ライフサイエンスコーパス: cisplatin

1 t than 2 cycles of bleomycin, etoposide, and cisplatin.

2 strongly sensitizes SCLC cells and tumors to cisplatin.

3 nd sickness induced by lipopolysaccharide or cisplatin.

4 r EOC is platinum-based chemotherapy such as cisplatin.

5 treatment with clinically relevant doses of cisplatin.

6 d apoptosis before and after incubation with cisplatin.

7 BRD9 sensitizes cancer cells to olaparib and cisplatin.

8 is indicated before every administration of cisplatin.

9 p53, including 5-fluorouracil, etoposide and cisplatin.

10 potential resistance mechanism to PARPi and cisplatin.

11 with and after chemoradiotherapy with weekly cisplatin.

12 ting ZNF207/BuGZ sensitizes p53-null hESC to cisplatin.

13 in place of Cu(I) and transplatin instead of cisplatin.

14 ZH2 pathway re-sensitizes resistant cells to cisplatin.

15 MYXV that was enhanced by combined low-dose cisplatin.

16 pounds, aristolochic acid, aflatoxin B1, and cisplatin.

17 in cellular proliferation and sensitivity to cisplatin.

18 n human blood when a patient is treated with cisplatin.

19 U) displayed a GSH-dose dependent release of cisplatin.

20 ish the mechanism for potential synergy with cisplatin.

21 rol arm), for 5 d before each of 3 cycles of cisplatin.

22 nd L-mimosine in the safer administration of cisplatin.

23 sslinks caused by the chemotherapeutic agent cisplatin.

24 promoted resistance to the chemotherapeutic cisplatin.

25 nd conferred resistance to the platinum drug cisplatin.

26 Each cycle consisted of cisplatin 20 mg/m(2) and etoposide 100 mg/m(2) on days 1

27 Treatment for patients in arm A consisted of cisplatin 25 mg/m(2) and gemcitabine 600 mg/m(2) intrave

28 wed by 250 mg/m(2)/wk, or weekly intravenous cisplatin 40 mg/m(2), during RT.

29 er were randomly assigned 1:1 to intravenous cisplatin 60 mg/m(2) (day 1) plus FU 1,000 mg/m(2) (days

30 mg/mL per min administered intravenously) or cisplatin (70 mg/m(2) body surface area administered int

31 Chemotherapy was either cisplatin (70 mg/m(2)) or carboplatin (area under the cu

32 platin area under the curve 5-6 mg/mL/min or cisplatin 75-80 mg/m(2) on day 1 of each cycle.

33 -day cycles of pemetrexed (500 mg/m(2)) plus cisplatin (75 mg/m(2)) on day 1, then nintedanib (200 mg

34 /m(2)) with carboplatin (5 mg/mL per min) or cisplatin (75 mg/m(2); investigator's choice) every 3 we

35 f individual cells in a clonal population to cisplatin, a DNA-damaging chemotherapeutic agent.

36 arget of rapamycin) on resistance of CSCs to cisplatin, a prototypic platinum-based chemotherapeutic

37 und that the cell cycle phase at the time of cisplatin addition was not predictive of outcome, the pr

38 is unable to fully protect ssDNA created by cisplatin adducts.

39 napse of GLAST KO mice is more vulnerable to cisplatin administration during the active phase (nightt

40 ndings suggest that the current protocols of cisplatin administration in humans during daytime may ca

41 Dose-limiting toxicities for cisplatin administration, including ototoxicity and neph

42 h the conjugate is 15-fold greater than with cisplatin after 5 h.

43 combined with D-CAN was more effective than cisplatin alone in suppressing growth of mouse prostate

44 Cisplatin also increased the fraction of CSCs in vivo.

45 ity with a half-life of ~ 8 h, and combining cisplatin and amino acid deprivation synergistically red

46 s and synergistic action in combination with cisplatin and amphotericin B against cancer and fungal c

47 omycin, an established CSC-potent agent, and cisplatin and carboplatin, clinically used platinum drug

48 to 94%) and 78% (95% CI, 71% to 85%) in the cisplatin and cetuximab groups, respectively (adjusted h

49 , there was a significant difference between cisplatin and cetuximab in 2-year overall survival (97.5

50 rol arm received induction chemotherapy with cisplatin and docetaxel, followed by concomitant chemora

51 BC cells to the cytotoxic chemotherapy drugs cisplatin and doxorubicin alter arginine and polyamine m

52 d induction of p21 that was synergistic with cisplatin and doxorubicin.

