ライフサイエンスコーパス: cisplatin

1 t with the platinum-based chemotherapy agent cisplatin.

2 ogenic differentiation and sublethal dose of cisplatin.

3 epithelial ovarian cancer cells resistant to cisplatin.

4 chanism of chemoresistance of advanced BC to cisplatin.

5 cancer cells renders cells hypersensitive to cisplatin.

6 es to shikonin but enhances the responses to cisplatin.

7 ression was further increased in response to cisplatin.

8 aluation, sensitized chemoresistant cells to cisplatin.

9 ptosis as seen in the combination of 4j with cisplatin.

10 endent increase in p53 expression induced by cisplatin.

11 ath in gallbladder cancer cells treated with cisplatin.

12 hout compromising the antitumour efficacy of cisplatin.

13 gallbladder cancer cells in the presence of cisplatin.

14 ditional benefit accrued in combination with cisplatin.

15 m is better suited for real time analysis of cisplatin.

16 y standard of care chemotherapeutics such as cisplatin.

17 1g-i interacted synergistically with cisplatin.

18 Purpose Chemoradiation with cisplatin 100 mg/m(2) given once every 3 weeks is the st

19 n 30 mg/m(2) given once a week compared with cisplatin 100 mg/m(2) given once every 3 weeks, both adm

20 zed trial, we assessed the noninferiority of cisplatin 30 mg/m(2) given once a week compared with cis

21 four) to intravenous chemotherapy of either cisplatin (50 mg/m(2) on day 1 or 2) plus paclitaxel (13

22 atients were randomized to weekly concurrent cisplatin (50 mg/m2), paclitaxel (25 mg/m2), and daily r

23 herapy (epirubicin 50 mg/m(2) intravenously; cisplatin 60 mg/m(2) intravenously; capecitabine 625 mg/

24 weekly cycles of epirubicin [50 mg/m(2)] and cisplatin [60 mg/m(2)] intravenously on day 1, and capec

25 ekly ADI-PEG 20 36 mg/m(2) plus three-weekly cisplatin 75 mg/m(2) and pemetrexed 500 mg/m(2).

26 750 mg/day or platinum-based chemotherapy ([cisplatin 75 mg/m(2) or carboplatin AUC 5-6 plus pemetre

27 2), together with pemetrexed 500 mg/m(2) and cisplatin 75 mg/m(2) which were given every three weeks

28 and fluorouracil (CF; two 3-weekly cycles of cisplatin [80 mg/m(2) intravenously on day 1] and fluoro

29 ine starvation has a synergistic effect with cisplatin, a component of the current medulloblastoma ch

30 Cisplatin accumulation is consistently high in the stria

31 We demonstrated that cisplatin activates ATR, CHK1 and WEE1, which shut down

32 , consistent with the cationic nature of the cisplatin adduct following aquation.

33 forskolin enhanced clearance of intrastrand cisplatin-adducts in melanocytes or MC1R-transfected HEK

34 and progression-free survival upon receiving cisplatin after operation.

35 EGylated particles (median survival=40days), cisplatin alone (median survival=12days) or saline-treat

36 atin extended overall survival compared with cisplatin alone.

37 r agents, as well as more recently developed cisplatin analogs.

38 rmia (42 degrees C) plus local chemotherapy (cisplatin and 5-fluorouracil), (b) chemotherapy alone, (

39 Although cisplatin and carboplatin are used primarily in germ cel

40 n used to treat cell lines and compared with cisplatin and carboplatin at different concentrations.

41 We show that oxaliplatin, unlike cisplatin and carboplatin, does not kill cells through t

42 sion of VEGFR2 correlated with resistance to cisplatin and combination with VEGFR2-inhibitor apatinib

43 ung cancer is initially highly responsive to cisplatin and etoposide but in almost every case becomes

44 that PID1 increased the apoptosis induced by cisplatin and etoposide in medulloblastoma and glioblast

45 Conclusion The addition of bevacizumab to cisplatin and etoposide in the first-line treatment of E

46 e and tumour stage, to receive two cycles of cisplatin and fluorouracil (CF; two 3-weekly cycles of c

47 es of concurrent cetuximab and two cycles of cisplatin and fluorouracil.

