ライフサイエンスコーパス: oxaliplatin

1 t of gemcitabine, capecitabine, cisplatin or oxaliplatin.

2 pretreatment sensitized HCT116-OxR cells to oxaliplatin.

3 ent with the clinically used anticancer drug oxaliplatin.

4 the neuropathic hypersensitivity induced by oxaliplatin.

5 axel and with beneficial effects extended to oxaliplatin.

6 ged a cumulative dose of 1,426 +/- 204 mg/m2 oxaliplatin.

7 tients receiving i.v. mangafodipir following oxaliplatin.

8 nts received an average of 880 +/- 239 mg/m2 oxaliplatin.

9 leucovorin and fluorouracil with or without oxaliplatin.

10 djuvant chemotherapy with 5-fluorouracil and oxaliplatin.

11 umour), and previous adjuvant treatment with oxaliplatin.

12 re examined in mice following treatment with oxaliplatin.

13 effect, especially when in combination with oxaliplatin.

14 ontrol arm, 1) or with (experimental arm, 2) oxaliplatin.

15 cancer, and previous adjuvant treatment with oxaliplatin.

16 of gemcitabine, capecitabine, cisplatin, or oxaliplatin.

17 in cancer patients requiring treatment with oxaliplatin.

18 raction with 5-fluorouracil, irinotecan, and oxaliplatin.

19 in PGE(2) synthesis, sensitized OXR cells to oxaliplatin.

20 ith 5-fluorouracil (3.1, 31, or 310 muM) and oxaliplatin (0.7 or 7 muM) or radiation (2 or 4.5 Gy).

21 ay GEMOX regimen (gemcitabine 1000 mg/m2 and oxaliplatin 100 mg/m2 Day 1, every 2 weeks), and 20 pati

22 (2) repeated every 2 weeks (regimen one), or oxaliplatin 130 mg/m(2) administered intravenously over

23 m(2) repeated every 2 weeks (regimen one) or oxaliplatin 130 mg/m(2) intravenously over 2 h and oral

24 were randomly assigned to receive XELOX, as oxaliplatin 130 mg/m(2) on day 1 and capecitabine 1,000

25 er 3 h on day 1) before BEP plus intravenous oxaliplatin (130 mg/m(2) over 3 h on day 10; two cycles)

26 d modified FOLFIRINOX treatment (85 mg/m2 of oxaliplatin, 180 mg/m2 of irinotecan hydrochloride, 400

27 mg/kg), the third irinotecan (80 mg/kg) plus oxaliplatin (5 mg/kg), and the fourth vehicle (0.9% NaCl

28 was given irinotecan (100 mg/kg), the second oxaliplatin (5 mg/kg), the third irinotecan (80 mg/kg) p

29 ILIV trial in which cancer patients received oxaliplatin, 5-fluorouracil and irinotecan via chronomod

30 0003594), in which different combinations of oxaliplatin, 5-fluorouracil, and irinotecan were investi

31 mg/m(2) twice daily on days 1-14 and 22-35), oxaliplatin (50 mg/m(2) on weeks 1, 2, 4, and 5), and ra

32 on-CRC = 37), Oxaliplatin (n = 10) (CRC), or Oxaliplatin + 5FU (n = 12) (CRC).

33 1000 mg/m intravenously over 100 minutes and oxaliplatin 80 mg/m intravenously over 2 hours, every 2

34 Chemotherapy consisted of oxaliplatin 85 mg/m(2) administered intravenously over 2

35 the discretion of the treating investigator, oxaliplatin 85 mg/m(2) in a 2-h infusion, bolus fluorour

36 EMOX (gemcitabine 1,000 mg/m(2) on day 1 and oxaliplatin 85 mg/m(2) infused on day 2 of a 2-week cycl

37 Chemotherapy consisted of oxaliplatin 85 mg/m(2) intravenously over 2 h and fluoro

38 llocated to receive either FOLFIRINOX alone (oxaliplatin 85 mg/m(2), irinotecan 180 mg/m(2), leucovor