53 led to an enhanced tumor cell sensitivity to cisplatin and dramatically improved chemotherapeutic res

54 h deliver Rac1-targeting siRNA together with cisplatin and effectively reverses NAC-chemoresistance i

55 x cholangiocarcinoma cell lines treated with cisplatin and gemcitabine (CG) seeking changes in cell v

56 These data establish cisplatin and gemcitabine as a standard approach in gBRC

57 Cisplatin and gemcitabine is an effective regimen in adv

58 enter, two-arm phase II trial to investigate cisplatin and gemcitabine with or without veliparib in g

59 e and absence of sublethal concentrations of cisplatin and identified 137 genes whose loss selectivel

60 ting that DNA repair after dual treatment of cisplatin and KU55933 was not sufficient to prevent the

61 , aldosterone, angiotensin II, high glucose, cisplatin and lipopolysaccharide, but was induced by ari

62 , high glucose, angiotensin II, aldosterone, cisplatin and lipopolysaccharide.

63 erty of TNBC cells, compared to conventional cisplatin and miriplatin.

64 Rad51 downregulation by the combination of cisplatin and Nutlin-3 inhibits homologous recombination

65 ll sensitivity to DNA-damage agents, such as cisplatin and olaparib.

66 cally, G1 delays increase drug resistance to cisplatin and paclitaxel by reducing their ability to da

67 esistance to the frontline chemotherapeutics cisplatin and paclitaxel.

68 Treatment of BNC tumor-bearing mice with cisplatin and pemetrexed, the current frontline treatmen

69 conjugation between platinum(IV) prodrugs of cisplatin and perfluoroaryl peptide macrocycles to incre

70 Thresholds of cisplatin and radiation exposure exist, above which risk

71 er (HNSCC) patients treated with concomitant cisplatin and radiotherapy.

72 liferation status in regulating responses to cisplatin and suggest that slowly proliferating cells wi

73 latform provides a framework for preclinical cisplatin and TCZ dose and frequency evaluation to be te

74 ls after treatment with the chemotherapeutic cisplatin and that overexpression of SOX9 correlates wit

75 EZH2 depletion causes cellular cisplatin and UV hypersensitivity in an epistatic manner

76 enografts were used to examine the effect of cisplatin and/or temsirolimus on CSCs in vivo.

77 B knockdown re-sensitises resistant cells to cisplatin, and A3B knockout enhances sensitivity to chem

78 fic Vgf gene ablation exacerbates ischemia-, cisplatin-, and rhabdomyolysis-associated AKI in vivo an

79 ional stress response in RTECs to ischemia-, cisplatin-, and rhabdomyolysis-associated renal injury.

80 These metabolic effects of cisplatin are abolished by pre-treatment with the GFRAL

81 ulated radiotherapy with concurrent low-dose cisplatin are favorable in patients with human papilloma

82 these events precluded the administration of cisplatin at the planned date, and no subsequent cases o

83 fety and efficacy of adding pembrolizumab to cisplatin-based chemoradiotherapy in patients with LA HN

84 Pembrolizumab in combination with weekly cisplatin-based chemoradiotherapy is safe and does not i

85 Cisplatin-based chemotherapeutic regimens are frequently

86 It is hypothesized that cisplatin-based chemotherapy (CBCT) reduces the occurren

87 poor outcomes associated with resistance to cisplatin-based chemotherapy.

88 All patients were treated with cisplatin-based combination chemotherapy.

89 s a powerful tool to boost response rates to cisplatin-based therapy in vitro.

