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-induced activation of caspase-3-like proteases was

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

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

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

12 1 protein, and we determined that the SKOV-3 CDDP/R cell line is significantly more proficient at DNA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 ts confirmed the synergy between polymet and CDDP.

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

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

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

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

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

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

44 caspase activation and apoptosis induced by CDDP.

45 ubclinical renal tubular toxicity induced by CDDP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 to potentiate the cytotoxicity of cisplatin (CDDP).

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

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

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

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

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

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

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

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

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

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

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

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

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

79 cellular transport of melanosomes containing CDDP.

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

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

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

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

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

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

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

87 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

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

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

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

91 linked to changes in cell survival following CDDP treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 lls abrogated cellular migration and induced CDDP sensitivity.

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

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

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

136 1 plays a role in DNA damage repair-mediated CDDP resistance.

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

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

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

140 b HER2 were unaltered by coadministration of CDDP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 The sequence of CDDP before TPT induced significantly worse neutropenia

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

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

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

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

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

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

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

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

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

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

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

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

170 coexposure completely reversed HRG-promoted CDDP resistance.

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

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

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

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

175 53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 ism underlying intrinsic tumor resistance to CDDP remains elusive.

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

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

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

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

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

208 lear factor kappaB activation in response to CDDP.

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

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

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

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

213 g CDDP exposure and increased sensitivity to CDDP.

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

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

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

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

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

219 sistant cancer cells promoted apoptosis upon CDDP treatment.

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

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

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

223 or concurrent chemoradiotherapy with weekly CDDP.

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

225 ose) polymerase upon treatment of cells with CDDP.

226 HER2 was unaffected by coadministration with CDDP.

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

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

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

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

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

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

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

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

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

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