48 [paclitaxel and gemcitabine] v 10.7 months [cisplatin and gemcitabine]; HR, 1.46; P = .02).

49 Cisplatin and its platinum analogs, carboplatin and oxal

50 aling (SSA), and in conferring resistance to cisplatin and olaparib in human cancer cells.

51 ing USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (olaparib) while overexpres

52 0.3 (paclitaxel and pemetrexed) versus 11.6 (cisplatin and pemetrexed) months for ERCC1-negative pati

53 8.0 (paclitaxel and pemetrexed) versus 9.6 (cisplatin and pemetrexed) months for ERCC1-positive pati

54 It has high specificity for cisplatin and potentially other Pt(II) drugs and does no

55 on did not impair the anticancer efficacy of cisplatin and radiotherapy in tumor-bearing mice.

56 biting PKM2 augments the chemosensitivity to cisplatin and reduces BC growth and progression.

57 be simultaneously filled by introducing both cisplatin and triflate concurrently, providing the first

58 G2-M cell cycle checkpoint simultaneously by cisplatin and WEE1 inhibition is promising for TNBCs tre

59 ratios (ORs) in relation to age, cumulative cisplatin and/or bleomycin dose, time since chemotherapy

60 on days 1-4]) or four cycles of epirubicin, cisplatin, and capecitabine (ECX; four 3-weekly cycles o

61 ab group; n=304) or placebo plus epirubicin, cisplatin, and capecitabine (placebo group; n=305).

62 mly assigned to rilotumumab plus epirubicin, cisplatin, and capecitabine (rilotumumab group; n=304) o

63 ics of rilotumumab combined with epirubicin, cisplatin, and capecitabine, and to assess potential bio

64 o surgery alone or perioperative epirubicin, cisplatin, and fluorouracil chemotherapy in the Medical

65 al implementation of oxaliplatin relative to cisplatin, and it might enable mechanistically informed

66 ose, safety, and tolerability of ADI-PEG 20, cisplatin, and pemetrexed in patients with ASS1-deficien

67 he addition of cetuximab to radiotherapy and cisplatin, and there is a significant interaction betwee

68 rred when yeast lacking RAD1 were exposed to cisplatin, and we characterized this interaction using w

69 transfer experiments and protected mice from cisplatin- and doxorubicin-induced nephrotoxic injury.

70 d using (18)F-FPMA for coordination with the cisplatin-aqua complex.

71 as the labeling agent to coordinate with the cisplatin-aqua complex.

72 line chemotherapeutic agents (paclitaxel and cisplatin) are described within three distinct in vitro

73 Conclusion Once-every-3-weeks cisplatin at 100 mg/m(2) resulted in superior LRC, albei

74 ractionation RT (70 Gy/35 over 7 weeks) plus cisplatin at 100 mg/m2 intravenous for 3 doses (arm A) v

75 eit with more toxicity, than did once-a-week cisplatin at 30 mg/m(2), and should remain the preferred

76 inued widespread use, the genomic effects of cisplatin-based chemotherapy and implications for subseq

77 l cancer cannot receive standard, first-line cisplatin-based chemotherapy because of renal dysfunctio

78 For individuals with stage IB, adjuvant cisplatin-based chemotherapy is not recommended for rout

79 Recommendations Adjuvant cisplatin-based chemotherapy is recommended for routine

80 uencing of matched pre- and post-neoadjuvant cisplatin-based chemotherapy primary bladder tumor sampl

81 seminoma can be successfully treated with a cisplatin-based chemotherapy regimen adequate for stage.