90 pse after adjuvant bleomycin, etoposide, and cisplatin (BEP) from 18 centers/11 countries were collec

91 Treatment with bleomycin-etoposide-cisplatin (BEP; n = 1,819) was associated with increased

92 re improved to 4.3 d; performance as good as cisplatin but with the advantage of no weight loss in th

93 after treatment at nighttime suggesting that cisplatin can modulate the molecular clock.

94 of female reproductive system cancers, while cisplatin (CDDP) resistance is the one of main reasons f

95 (ypT0/is, N0) after neoadjuvant single-agent cisplatin (CDDP) versus doxorubicin-cyclophosphamide (AC

96 We found that in response to cisplatin, cells either arrested or died, and the ratio

97 ion) and suggests a new strategy to modulate cisplatin chemosensitivity by targeting the PRIMPOL path

98 and resistant to docetaxel, cabazitaxel, and cisplatin chemotherapy.

99 umor responses alone and in combination with cisplatin chemotherapy.

100 f platinum-based chemotherapy, in particular cisplatin (cis-diammine dichloroplatinum II).

101 that uses platinum complexes [K(2)PtCl(4) or Cisplatin (CisPt)] for drug activation.

102 ir sublines adapted to the anti-cancer drugs cisplatin (COLO-704(r)CDDP(1000), EFO-21(r)CDDP(2000), E

103 responses of HNSCC to tocilizumab (TCZ) and cisplatin combination therapy.

104 Importantly, cisplatin combined with D-CAN was more effective than ci

105 potent toward MCF7 cancer cells (similar to cisplatin), complexes bearing the tether-ring structure,

106 tes of primordial follicles was dependent on cisplatin concentration and administration frequency.

107 827 cells, TTF-1 desensitized these cells to cisplatin; concomitantly, TTF-1 conferred an increase in

108 pendent cellular evasion of apoptosis during cisplatin could be observed, leading to three different

109 The primary endpoint occurred in 8 of 470 cisplatin cycles (1.7%, 95%CI 0.5-2.9).

110 aired uCrCl and eGFR determinations from 470 cisplatin cycles from 121 patients were analyzed [median

111 ependent deacetylase, protected neurons from cisplatin cytotoxicity by promoting transcription-couple

112 over, animals co-injected with melatonin and cisplatin did not display any significant differences fr

113 uencing (XR-seq) method to better understand cisplatin DNA damage and repair.

114 Cisplatin kills cells by forming cisplatin-DNA adducts, most commonly the Pt-d(GpG) diadd

115 le checkpoints in combination with repair of cisplatin-DNA lesions in vivo using RNAi nanocarriers, a

116 d by concomitant chemoradiation therapy with cisplatin, docetaxel, and 45Gy.

117 5 days; 88.1% of patients completed the goal cisplatin dose of >= 200 mg/m(2).

118 the proliferation status interacted with the cisplatin dose to further guide this decision.

119 We propose that cells adapt to repeated cisplatin doses by activating PRIMPOL repriming under co

120 1-deficient cancer cells exposed to multiple cisplatin doses, mimicking a clinical treatment regimen.

121 ations for the effective distribution of the cisplatin drug.

122 nhibitor of this pathway, JH-RE-06, promotes cisplatin efficacy in cancer cells and mouse xenograft m

123 As a result, miR-1291 largely improved cisplatin efficacy in the inhibition of PC cell viabilit

124 r gemcitabine plus carboplatin, depending on cisplatin eligibility) administered intravenously for up

125 -web response system, with stratification by cisplatin eligibility, PD-L1 status, and presence or abs

126 at the combination treatment of anti-PD1 and cisplatin enriched BMI1(+) CSCs in HNSCC while inhibitin

127 nce with 2 cycles of adjuvant etoposide plus cisplatin (EPx2) after therapeutic primary RPLND.

128 N overexpression also suppressed response to cisplatin-etoposide chemotherapy, with similar findings

129 Relative to no cisplatin exposure, patients receiving < 200 mg/m(2) wer

130 rated that continuous treatment with 2 mg/kg cisplatin for 15 days can activate primordial follicles,

131 trate that continuous treatment with 2 mg/kg cisplatin for 15 days leads to the same consequence as w

132 Phase IB data from a trial that used cisplatin, gemcitabine, and veliparib treatment demonstr

133 % CI, 4% to 14%) in the cetuximab versus the cisplatin group (Gray's test P = .0036).

