated with CDDP + DTIC + BCNU (CDB) with or without TAM.

273 NSCLC cells treated with CDDP plus pyridoxine in vitro elicited a protective anti

274 n-dependent cell death in cells treated with CDDP; however, the molecular events underlying this deat

275 n the resistance of tumors to treatment with CDDP and indicate that c-Jun is a molecular target for i

276 Treatment with CDDP and TMZ also remodels the innate immune microenviro

277 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via