82 All four cisplatin-based chemotherapy regimens were used: 377 (25

83 sticular cancer, and previously treated with cisplatin-based chemotherapy were recruited from July 20

84 Inhibiting AP-1 or BMI1 sensitized tumors to cisplatin-based chemotherapy, and it eliminated lymph no

85 and genomic dynamics of tumor evolution with cisplatin-based chemotherapy, suggest mechanisms of clin

86 Cisplatin-based chemotherapy.

87 utive patients with GCT who progressed after cisplatin-based combination chemotherapy and were subseq

88 He received four cycles of cisplatin-based neoadjuvant chemotherapy followed by rad

89 hree or four cycles of bleomycin, etoposide, cisplatin (BEPX3/BEPX4).

90 other DNA-targeted chemotherapeutics such as cisplatin by its potency, cellular mechanism, and select

91 utes to NPC's resistance to radiotherapy and cisplatin by regulating DNA damage and repair pathways.

92 The platinum-based anticancer agents cisplatin, carboplatin, and oxaliplatin represent a spec

93 had completed a multidrug induction regimen (cisplatin, carboplatin, cyclophosphamide, vincristine, a

94 olyethylene glycol (PEG) and are loaded with cisplatin (CDDP) could be delivered across both the bloo

95 strated its capacity in targeted delivery of Cisplatin (CDDP), a drug having physicochemical properti

96 Cisplatin chemotherapy causes permanent hearing loss in

97 rate in vivo, and reduces survival following cisplatin chemotherapy in vivo.

98 Cisplatin chemotherapy is commonly used to treat cancer

99 f biological action was closely aligned with cisplatin [cis-PtCl2(NH3)2].

100 4 plays a major role in sensitizing TGCTs to cisplatin, consistent with shielding of platinum-DNA add

101 (control group) in addition to their planned cisplatin-containing chemotherapy regimen, using permute

102 onding ex vivo Notably, explant responses to cisplatin correlated significantly with patient survival

103 hesis (TLS) under these conditions, SAHA and cisplatin cotreatment promoted focal accumulation of the

104 ions were conducted at baseline, before each cisplatin cycle, and at the end of therapy.

105 The median number of pemetrexed and cisplatin cycles was six; the median treatment duration

106 The enhanced cisplatin cytotoxicity in histone H4 knockdown cells was

107 ors consistent with known characteristics of cisplatin damage and repair.

108 hancement of ATR and XPA's associations with cisplatin-damaged DNA, indicating that ATR phosphorylati

109 ics of ATR-pS435 and XPA's associations with cisplatin-damaged DNA.

110 luding one-, two-, and three-drug schemes of cisplatin (DDP), bevacizumab (BEV), and paclitaxel (PTX)

111 Mechanistically, cisplatin decreased spare respirator capacity of brain s

112 hromatin in regulating genome targeting with cisplatin derivatives and associated cellular responses.

113 Cisplatin derivatives can form various types of DNA lesi

114 ment of an XPA-ATR-pS435 complex to sites of cisplatin DNA damage.

115 B4 specifically inhibits repair of the major cisplatin-DNA adducts in TGCT cells by using the human T

116 n testes, uniquely blocks excision repair of cisplatin-DNA adducts, 1,2-intrastrand cross-links, to p

117 in sensitivity to three chemotherapy drugs: cisplatin, docetaxel, and doxorubicin.

118 lfate 16 g/m(2) intravenously 6 h after each cisplatin dose or observation.

119 In vitro, cisplatin dose-dependently increased ROS generation in L

120 ncidence of hearing loss 4 weeks after final cisplatin dose.

121 Neoadjuvant chemotherapy comprising cisplatin, doxorubicin, and methotrexate with intercalat

122 ng in vivo inhibits tumour growth, increases cisplatin efficacy and OS.