134 1904) were similar between the cetuximab and cisplatin groups.

135 ation >= 34 Gy, abdominal radiation > 40 Gy, cisplatin >= 600 mg/m(2), amputation, or lung surgery ha

136 ng VRAC activity by hypotonic cell swelling, cisplatin, GTPgammaS, or the cytokines TNF or interleuki

137 of platinum compounds in the cochlea, rather cisplatin had a dose-dependent impact on cochlear clock

138 on theory analysis revealed that the dose of cisplatin had the greatest influence on the cells' decis

139 combination of the NAMPT inhibitor FK866 and cisplatin improved the survival of EOC-bearing mice.

140 alone in a platinum-sensitive model or with cisplatin in a platinum-resistant model increases surviv

141 r proliferation and increased sensitivity to cisplatin in a SASH1-dependent manner.

142 ction of CSCs (P < 0.05) even in presence of cisplatin in a short-term in vivo experiment.

143 ate reversed chemoresistance to sorafenib or cisplatin in HCC stem cells derived from four HCC cell l

144 S) machinery, could potentiate the action of cisplatin in non-small cell lung cancer (NSCLC) treatmen

145 1 was 12-fold more toxic than cisplatin in T98g cells and 6-fold more toxic in T98g ce

146 itination enhances the antitumor efficacy of cisplatin in vitro and in vivo.

147 from (1) increased PRPP consumption, because cisplatin increased protein PARylation and PARP1 shRNA k

148 We observed that cisplatin induced mTOR and S6K1 phosphorylation, increas

149 the substrate Leu-FC can effectively monitor cisplatin induced overexpression of LAP activity in HepG

150 ain inhibitors could be developed to prevent cisplatin induced peripheral neuropathy.

151 y for protecting renal tubular cells against cisplatin-induced AKI by enhancing autophagy via AMPK-al

152 th controls after either ischemia-induced or cisplatin-induced AKI.

153 mTOR inhibition (e.g., temsirolimus) blocked cisplatin-induced Bmi-1 expression and salisphere format

154 ational spectrum compared with the repair of cisplatin-induced crosslinks.

155 euronal cells and protection of neurons from cisplatin-induced cytotoxicity and CIPN in mice.

156 air cells in the zebrafish otic vesicle from cisplatin-induced damage and preserved zebrafish larval

157 upled nucleotide excision repair (TC-NER) of cisplatin-induced DNA cross-links.

158 nhibition does not increase DNA repair after cisplatin-induced DNA damage and exacerbates tubular inj

159 did not ameliorate, but instead exacerbated cisplatin-induced DNA damage and tubular injury, thereby

160 chromatin accessibility, and sensitivity to cisplatin-induced DNA damage.

161 3(R158G) could render cancers susceptible to cisplatin-induced DNA stress.

162 al otoprotection against aminoglycoside- and cisplatin-induced hair cell death.

163 ut animals exhibited increased resistance to cisplatin-induced kidney injury, but not to folic acid-i

164 YM-5478, reduces allodynia in a rat model of cisplatin-induced neuropathy and attenuates the associat

165 ides insights into the mechanisms underlying cisplatin-induced oto- and nephrotoxicity and compelling

166 ike neuronal cells in DRG is associated with cisplatin-induced peripheral neuropathy (CIPN) in mice.

167 emonstrate that SIRT2 protected mice against cisplatin-induced peripheral neuropathy (CIPN).

168 l death in vitro Importantly, aggravation of cisplatin-induced renal injury caused by Vgf gene ablati

169 nd rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro Importantly,

170 mor cell apoptosis, Rev7 deletion promoted a cisplatin-induced senescence phenotype.