39 2206 135 mg orally once per week or mFOLFOX (oxaliplatin, 85 mg/m2 intravenous, and fluorouracil, 240

40 Oxaliplatin, a commonly used chemotherapeutic agent, is

41 travenous calcium/magnesium before and after oxaliplatin, a placebo before and after, or calcium/magn

42 Oxaliplatin, a platinum-based chemotherapeutic drug, whi

43 tially respond to the chemotherapeutic agent oxaliplatin, acquired resistance to this treatment remai

44 The impact of oxaliplatin added to FU + LV on the time course of recur

45 nter trial to evaluate the benefit of FU and oxaliplatin administered as modified FOLFOX6 (mFOLFOX6;

46 No benefit was observed with the addition of oxaliplatin, administered as mFOLFOX6, versus infusional

47 y, nearly all patients acquire resistance to oxaliplatin after long-term use, limiting its therapeuti

48 Oxaliplatin also significantly reduced risk of death fro

49 Here we focus on oxaliplatin, an immunogenic chemotherapeutic agent that

50 We show that cisplatin and an oxaliplatin analogue can specifically bind to the hetero

51 26) or in combination with chemotherapy [C26 oxaliplatin and 5-fluorouracil (oxfu)] and to evaluate t

52 nd markedly enhances PDA cell sensitivity to oxaliplatin and 5-fluorouracil under physiologic low oxy

53 i synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi ther

54 are being offered adjuvant chemotherapy with oxaliplatin and a fluoropyrimidine.

55 oard meeting, and adjuvant chemotherapy with oxaliplatin and capecitabine was recommended.

56 gimens included in our analyses were: XELOX (oxaliplatin and capecitabine); leucovorin and fluorourac

57 two common platinum-based chemotherapeutics, oxaliplatin and carboplatin.

58 Oxaliplatin and dihydroartemesinin have contrasting phys

59 gainst DNA damage and cell death mediated by oxaliplatin and doxorubicin treatments.

60 ned to folinic acid and fluorouracil (FF) or oxaliplatin and FF (OFF).

61 survival, a significant interaction between oxaliplatin and fluoropyrimidine was recorded in the mul

62 e survival is increased with the addition of oxaliplatin and fluorouracil chemotherapy.

63 ultaneous delivery of two chemotherapeutics, oxaliplatin and gemcitabine monophosphate (GMP), at 30 w

64 g, fluorouracil, leucovorin, irinotecan, and oxaliplatin and gemcitabine plus nanoparticle albumin-bo

65 A strong synergistic therapeutic effect of oxaliplatin and GMP was observed in vitro against AsPc-1

66 in combination with FOLFIRINOX chemotherapy (oxaliplatin and irinotecan plus leucovorin and fluoroura

67 with poor prognosis, and were refractory to oxaliplatin and irinotecan.

68 effects were monitored for up to 8 cycles of oxaliplatin and mangafodipir.

69 Synergy between oxaliplatin and pyrolipid-induced PDT kills tumour cells

70 the lowest for irinotecan, intermediate for oxaliplatin and the largest for 5-fluorouracil.

71 ps who received capecitabine with or without oxaliplatin and those who received leucovorin and fluoro

72 XELOX) were pooled to examine the impact of oxaliplatin and tumor-specific factors on the time cours

73 , folinic acid [leucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nab-paclitaxel remain

74 , folinic acid [leucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nanoparticle albumin-b

75 mbination of 5-fluorouracil, leucovorin, and oxaliplatin), and IL-12, successfully stimulates central

76 ine; FOLFOX-4 (leucovorin, fluorouracil, and oxaliplatin); and modified FOLFOX-6 (mFOLFOX-6).

77 r after first-line therapy with bevacizumab, oxaliplatin, and a fluoropyrimidine.