123 t study reports a simple approach to improve cisplatin efficacy in the treatment of colon cancer thro

124 herapy consisted of one cycle of intravenous cisplatin (either 80 mg/m(2) on day 1 or 20 mg/m(2) per

125 rs (TCSs) after four cycles of etoposide and cisplatin (EPX4) or three or four cycles of bleomycin, e

126 rapeutic agents (5-fluoruracil, carboplatin, cisplatin, eribulin, and paclitaxel), based on their con

127 cell tumors (MGCT) if the administration of cisplatin, etoposide, and bleomycin (PEb) is reduced fro

128 ificant difference in response rates between cisplatin-etoposide and carboplatin-paclitaxel (58% vs 5

129 o compare outcomes and toxic effects between cisplatin-etoposide and carboplatin-paclitaxel in patien

130 Cisplatin-etoposide and carboplatin-paclitaxel regimens

131 45 days, starting on day 22 after commencing cisplatin-etoposide chemotherapy (given as four to six c

132 atients were included from 31 studies in the cisplatin-etoposide groups (median age, 61 years; 65% ma

133 For cisplatin-etoposide vs carboplatin-paclitaxel, there was

134 Cisplatin-etoposide was associated with higher grade 3 t

135 otherapy (RT) with carboplatin-paclitaxel or cisplatin-etoposide were identified using electronic dat

136 progressed with age and were exacerbated on cisplatin exposure.

137 ncomitant loss of Lkb1, combined AZD1775 and cisplatin extended overall survival compared with cispla

138 stage I to III SCCAC received CRT including cisplatin, fluorouracil, and radiation therapy to the pr

139 l cycles of VI intermixed with six cycles of cisplatin/fluorouracil/vincristine/doxorubicin (C5VD), a

140 In contrast, the cochlea retains cisplatin for months to years after treatment in both mi

141 Cisplatin impaired performance in the novel object/place

142 eached; 80% long-term survivors) compared to cisplatin in conventional un-PEGylated particles (median

143 particles also provide controlled release of cisplatin in effective concentrations to kill the tumor

144 efficiency and enhanced cytotoxic effects of cisplatin in NSCLC cells.

145 ry nature of neural projections activated by cisplatin in rats and reveal the necessity of specific h

146 r results demonstrate long-term retention of cisplatin in the human cochlea, and they point to the st

147 racter results in selective guest binding of cisplatin in the peripheral cavities, with triflate bind

148 uminescence in the liver (APAP) and kidneys (cisplatin) in vivo and ex vivo, whilst qPCR, Taqman low-

149 Etoposide and cisplatin increased NFkappaB promoter reporter activity

150 asome inhibitor, bortezomib, suggesting that cisplatin induced proteasome dependent degradation of PI

151 hich shut down DNA replication and attenuate cisplatin induced-lethality.

152 ey dysfunction and a lower mortality rate in cisplatin-induced AKI.

153 ereas MIOX gene disruption protects against, cisplatin-induced AKI.

154 Inhibition of lPBN-->CeA neurons attenuated cisplatin-induced anorexia and body weight loss signific

155 inhibition of NTS-->lPBN neurons attenuated cisplatin-induced anorexia and body weight loss signific

156 at CeA glutamate receptor signaling mediates cisplatin-induced anorexia and body weight loss.

157 BN-->CeA projection neurons are required for cisplatin-induced anorexia and weight loss, we inhibited

158 specific hindbrain-forebrain projections for cisplatin-induced anorexia and weight loss.

159 expression, thereby sensitizing NPC cells to cisplatin-induced apoptosis both in vitro and in vivo.

160 lated histone H4 expression, which increased cisplatin-induced apoptosis in lung cancer cells.

161 trate for the first time that etoposide- and cisplatin-induced apoptosis in medulloblastoma and gliob

162 PID1 siRNA diminished cisplatin-induced apoptosis, suggesting that PID1 is req

163 ing pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for the first time found

164 iously reported role of MOAP-1 in modulating cisplatin-induced apoptosis.

165 and sensitized otherwise resistant cells to cisplatin-induced apoptosis.

166 ptosis, suggesting that PID1 is required for cisplatin-induced apoptosis.

167 T-mu treatment prevented CICI and associated cisplatin-induced changes in coherency of myelin basic p

168 cAMP-enhanced repair of cisplatin-induced DNA damage was dependent on PKA-mediat

169 The cisplatin-induced DNA-PK activation was suppressed in hi

170 evidence that excitatory projections mediate cisplatin-induced energy balance dysregulation.

