ライフサイエンスコーパス: resistant cell

1 7 cells, but remained relatively constant in resistant cells.

2 toxic agents and how they are deregulated in resistant cells.

3 potent activity against chemotherapeutically resistant cells.

4 partially restored tamoxifen sensitivity of resistant cells.

5 ing a novel set of target genes in tamoxifen-resistant cells.

6 ansform into permanent and irreversible drug-resistant cells.

7 ression by activating NF-kappaB in apoptosis-resistant cells.

8 ion profile of EGFR in TKI-sensitive and TKI-resistant cells.

9 on in sensitive cells was much lower than in resistant cells.

10 t strategies to combat the emergence of drug-resistant cells.

11 y cotargeting IGF-1R and HER2 in trastuzumab-resistant cells.

12 or PARP-1 increased cisplatin sensitivity in resistant cells.

13 as delayed in animals lacking IL-33 in radio-resistant cells.

14 nd limit in-vitro cell growth of vemurafenib-resistant cells.

15 1 and Trex1, are highly enriched in the 6-TG resistant cells.

16 , was significantly elevated in enzalutamide-resistant cells.

17 demonstrated specific activity in paclitaxel-resistant cells.

18 fer sensitivity to shear stress on otherwise resistant cells.

19 r regression due to the emergence of therapy-resistant cells.

20 ependent apoptotic cell death selectively in resistant cells.

21 STAT3 signaling is induced in BRAF-inhibitor-resistant cells.

22 a cells, wherein miR-137 is downregulated in resistant cells.

23 atin-induced apoptosis in acquired cisplatin-resistant cells.

24 invariably limited by the emergence of drug-resistant cells.

25 nced signaling and can sensitize Apo2L/TRAIL-resistant cells.

26 ion could be a significant trait of the drug-resistant cells.

27 ing attributed to a growing fraction of drug-resistant cells.

28 and clonogenic survival of both trastuzumab-resistant cells.

29 se (UGT1A) family of enzymes are elevated in resistant cells.

30 this information to more effectively target resistant cells.

31 h were significantly upregulated in the CDDP-resistant cells.

32 estored by introduction of a WDR85 cDNA into resistant cells.

33 vivin restored sensitivity to trastuzumab in resistant cells.

34 was analysed after the selection of anoikis-resistant cells.

35 n2 mRNA and protein levels compared with PDT-resistant cells.

36 tumors derived from cisplatin-sensitive and -resistant cells.

37 manipulated to resurrect ATRA sensitivity to resistant cells.

38 the invariably rapid emergence of stem-like resistant cells.

39 macrophage pool was delayed in the apoptosis-resistant cells.

40 l prognoses, tumor metastases, and multidrug resistant cells.

41 (mC46) as the means for developing infection-resistant cells.

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

43 levels, triggering apoptosis of trastuzumab-resistant cells.

44 WEE1 and CHK1 occurred commonly in cisplatin-resistant cells.

45 uced cell death in both parental and ABT-737-resistant cells.

46 tive cells to exploit their competition with resistant cells.

47 TP and improves IFNalpha response in insulin-resistant cells.

48 TGER4) is upregulated after demethylation in resistant cells.

49 to CIBM, but also the proliferation of CIBM resistant cells.

50 ability to inhibit the proliferation of CIBM resistant cells.

51 aling could increase GC-induced apoptosis in resistant cells.

52 nation, which was also effective in imatinib-resistant cells.

53 enhancing NK cell cytotoxicity to cisplatin-resistant cells.

54 was induced after co-culture with cisplatin-resistant cells.

55 eeded to design future therapies that target resistant cells.

56 d by proteasomal degradation of EZH2 in drug-resistant cells.

57 ssion, followed by the eventual outgrowth of resistant cells.

58 driving effects of Indomethacin in cisplatin-resistant cells.

59 stance but acts as a tumor suppressor in TAM-resistant cells.

60 ns, with a similar potency observed for drug-resistant cells.

61 R calcium ATPase 2b (SERCA2b) function in AI-resistant cells.

62 ilization enhances cytotoxicity to multidrug-resistant cells.

63 ates revealed higher potency than MTX on MTX-resistant cells.

64 entify any acquired mutations in FLT3 in the resistant cells.

65 titumoral effects of PI3Kalpha inhibition in resistant cells.