78 th a first-line combination regimen of 5-FU, oxaliplatin, and bevacizumab (FOLFOX-bevacizumab), as co

79 perative cycles of fluorouracil, leucovorin, oxaliplatin, and docetaxel (FLOT) followed by surgery an

80 istische Onkologie-fluorouracil, leucovorin, oxaliplatin, and docetaxel) trial is a prospective, phas

81 chemotherapy with fluorouracil/folinic acid, oxaliplatin, and irinotecan (FOLFOXIRI) in a two-to-one

82 it from infusional fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab

83 chemotherapy with fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) showed superior

84 The combination of fluorouracil, oxaliplatin, and irinotecan plus bevacizumab (FOLFOXIRI-

85 all survival than both IROX [irinotecan plus oxaliplatin] and IFL [irinotecan and bolus fluorouracil

86 num-based drugs (cisplatin, carboplatin, and oxaliplatin) are widely used therapeutic agents for canc

87 Platinum-based chemotherapies, including oxaliplatin, are a mainstay in the management of solid t

88 in and its platinum analogs, carboplatin and oxaliplatin, are some of the most widely used cancer che

89 t that nanomedicine mimicking irinotecan and oxaliplatin as parts of FOLFIRINOX regimen may further i

90 as fluorouracil, leucovorin, irinotecan, and oxaliplatin as well as gemcitabine/nab-paclitaxel are ac

91 613 in combination with modified FOLFIRINOX (oxaliplatin at 65 mg/m(2), leucovorin at 400 mg/m(2), ir

92 Notably, CRLX101 was more effective than oxaliplatin at enhancing the efficacy of chemoradiothera

93 nt chemotherapy, 108 patients (60%) received oxaliplatin based regimen and 99 patients (55%) complete

94 The OS benefit of oxaliplatin-based adjuvant chemotherapy, increasing over

95 Oxaliplatin-based adjuvant therapy is the standard of ca

96 ation were randomly assigned (1:1) to either oxaliplatin-based chemotherapy (FOLFOX: leucovorin, fluo

97 the association of sinusoidal dilatation and oxaliplatin-based chemotherapy but not for estroprogesta

98 s of colorectal cancer patients treated with oxaliplatin-based chemotherapy.

99 ls that compared 6 months versus 3 months of oxaliplatin-based chemotherapy.

100 hree cycles of fluorouracil, leucovorin, and oxaliplatin before fluorouracil/oxaliplatin CRT (50.4 Gy

101 disease (PD1); and p2, during capecitabine + oxaliplatin + bevacizumab or another reintroduction trea

102 y of a subset of Pt(II) compounds, including oxaliplatin but not cisplatin, to induce cytotoxicity vi

103 fibers by light elicits pain behavior in the oxaliplatin but not the CCI model.

104 sistant clones exhibit cross-resistance with oxaliplatin but not with ionising radiation or 5-fluorur

105 ropathic pain evoked by the chemotherapeutic oxaliplatin, but not in the chronic constriction injury

106 NCE STATEMENT The first-line cytostatic drug oxaliplatin can cause acute peripheral pain and chronic

107 n (FOLFOX) every 2 weeks or capecitabine and oxaliplatin (CAPOX) in different doses and methods every

108 Among other substances, oxaliplatin causes CIPN in up to 80% of treated patients

109 We aimed to assess whether gemcitabine and oxaliplatin chemotherapy (GEMOX) would increase relapse-

110 s revealed specific morphological effects of oxaliplatin chemotherapy, radiotherapy, and photodynamic

111 acid [leucovorin calcium], fluorouracil, and oxaliplatin) chemotherapy with or without cetuximab (Nor

112 ropriately selected immunogenic drugs (e.g., oxaliplatin combined with cyclophosphamide for treatment

113 A fluoropyrimidine plus irinotecan or oxaliplatin, combined with bevacizumab (a monoclonal ant

114 ned, most of whom received fluorouracil- and oxaliplatin-containing chemotherapy regimens.