171 Additionally, the cisplatin-induced enhancement of p53 activation, NF-kapp

172 assess sodium thiosulfate for prevention of cisplatin-induced hearing loss in children and adolescen

173 ETATION: Sodium thiosulfate protects against cisplatin-induced hearing loss in children and is not as

174 in preclinical studies in animals to prevent cisplatin-induced hearing loss with timed administration

175 NBCs and cisplatin resistant cancer cells to cisplatin-induced lethality, because it not only impairs

176 atinum-induced damage and protection against cisplatin-induced mutagenesis.

177 that was associated with protection against cisplatin-induced ototoxic effects in 2 independent coho

178 Cisplatin-induced ototoxic effects were independently di

179 ween protein-coding variation in SLC16A5 and cisplatin-induced ototoxic effects.

180 Cisplatin-induced ototoxic effects.

181 ing a role for SLC16A5 in the development of cisplatin-induced ototoxic effects.

182 showed that RAD6 is necessary for overcoming cisplatin-induced replication fork stalling, as replicat

183 To investigate the role of MIOX in cisplatin-induced tubular AKI, we generated conditional

184 ced or metastatic urothelial cancer who were cisplatin ineligible.

185 a new treatment option for patients who are cisplatin-ineligible or not suitable candidates for chem

186 re, single-arm, phase 2 study (KEYNOTE-052), cisplatin-ineligible patients with advanced urothelial c

187 ty and safety of first-line pembrolizumab in cisplatin-ineligible patients with locally advanced and

188 mour activity and acceptable tolerability in cisplatin-ineligible patients with urothelial cancer, mo

189 reatment for metastatic urothelial cancer in cisplatin-ineligible patients.

190 SMI#9 pretreatment synergistically increased cisplatin inhibition of MDA-MB-231 triple-negative breas

191 Cisplatin is a particularly potent chemotherapeutic agen

192 Chemoresistance to cisplatin is a principal cause of treatment failure and

193 The hypersensitivity of TGCTs to cisplatin is a subject of widespread interest.

194 y to these chemotherapeutic agents including cisplatin is common.

195 In most organs cisplatin is detected within one hour after injection, a

196 Cisplatin is one of the most commonly used therapeutic d

197 Cisplatin is the most commonly used anticancer drug for

198 of the first metal based therapeutic agent, cisplatin, launched a new era in the application of tran

199 We describe the development of cisplatin-loaded nanoparticles that are small enough (70

200 This result differs from cisplatin mutation signatures in XPF-deficient Caenorhab

201 in patients (both post-platinum therapy and cisplatin-naive) treated with avelumab and to assess ant

202 dose of 12 mg/m(2) on day 1) or intravenous cisplatin (one dose of 60 mg/m(2) on days 1 and 29), wit

203 ined with up to six cycles of etoposide plus cisplatin or carboplatin every 3 weeks, until disease pr

204 hether the cochlea has unique sensitivity to cisplatin or is exposed to higher levels of the drug.

205 Combinations of cisplatin or PARP inhibitors enhanced the antitumor cell

206 gle-agent efficacy, augmented the effects of cisplatin or the PARP inhibitor olaparib, and improved t

207 In contrast to cisplatin or the progenitor RAPTA-C anticancer drugs, th

208 o maintenance chemotherapy (fluorouracil and cisplatin) or no maintenance chemotherapy.

209 Senescence occurred following cisplatin- or Taxol-treatment in cell lines from both ca

210 important therapeutic target for preventing cisplatin ototoxicity.

211 t, and more so when used in combination with cisplatin+pemetrexed, the current standard of care.