171 ted NAD(+) biosynthesis in the production of cisplatin-induced senescence-associated cancer stem cell

172 acokinetics of platinum therapy, we profiled cisplatin-induced signalling, DNA-damage and apoptotic r

173 nd KU55933 was not sufficient to prevent the cisplatin-induced tubular injury.

174 Myr-Akt1 or phosphomimetic HK2-T473D rescued cisplatin-induced tumor suppression in Skp2 knockdown st

175 Here, we show that cisplatin induces senescent-like neuronal cells in prima

176 The cancer-therapeutic drug, cisplatin, induces the release of GDF15 and activates GF

177 inoma(1,2), with one study reporting data in cisplatin-ineligible patients who received anti-PD-L1 mo

178 meaningful and durable clinical response in cisplatin-ineligible patients with advanced UC and is as

179 h localized urothelial carcinoma, especially cisplatin-ineligible patients with high-risk features wh

180 a first-line treatment in February 2020 for cisplatin-ineligible patients with locally advanced or m

181 rvalumab) plus anti-CTLA-4 (tremelimumab) in cisplatin-ineligible patients, with all tumors identifie

182 patients with locally advanced or metastatic cisplatin-ineligible urothelial carcinoma (UC).

183 bstrate for purine nucleotide synthesis, and cisplatin inhibited de novo purine synthesis and DNA syn

184 sine combined with a sub-therapeutic dose of cisplatin inhibited growth of ectopic hepatomas in mice.

185 SNI-1 also enhanced ADR or cisplatin inhibition of murine TNBC tumors in vivo and r

186 cute renal tubular damage in mice exposed to cisplatin insult, associated with enhanced autophagy in

187 Cisplatin is a commonly used chemotherapy agent with sig

188 Cisplatin is a mainstay of cancer chemotherapy.

189 Cisplatin is a standard of care for lung cancer, yet pla

190 Although the combination of gemcitabine and cisplatin is a standard regimen of choice, there are no

191 uced by roughly 3 orders of magnitude if the cisplatin is apportioned between 5 optimally spaced loca

192 The chemotherapeutic agent cisplatin is renowned for its ototoxic effects.

193 Radiotherapy plus cisplatin is the standard of care for eligible patients

194 an and mouse cell lines we examined in vitro cisplatin/JH-RE-06 treatment does not increase apoptosis

195 the opposite was true in cells treated with cisplatin/JH-RE-06.

196 d against FR-positive paclitaxel (KB-PR) and cisplatin (KB-CR) resistant models.

197 Cisplatin kills cells by forming cisplatin-DNA adducts,

198 mice lacking GLAST the effects of a low-dose cisplatin known not to cause any detectable change in he

199 ls in the cochlea are established targets of cisplatin, less is known regarding the afferent synapse,

200 Cisplatin-loaded GSH-sensitive nanoparticles (CGPU) disp

201 Until now, the involvement of GLAST in cisplatin-mediated ototoxicity remains unknown.

202 circadian regulation of the vulnerability to cisplatin-mediated ototoxicity.

203 While cisplatin monotherapy resulted in tumor cell apoptosis,

204 r data support that fertoprotectants against cisplatin must target molecules that control cell death

205 (n=326) or placebo plus fluoropyrimidine and cisplatin (n=319).

206 eceive ramucirumab plus fluoropyrimidine and cisplatin (n=326) or placebo plus fluoropyrimidine and c

207 no expression of GULP1 was observed in most cisplatin nonresponder cases.

208 activate p53, which increased robustly with cisplatin/Nutlin-3 combination and enhanced antitumor ef

209 n DNA damage resulting from HR inhibition by cisplatin/Nutlin-3.

210 g cancer cells was observed compared to free cisplatin of equivalent concentration (survival fraction

211 ylated arginine deiminase) and chemotherapy (cisplatin), offering new insights into development of ra

212 ineoplastic DNA-damaging agents doxorubicin, cisplatin, olaparib, and gamma-irradiation (IR) enhances

213 of intravenous oxaliplatin or 80 mg/m(2) of cisplatin on day 1, 850 mg/m(2) of oral capecitabine twi

214 ds did not abrogate the cytotoxic effects of cisplatin on human cancer cells.