115 of patients with colorectal cancer receiving oxaliplatin-containing therapy.

116 covorin, and oxaliplatin before fluorouracil/oxaliplatin CRT (50.4 Gy) or to group B for consolidatio

117 0.33 percentage injected dose per gram), but oxaliplatin/cyclophosphamide treatment led to close to a

118 tically significant increase in signal after oxaliplatin/cyclophosphamide was also observed in the A9

119 nd A9F1) undergoing 2 types of chemotherapy: oxaliplatin/cyclophosphamide, shown to induce immunogeni

120 ive oxygen species (ROS), a key component of oxaliplatin cytotoxicity, was significantly increased by

121 ceiving the platinum-based chemotherapy drug oxaliplatin develop peripheral neurotoxicity.

122 Patients with stage II disease receiving oxaliplatin did not exhibit a significant reduction in r

123 ng of outcomes between treatment groups (ie, oxaliplatin did not simply postpone recurrence or death

124 this combinatorial approach and proxies for oxaliplatin-DNA damage, we observed no significant diffe

125 howed higher tumor mass Pt accumulation than oxaliplatin, due to its higher lipophilicity, with negli

126 cer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combination as em

127 Patients treated with oxaliplatin experienced significantly more grade 3 or 4

128 Inhibition of miR-181a-5p coupled with oxaliplatin exposure in pancreatic cell lines decreased

129 X (leucovorin, fluorouracil, irinotecan, and oxaliplatin; favorable comorbidity profile) or gemcitabi

130 lexes, including cisplatin, carboplatin, and oxaliplatin, finding that DMSO reacted with the complexe

131 e addition of cetuximab to standard adjuvant oxaliplatin, fluorouracil, and leucovorin chemotherapy (

132 e MOSAIC (Multicenter International Study of Oxaliplatin/Fluorouracil/Leucovorin in the Adjuvant Trea

133 fluorouracil, irinotecan hydrochloride, and oxaliplatin (FOLFIRINOX) versus gemcitabine alone, prese

134 (leucovorin), fluorouracil, irinotecan, and oxaliplatin (FOLFIRINOX), restrict their full utility in

135 5-fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX).

136 hs of adjuvant fluorouracil, leucovorin, and oxaliplatin (FOLFOX) every 2 weeks or capecitabine and o

137 d therapy with fluorouracil, leucovorin, and oxaliplatin (FOLFOX) versus a non-platinum-containing re

138 th combination leucovorin, fluorouracil, and oxaliplatin (FOLFOX)-based adjuvant chemotherapy is cont

139 es to standard fluorouracil, leucovorin, and oxaliplatin (FOLFOX)-based chemotherapy in patients with

140 ive infusional fluorouracil, leucovorin, and oxaliplatin (FOLFOX)/bevacizumab with selective rather t

141 ompared with those given 5-fluorouracil plus oxaliplatin (FOLFOX; cycle 1 mean grade nausea 1.1 [SD 1

142 cil plus leucovorin (LV5FU2) and LV5FU2 plus oxaliplatin (FOLFOX4) arms were 67.1% versus 71.7% (haza

143 treated with a fluorouracil, leucovorin, and oxaliplatin (FOLFOX4) regimen.

144 rinotecan+folinic acid] than to FOLFOX (5-FU+oxaliplatin+folinic acid), not only between isogenic tum

145 fluorouracil (FU) and oxaliplatin using the oxaliplatin, folinic acid, and FU (OFF) regimen.

146 Chemotherapy was FOLFOX (folinic acid and oxaliplatin followed by bolus and infused fluorouracil).

147 man serum, potassium iodide and doxorubicin/ oxaliplatin for both ex vivo and in vitro experiments.

148 y end point was improvement of 3-year DFS by oxaliplatin from 65% to 72% (hazard ratio [HR], 0.763).