212 Male C57BL/6J mice injected with cisplatin +/- PFT-mu for two 5-day cycles were assessed

213 plasma mass spectrometry (ICP-MS) to examine cisplatin pharmacokinetics in the cochleae of mice and h

214 CLC were randomly assigned to receive either cisplatin plus etoposide (arm A) or the same regimen wit

215 efficacy of adding bevacizumab to first-line cisplatin plus etoposide for treatment of extensive-dise

216 ratio to up to six cycles of pemetrexed and cisplatin plus nintedanib (200 mg twice daily) or placeb

217 with advanced HNSCC from a phase 3 trial of cisplatin plus radiotherapy with or without cetuximab (N

218 lerated-fractionation RT was not superior to cisplatin plus standard-fractionation RT in LA-SCCHN and

219 ty polypyridyl [Pd3(L)4](6+) cages that bind cisplatin [Pt(NH3)2Cl2] within their internal cavities a

220 eously inhibiting Bmi1 or AP1, combined with Cisplatin, reduces tumor growth effectively in preclinic

221 cal regulator of ovarian cancer stemness and cisplatin resistance by inducing the expressions of plur

222 RP-1 levels and suggests that MKP-1-mediated cisplatin resistance can be bypassed by PARP-1 inhibitio

223 rthermore, 4j almost completely reversed the cisplatin resistance in Cal27CisR.

224 otic MOAP-1 and suggest that UBR5 can confer cisplatin resistance in ovarian cancer.

225 ein was found to contribute to radiation and cisplatin resistance of cells, responses that could be a

226 oly(ADP-ribose) (PAR) protein expression and cisplatin resistance while its downregulation suppresses

227 -type cells, signifying that they circumvent cisplatin resistance.

228 nostic anticancer agents that can circumvent cisplatin resistance.

229 resses PARP-1 and PAR protein expression and cisplatin resistance.

230 ated protein kinase phosphatase-1 (MKP-1) in cisplatin resistance.

231 or TNBCs treatment, and for overcoming their cisplatin resistance.

232 ration could be considered as a biomarker of cisplatin resistance.

233 id raft localization for CSC maintenance and cisplatin resistance.

234 Induced cisplatin-resistance is strongly associated with PKM2 ov

235 y to the comparative uptake of Pt-species in cisplatin resistant and sensitive cell lines (A2780cis a

236 WEE1 inhibition sensitizes TNBCs and cisplatin resistant cancer cells to cisplatin-induced le

237 These effects were more pronounced for the cisplatin resistant subline Cal27CisR.

238 Pt-DA showed photocytotoxicity against cisplatin-resistant A2780Cis human ovarian cancer cells

239 les and delivered to cisplatin-sensitive and cisplatin-resistant A549-lung adenocarcinoma cells.

240 Complexes 9, 10, and 13 were as effective in cisplatin-resistant cells as wild-type cells, signifying

241 We found cisplatin-resistant cells more resistant to NK cell cyto

242 gly associated with PKM2 overexpression, and cisplatin-resistant cells respond sensitively to shikoni

243 We also observed increased susceptibility of cisplatin-resistant cells to NK cell cytotoxicity when n

244 effect in enhancing NK cell cytotoxicity to cisplatin-resistant cells.

245 n NK cells was induced after co-culture with cisplatin-resistant cells.

246 partially driving effects of Indomethacin in cisplatin-resistant cells.

247 nd enhanced the cisplatin sensitivity of the cisplatin-resistant head-neck cancer cell line Cal27CisR

248 bited the growth of subcutaneously implanted cisplatin-resistant human ovarian cancer cells in athymi

249 Importantly, we found that cisplatin-resistant ovarian cancer cell lines exhibit lo

250 Furthermore, we showed that acquired cisplatin-resistant ovarian cancer cells expressed high

251 xpression was higher in ovarian cancers from cisplatin-resistant patients than from cisplatin-respons

252 icancer agent, KuQs have been tested against Cisplatin-resistant SKOV3 and SW480 cancer cell lines.

253 In explant tissue, cisplatin-resistant tumors excluded platinum ions from t

254 ay activities to build a predictive model of cisplatin response.

255 from cisplatin-resistant patients than from cisplatin-responsive patients.

256 on Addition of nintedanib to pemetrexed plus cisplatin resulted in PFS improvement.