215 The impact of mTOR inhibitors and/or cisplatin on MEC stemness was examined with salisphere a

216 irolimus, BKM120, AZD8055, PF4708671) and/or cisplatin on survival of human MEC cells.

217 nificant differences from those treated with cisplatin only contrary to the known results.

218 iation (3 x 8 Gy), (3) cyclophosphamide, (4) cisplatin or (5) doxorubicin, all followed by nivolumab.

219 ith the combination of pemetrexed and either cisplatin or carboplatin (platinum-based chemotherapy) (

220 t-line durvalumab plus etoposide with either cisplatin or carboplatin (platinum-etoposide) showed a s

221 ndard-of-care chemotherapy (gemcitabine plus cisplatin or gemcitabine plus carboplatin, depending on

222 , but not that of gemcitabine, capecitabine, cisplatin, or oxaliplatin.

223 ng enzyme superfamily, mediates reduction of cisplatin ototoxicity by removing 4-hydroxynonenal (4-HN

224 Multiple doses of caffeine exacerbated cisplatin ototoxicity which was associated with damage t

225 We also show that predictions of cisplatin PDs match previously reported patient data.

226 Median overall survival was 12.3 months for cisplatin plus FU (95% CI, 9.2 to 17.7 months) compared

227 of 91 patients were randomly assigned: 46 to cisplatin plus FU and 45 to carboplatin plus paclitaxel.

228 ore serious adverse events were noted in the cisplatin plus FU arm (62%) compared with the carboplati

229 s 5.7 months (95% CI, 3.3 to 9.0 months) for cisplatin plus FU compared with 8.1 months (95% CI, 6.6

230 ORR was 57% (95% CI, 39.4% to 73.7%) for cisplatin plus FU versus 59% (95% CI, 42.1% to 74.4%) fo

231 nd we found that treating cells for 6 h with cisplatin reduced intracellular PRPP availability.

232 Cetuximab is inferior to cisplatin regarding locoregional control for concomitant

233 hanisms and may be useful for development of cisplatin-related treatment strategies.

234 Furthermore, we show that neurotoxicity of cisplatin requires activation of Sarm1, a key regulator

235 2A to be part of the underlying mechanism of cisplatin resistance in MPM.

236 creen, we identified important regulators of cisplatin resistance in SCLC cells, including EZH2.

237 nucleotide excision repair (NER) and govern cisplatin resistance in SCLC.

238 beyond its catalytic activity for overcoming cisplatin resistance in SCLC.

239 Our results shed new lights on cisplatin resistance mechanisms and may be useful for de

240 ins (MT) has been identified as a reason for cisplatin resistance, which often leads to early therapy

241 cancer therapeutic intervention to overcome cisplatin resistance.

242 ibition is not required for full reversal of cisplatin resistance.

243 e the top biologic processes responsible for cisplatin resistance.

244 Cisplatin-resistant cells, however, can demonstrate incr

245 X1, and other candidate antioxidant genes in cisplatin-resistant cells.

246 he BMI1 inhibitor has therapeutic effects in cisplatin-resistant tumors and can reduce metastases ini

247 he drug's side effects, and allow its use in cisplatin-resistant tumors.

248 enocarcinoma improves long-term survival and cisplatin response beyond those of the synthetic lethal

249 d -independent roles of Rev7 are relevant to cisplatin response.

250 istently Sym004 efficacy and potentiation of cisplatin responses correlated with EGFR surface express

251 Augmentation of cisplatin's biochemical and cytotoxic effects by amino a

252 Amino acid deprivation enhanced cisplatin's cytotoxicity, increasing cellular apoptosis

253 esis, with amino acid deprivation augmenting cisplatin's effects.

254 Drug profiling reveals cisplatin sensitivities consistent with patient response

255 late BRCA1 transcription, thereby increasing cisplatin sensitivity and serving as a treatment efficac

256 While RAD5OE and rad5Delta both cause cisplatin sensitivity and share many genetic interaction

257 al fraction of genes whose disruptions cause cisplatin sensitivity or resistance overlap with those w

258 Moreover, Rev7 deficiency promoted greater cisplatin sensitivity than that previously shown followi

259 e the top biologic processes responsible for cisplatin sensitivity.