149 However, Gemcitabine/Oxaliplatin (GEMOX) combination and Gemcitabine/Carbopla

150 OX [infusional fluorouracil, leucovorin, and oxaliplatin] had longer overall survival than both IROX

151 imidines and more recently combinations with oxaliplatin-has reduced the risk of tumor recurrence and

152 antly, two compounds, 14Ru and 18Ru, matched oxaliplatin IC50 (0.45 muM), the standard metallodrug us

153 y, concomitant fluorouracil, and concomitant oxaliplatin in groups A and B, respectively); 92% versus

154 ied to map the penetration and metabolism of oxaliplatin in hyperthermic intraperitoneal chemotherapy

155 nd FANCD2 monoubiquitinations are induced by oxaliplatin in parental HCT116 cells.

156 ar overall survival (OS) benefit of adjuvant oxaliplatin in stage II to III resected colon cancer.

157 polymer (NCP) core-shell nanoparticles carry oxaliplatin in the core and the photosensitizer pyropheo

158 covorin and fluorouracil plus irinotecan and oxaliplatin) in patients with locally advanced pancreati

159 combination with DNA damaging agents (MMC or oxaliplatin) in PDA cell lines that are either DNA repai

160 ium/magnesium did not substantially decrease oxaliplatin-induced acute neuropathy.

161 line (LPC) 18:1, LPC 16:0, and 9,10-EpOME in oxaliplatin-induced acute pain.

162 gnificantly altered in nervous tissue during oxaliplatin-induced acute pain.

163 ting signaling lipid pathways may ameliorate oxaliplatin-induced acute peripheral pain and the subseq

164 LPC-mediated lipid signaling is involved in oxaliplatin-induced acute peripheral pain.

165 shed OCT2 activity, significantly mitigating oxaliplatin-induced acute sensory neuropathy.

166 small molecule inhibitor, L-161,982 enhanced oxaliplatin-induced apoptosis in OXR cells.

167 rred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduced the e

168 an icilin-induced WDS (at 11.5 mg/kg ip), an oxaliplatin-induced cold allodynia (at 10-30 mug sc), an

169 inesterase inhibitor, prevented and reversed oxaliplatin-induced cold and mechanical allodynia as wel

170 In contrast, the levels of oxaliplatin-induced DNA damage were significantly lower

171 e pIC using oxotremorine completely reversed oxaliplatin-induced mechanical allodynia.

172 Oxaliplatin-induced mechanical hyperalgesia was reduced

173 ter compounds (9-12) showed that they reduce oxaliplatin-induced neuropathic pain by a mechanism invo

174 icin-induced neurogenic pain, and notably in oxaliplatin-induced neuropathic pain in mice.

175 e G-protein coupled receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice.

176 h 3 by different paradigms in a rat model of oxaliplatin-induced neuropathic pain, showed the better

177 enrolled 23 cancer patients with grade >/= 2 oxaliplatin-induced neuropathy in a phase II study, with

178 lipoyl-derivative 15 was also able to revert oxaliplatin-induced neuropathy in the mouse.

179 Given that the clinical course of oxaliplatin-induced neuropathy is not well defined, the

180 Acute oxaliplatin-induced neuropathy symptoms do not always co

181 nvolved in pain processing in a rat model of oxaliplatin-induced neuropathy using HRMAS (1)H-NMR spec

182 e profile being able to fully counteract the oxaliplatin-induced neuropathy.

183 cidic media, were tested in a mouse model of oxaliplatin-induced neuropathy.

184 sporter 2 (OCT2) in satellite glial cells in oxaliplatin-induced neurotoxicity, and demonstrate that

185 t using calcium/magnesium to protect against oxaliplatin-induced neurotoxicity.