257 of resistant cells to high concentrations of cisplatin revealed transcriptomic changes in potential k

258 rain-forebrain projections are necessary for cisplatin's untoward effects on energy intake, elucidati

259 aluronic-Acid nanoparticles and delivered to cisplatin-sensitive and cisplatin-resistant A549-lung ad

260 latinum ions from tumor areas in contrast to cisplatin-sensitive tumors.

261 a positive correlation was observed between cisplatin sensitivity and TP53 mutation status (P = 0.00

262 and that silencing MKP-1 or PARP-1 increased cisplatin sensitivity in resistant cells.

263 chemosensitizing properties and enhanced the cisplatin sensitivity of the cisplatin-resistant head-ne

264 Furthermore, their ability to enhance cisplatin sensitivity was analyzed in Cal27 and Cal27Cis

265 Variations in cisplatin sensitivity were noted with approximately 50%

266 Intact TP53 did not predict cisplatin sensitivity, but a positive correlation was ob

267 inhibitor apatinib synergistically increased cisplatin sensitivity.

268 We report the first electrochemical cisplatin sensor fabricated with a thiolated and methyle

269 red squalenoylated nanoparticles loaded with cisplatin (SQ-CDDP NP).

270 Moreover, combining HL001 with cisplatin synergistically enhance tumor regression in or

271 e signal-on sensors are capable of detecting cisplatin, the signal-on sensing mechanism is better sui

272 s, to potentiate the sensitivity of TGCTs to cisplatin therapy.

273 ctra matching, the promiscuity of binding of cisplatin to ubiquitin is revealed, with 14 different bi

274 exert additive effects with agents, such as cisplatin, to impair tumor growth, and observational stu

275 Shikonin and cisplatin together exhibit significantly greater inhibit

276 In syngeneic mice, shikonin and cisplatin together, but not as single-agents, markedly r

277 NA-PK reduced expression of RIP1 and IAPs in cisplatin-treated cells.

278 review mechanism for audiologic results for cisplatin-treated children in the cooperative group sett

279 cation of intracellular hydrogen peroxide in Cisplatin-treated human renal HK-2 cells.

280 l comparison of tissue lipids in control and cisplatin-treated kidneys.

281 ptosis, but these effects were attenuated in cisplatin-treated MIOX(-/-) mice.

282 with cisplatin-treated wild-type (WT) mice, cisplatin-treated MIOX-TG mice had even greater increase

283 ta activity was essential for mutagenesis in cisplatin-treated rad1Delta cells.

284 Compared with cisplatin-treated wild-type (WT) mice, cisplatin-treated

285 ntensities in kidney sections of control and cisplatin-treated Wistar rats.

286 the 2D monolayer and 3D diffuse models while cisplatin treatment afforded an increase in ALDH1A3 expr

287 immunity in the setting of radiotherapy and cisplatin treatment and to evaluate the interaction of t

288 Finally, we demonstrated that combined cisplatin treatment and WEE1 inhibition synergistically

289 utic drugs for cancer therapy, yet prolonged cisplatin treatment frequently results in drug resistanc

290 ation than their sensitive counterparts upon cisplatin treatment, consistent with the previously repo

291 16A5-silencing altered cellular responses to cisplatin treatment, supporting a role for SLC16A5 in th

292 ferences in cell cycle progression following cisplatin treatment.

293 Activated by Designer Drugs (DREADDs) before cisplatin treatment.

294 active oxygen species (ROS) generation after cisplatin treatment.

295 in probe-to-probe spacing enables binding of cisplatin via the intrastrand GNG motif (N = A), generat

296 ith standard-fractionation RT plus high-dose cisplatin vs accelerated-fractionation RT plus the anti-

297 topic glioma was significantly enhanced when cisplatin was delivered in brain penetrating nanoparticl

298 icity-related deaths that were observed when cisplatin was infused into the brain without a delivery

299 ge of a novel azide-containing derivative of cisplatin we named APPA, a cellular pre-extraction proto

300 hearing loss with timed administration after cisplatin without compromising the antitumour efficacy o