260 synergistic attenuation of tumor growth with cisplatin, suggesting ITPKB as a promising synthetic let

261 as with the continuous treatment of 5 mg/kg cisplatin: the death of oocytes in primordial follicles

262 ith DNA mismatch or base excision repair and cisplatin therapy mechanisms.

263 function in patients with cancer undergoing cisplatin therapy.

264 ial amino acid could allow dose reduction of cisplatin; this could reduce the drug's side effects, an

265 he p53-MDM2-MDM4 complex and synergizes with cisplatin to intensify p53 function, which then downregu

266 ty analysis, the study was amended to reduce cisplatin to two cycles during CCR.

267 d and ATR expression was low in single agent cisplatin-treated cells, the opposite was true in cells

268 NAMPT inhibitors suppressed the outgrowth of cisplatin-treated EOC cells both in vitro and in vivo.

269 Pharmacological ATM inhibition by KU55933 in cisplatin-treated mice did not ameliorate, but instead e

270 -apoptotic signaling in tubular epithelia of cisplatin-treated mice, leading to marked mitochondrial

271 an increased expression level of MT2A after cisplatin treatment (from sixfold to fourfold).

272 ature of the persistent genomic damage after cisplatin treatment and also the resulting physiological

273 gful effect of MT2A knockdown and subsequent cisplatin treatment could be observed in MSTO-211H cells

274 line MRC-5, as well as their sensitivity to cisplatin treatment have been evaluated.

275 redox status, and sensitized cancer cells to cisplatin treatment in patient-derived xenografts.

276 One of the pathways activated by cisplatin treatment is the cGAS/STING pathway.

277 This suggests that cisplatin treatment of cells expressing APOBEC3A should

278 Cisplatin treatment produced prolonged activation of pro

279 obal impact of miR-509-3p overexpression and cisplatin treatment we performed Reverse Phase Protein A

280 significantly induced apoptotic rates during cisplatin treatment with strongest induction of apoptosi

281 s setting to reduce the toxicity of standard cisplatin treatment, but no randomised evidence exists f

282 ttenuated several DNA repair processes after cisplatin treatment, including single-strand DNA repair

283 of MT2A expression could be observed during cisplatin treatment, indicating a cell line-specific and

284 NA, but despite its overexpression following cisplatin treatment, RPA is unable to fully protect ssDN

285 and prevented neuronal cell death following cisplatin treatment.

286 GULP1 knockdown cells showed resistance to cisplatin treatment.

287 own of MT expression may improve response to cisplatin treatment.

288 r stem cells, as well as tumor relapse after cisplatin treatment.

289 rowth rate of 1.5 vs. 13 in saline) and free cisplatin (tumor growth rate of 5.9) in mouse xenograft

290 ndings that indicate chemotherapies, such as cisplatin used to treat BRCA-deficient tumors, do not in

291 kidney chips) and for intravenously injected cisplatin (using coupled bone marrow, liver and kidney c

292 y between radiotherapy (RT) with concomitant cisplatin versus concomitant cetuximab in patients with

293 istolochic acid, and repeated acute low-dose cisplatin was also alleviated in PT-DsbA-L-KO mice via t

294 ndergoing treatment with the anticancer drug cisplatin were studied.

295 sistance to gemcitabine, 5-fluorouracil, and cisplatin, whereas AsPC-1 cells with ZIP4 knockdown had

296 knockdown increases cellular sensitivity to cisplatin, whereas its overexpression promotes drug resi

297 The treatment of cells with cisplatin, which blocks replication, causes a significan

298 fense by WEE1 inhibition in combination with cisplatin, which causes DNA damage, serves as a promisin

299 inical problem of PSCC is chemoresistance to cisplatin, which is induced by Pten deficiency on the ba

300 ological properties of Pt(IV) derivatives of cisplatin with estramustine at the first axial position,