186 drugs, the contribution of these proteins to oxaliplatin-induced peripheral neurotoxicity remains con

187 cking the antioxidant functionality, reduced oxaliplatin-induced toxicity in microglia cells, the mos

188 ng G2A may be a promising approach to reduce oxaliplatin-induced TRPV1-sensitization and the hyperexc

189 hemotherapy was modified FOLFOX6 (85 mg/m(2) oxaliplatin infusion over 2 h, 200 mg leucovorin, and 40

190 modified de Gramont chemotherapy; 85 mg/m(2) oxaliplatin infusion over 2 h, L-leucovorin 175 mg or D,

191 rable comorbidity profile; fluorouracil plus oxaliplatin, irinotecan, or nanoliposomal irinotecan sho

192 ly nausea for patients given irinotecan plus oxaliplatin (IROX) compared with those given 5-fluoroura

193 in germ cell, breast and lung malignancies, oxaliplatin is instead used almost exclusively to treat

194 The oxalate leaving group of oxaliplatin is not required for NPM1 redistribution.

195 The platinum-based chemotherapeutic agent, oxaliplatin, is used to treat advanced colorectal cancer

196 Rather, oxaliplatin kills cells by inducing ribosome biogenesis

197 , irinotecan plus cisplatin (IC), or FOLFOX (oxaliplatin, leucovorin, and bolus and infusional fluoro

198 modified FOLFIRINOX chemotherapy (comprising oxaliplatin, leucovorin, irinotecan, and fluorouracil) i

199 Intralipid has been shown to reduce nano-oxaliplatin-mediated toxicity while improving bioavailab

200 d 5-fluorouracil, leucovorin, irinotecan and oxaliplatin (mFOLFIRINOX) is the standard-of-care adjuva

201 ed fluorouracil, leucovorin, irinotecan, and oxaliplatin (mFOLFIRINOX) was evaluated in patients with

202 combination of leucovorin, fluorouracil, and oxaliplatin (mFOLFOX6) regimen or the combination of leu

203 ostaglandin E2 and the chemotherapeutic drug oxaliplatin, modeling the inherent mechanisms underlying

204 In FOXFIRE, FOLFOX chemotherapy was OxMdG (oxaliplatin modified de Gramont chemotherapy; 85 mg/m(2)

205 Melphalan (n = 69) (CRC = 32, non-CRC = 37), Oxaliplatin (n = 10) (CRC), or Oxaliplatin + 5FU (n = 12

206 5-fluorouracil, leucovorin, irinotecan, and oxaliplatin) offers survival benefits superior to that o

207 ders of magnitude higher than reference drug oxaliplatin on three human (HCT 116, SW480, and HT-29) a

208 juvant FOLFOX (fluorouracil, leucovorin, and oxaliplatin) on study N08CB (North Central Cancer Treatm

209 enium complexes as compared to cisplatin and oxaliplatin, on both cisplatin-sensitive and cisplatin r

210 patients received 130 mg/m(2) of intravenous oxaliplatin or 80 mg/m(2) of cisplatin on day 1, 850 mg/

211 on of adjuvant fluorouracil, leucovorin, and oxaliplatin or capecitabine and oxaliplatin therapy (3 v

212 cell lines displaying acquired resistance to oxaliplatin or cisplatin.

213 to infusional fluorouracil, leucovorin, and oxaliplatin or fluorouracil, leucovorin, and irinotecan

214 owth when compared to NCP particles carrying oxaliplatin or GMP alone.

215 treatment, including a fluoropyrimidine and oxaliplatin or irinotecan.

216 erapy (FOLFOX: leucovorin, fluorouracil, and oxaliplatin) or FOLFOX plus single treatment SIRT concur

217 es for CRC patients using 5FU + Oxaliplatin, Oxaliplatin, or Melphalan were 83.3%, 66.7%, and 60.9%,

218 622 patients with mCRC treated with bev plus oxaliplatin- or irinotecan-based chemotherapy, and corre

219 ffect of anticancer drugs doxorubicin (DOX), oxaliplatin (OX) as well as OX-loaded liposomes, develop

220 Adding oxaliplatin (Ox) to the lymphodepletion regimen activate

221 of the ICD-inducing chemotherapeutic agent, oxaliplatin (OX).

222 Modification of oxaliplatin (OXA) into a lipophilic Pt(IV) complex [Pt(D

223 Resistance to oxaliplatin (OXA) is a complex process affecting the out

224 Oxaliplatin (OXA) is a valuable and largely used cancer

225 Response rates for CRC patients using 5FU + Oxaliplatin, Oxaliplatin, or Melphalan were 83.3%, 66.7%

226 rugs cyclophosphamide, gemcitabine (GEM) and oxaliplatin (OXP) for 24 hours in vitro.

227 These data add to the existing evidence that oxaliplatin plus capecitabine or leucovorin and fluorour

228 platinum drugs, cisplatin, carboplatin, and oxaliplatin, prevail in the treatment of cancer, but new

229 was utilized to develop a novel platinum(IV) oxaliplatin prodrug and incorporate it into a three-drug

230 Oxaliplatin-specific IgE was determined in oxaliplatin-reactive patients (who underwent DPT regardl

231 and oxaliplatin-ST in the largest series of oxaliplatin-reactive patients reported to date (74 oxali

232 latin-reactive patients reported to date (74 oxaliplatin-reactive patients).

233 ely test whether calcium/magnesium decreases oxaliplatin-related neurotoxicity.

234 ains the distinct clinical implementation of oxaliplatin relative to cisplatin, and it might enable m

235 nticancer agents cisplatin, carboplatin, and oxaliplatin represent a spectacular translational scienc

236 To identify molecular targets of oxaliplatin resistance in colorectal cancer, we performe

237 sed damage repair, is a major determinant of oxaliplatin resistance in these cell lines.

238 e for the COX-2/PGE(2)/EP4 signaling axis in oxaliplatin resistance via regulation of oxidative stres

239 ing an isogenic HCT116 colon cancer model of oxaliplatin resistance, we further show that gammaH2AX a

240 r cells with innate or acquired cisplatin or oxaliplatin resistance.

241 aliplatin sensitivity in a cellular model of oxaliplatin resistance.

242 of cancer cell lines including those showing oxaliplatin-resistance.

243 examined how this pathway was affected in an oxaliplatin resistant colon cancer cell line.

244 ncy in seven oxaliplatin-sensitive and three oxaliplatin-resistant colorectal cancer cell lines.

245 nd FANCD2 are constitutively up-regulated in oxaliplatin-resistant HCT116 (HCT116-OxR) cells and that

246 PGE(2) levels were significantly elevated in oxaliplatin-resistant HT29 cells (OXR) compared to naive

247 erent colorectal cancer cell lines and their oxaliplatin-resistant subclones, promoted DNA single- an

248 application of the ATR inhibitor VE-822 and oxaliplatin resulted in strong synergistic effects in si

249 When compared to oxaliplatin, Rh-PPO displays ninefold higher potency at

250 eoplastic and biological agents (paclitaxel, oxaliplatin, rituximab, infliximab, irinotecan, and othe

251 ng DNA damage and repair efficiency in seven oxaliplatin-sensitive and three oxaliplatin-resistant co

252 lved in the response to DNA stress, restored oxaliplatin sensitivity in a cellular model of oxaliplat

253 model, combined administration of VE-822 and oxaliplatin significantly increased survival by promotin

254 Addition of oxaliplatin significantly reduced the risk of recurrence

255 les bearing active formats of irinotecan and oxaliplatin, SN38 and 1,2-diaminocyclohexane-platinum (I

256 Sensitivity for oxaliplatin-specific IgE (0.35 UI/l cutoff point) was 34

257 ols; consequently, quality data are shown on oxaliplatin-specific IgE and oxaliplatin-ST in the large

258 ve patients (who underwent DPT regardless of oxaliplatin-specific IgE results).

259 Oxaliplatin-specific IgE was determined in oxaliplatin-r

260 logy Criteria for Adverse Events scale or an oxaliplatin-specific neuropathy scale.

261 ta are shown on oxaliplatin-specific IgE and oxaliplatin-ST in the largest series of oxaliplatin-reac

262 In contrast to conventional cisplatin or oxaliplatin, the mechanism of action (MoA) of 5 is funda

263 rently randomized to FU + LV with or without oxaliplatin; the latter analyses supported time-dependen

264 covorin, and oxaliplatin or capecitabine and oxaliplatin therapy (3 v 6 months) was performed.

265 These analyses support the addition of oxaliplatin to fluoropyrimidine-based adjuvant therapy i

266 hown to be significantly more cytotoxic than oxaliplatin to HCT116 cells, triggering higher levels of

267 cts synergistically with EGFR inhibitors and oxaliplatin to inhibit cell proliferation and induce apo

268 6 trial investigates whether the addition of oxaliplatin to preoperative capecitabine-based chemoradi

269 The addition of oxaliplatin to preoperative capecitabine-based chemoradi

270 he potential of ATR inhibition combined with oxaliplatin to sensitize cells to chemotherapy as a ther

271 the sciatic nerve and dorsal root ganglia of oxaliplatin treated mice.

272 s modeled over 6 years post treatment in all oxaliplatin-treated patients and patients concurrently r

273 nist, methoctramine, within the pIC, in both oxaliplatin-treated rats and spared nerve injury rats.

274 ch was confirmed by Western blot analysis in oxaliplatin-treated rats and the spared nerve injury mod

275 a lower level of acetylcholine in the pIC of oxaliplatin-treated rats, which was significantly increa

276 cancer, allows CTL-dependent eradication of oxaliplatin-treated tumours.

277 Here we investigated the effects of acute oxaliplatin treatment in a murine model, showing that ma

278 16:0 were significantly increased 24 h after oxaliplatin treatment in sciatic nerve, DRGs, or spinal

279 Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental

280 In wild-type mice, oxaliplatin treatment produced cold allodynia that could

281 Our analysis revealed that oxaliplatin treatment specifically increases one S1P spe

282 in almost 90% of patients immediately after oxaliplatin treatment, which is poorly understood mechan

283 lipids in nervous system tissues 24 h after oxaliplatin treatment, which revealed a crucial role of

284 decreased mechanical hypersensitivity after oxaliplatin treatment.

285 velop mechanical hypersensitivity 24 h after oxaliplatin treatment.

286 Exposure to oxaliplatin triggers alterations in peripheral neuropath

287 EFO-21(r)CDDP(2000), EFO-27(r)CDDP(2000)) or oxaliplatin (UKF-NB-3(r)OXALI(2000)), hence resulting in

288 se prostate cancer models were refractory to oxaliplatin unless genetically or pharmacologically depl

289 We show that oxaliplatin, unlike cisplatin and carboplatin, does not

290 nefit with second-line fluorouracil (FU) and oxaliplatin using the oxaliplatin, folinic acid, and FU

291 X6; infusional fluorouracil, leucovorin, and oxaliplatin) versus infusional FU/leucovorin (LV) in thi

292 ed in three phase 3 colon cancer trials when oxaliplatin was added to fluoropyrimidines, although the

293 Oxaliplatin was subsequently used in 55.9% (arm A) and 5

294 , sensitizes the cells to 5-fluorouracil and oxaliplatin.We investigated whether HSP110 T(17) could b

295 y with FOLFOX (fluorouracil, leucovorin, and oxaliplatin) were randomly assigned to intravenous calci

296 ers (OCTs), uptake carriers of metformin and oxaliplatin, were inhibited by several clinically used T

297 , were quickly reduced to their active form, oxaliplatin, when co-incubated with a macrocycle metallo

298 se B cells modulate the response to low-dose oxaliplatin, which promotes tumour-directed CTL activati

299 fectiveness of fluorouracil, leucovorin, and oxaliplatin with or without bevacizumab in the first-lin

300 d toxicity was observed with the addition of oxaliplatin, with grade 3/4 adverse events occurring in