66 ratin-19 (Krt19) marks long-lived, radiation-resistant cells above the crypt base that generate Lgr5(

67 AI-resistant cells activate endogenous cholesterol biosynth

68 , dual stimulation of NOD1 and TLR4 in radio-resistant cells alone was sufficient to mobilize HSCs, w

69 Resistant cells also acquired a TP53BP1 mutation that fa

70 Resistant cells also co-opt developmental pathways and d

71 nce of extinction-susceptible and extinction-resistant cells also suggests that the PAG plays a role

72 and GLI2 restored sensitivity to vemurafenib-resistant cells, an effect associated with both growth a

73 (Gamitrinib), which eradicated intrinsically resistant cells and augmented the efficacy of MAPKi by i

74 promoted the survival of aromatase inhibitor-resistant cells and elicited resistance in aromatase inh

75 restored the efficacy of SAIT301 in SAIT301-resistant cells and enhanced the efficacy in SAIT301-sen

76 able to restore differentiation in some ATRA-resistant cells and eradicate leukemia-initiating cells

77 o investigate miRNA/mRNA interactions in TMZ-resistant cells and has potential to identify drug resis

78 n human foreskin fibroblasts and WI-38 TRAIL-resistant cells and marginally sensitive MRC-5 cells com

79 The endogenous loss of EZH2 expression in resistant cells and primary blasts from a subset of rela

80 ta3 decreased AKT phosphorylation in SAIT301-resistant cells and restored SAIT301 responsiveness in H

81 3 induced substantial apoptosis in sorafenib-resistant cells and showed better survival benefits than

82 rongest changes was also induction of IL6 in resistant cells and the expression was further increased

83 Both the resistant cells and tumors from AI-resistant patients sh

84 very limited cross-resistance to nifurtimox-resistant cells and vice versa.

85 l structure amplifies the fitness penalty of resistant cells, and identifies their relative fitness a

86 ractory glioblastoma specimens, temozolomide-resistant cells, and resistant-xenograft models, we repo

87 2-sensitive cells, heavily methylated in the resistant cells, and reverted to low methylation in the

88 Our data indicate that cytarabine-resistant cells are more susceptible to natural killer (

89 mation or cell survival, suggesting that the resistant cells are no longer FLT3 dependent.

90 were to determine whether both sensitive and resistant cells are present in prostate cancers originat

91 wherein the continued growth of preexistent resistant cells are responsible for progression.

92 (VLA-4) activation and cooperation in shear-resistant cell arrest on VCAM-1 are ill defined.

93 fectively inhibit the growth of Enzalutamide-resistant cells as well as block the transcriptional act

94 9, 10, and 13 were as effective in cisplatin-resistant cells as wild-type cells, signifying that they

95 Selective sweeps, in which resistant cells become dominant in the population, are a

96 of breast cancer cells, including paclitaxel-resistant cells, blocked their invasion and proliferatio

97 stem-cell (CSC) fraction within trastuzumab-resistant cells both in vitro and in vivo.

98 eutic strategy to help destroy residual drug-resistant cells but also provides a sensitive imaging me

99 ss-resistance to radiation in EGFR inhibitor-resistant cells by modulating cell-cycle progression and

100 evels were substantially higher in CEM-C1-15-resistant cells, c-Jun was significantly induced in sens

101 These results indicate both susceptible and resistant cells can evolve within the same tumor.

102 In apoptosis-resistant cells, cFLIP restricts caspase-8 activity, res

103 inase (MAPK) kinase (MEK) phosphorylation in resistant cells compared with parental cells.

104 ned Herceptin-Her2 interactions in Herceptin-resistant cells, compared to those in Herceptin-sensitiv

105 improve antitumor activity against a therapy-resistant cell compartment.

106 Mechanistic investigations showed that resistant cells coordinately upregulated expression of c

107 We found that PI3K inhibitor (PI3Ki)-resistant cells cultured in the absence of PI3Ki develop

108 Targeting EPHA2 in erlotinib-resistant cells decreased S6K1-mediated phosphorylation

109 Furthermore, PLX-4032-resistant cells demonstrated collateral resistance to co

110 with mice orthotopically implanted with ENZA-resistant cells demonstrated that the combination of ENZ

111 The osmotic stress resistant cells developed a RVI response, and inhibition

112 Resistant cells display a spectrum of phenotypical chang

113 In resistant cells, dsRNA receptor overexpression restored

114 Thus, the proliferative defect of PI3Ki-resistant cells during drug holidays is caused by defect

115 heir resistant counterparts, indicating that resistant cells escaped drug treatments through one or m

116 lerant cells serve as a reservoir from which resistant cells eventually emerge, inhibiting the pathwa

117 Resistant cells exhibited attenuation in the formation o

118 Intrinsically resistant cells exploited an integrated stress response,

119 expression profiling of drug-sensitive and -resistant cells expose targetable metabolic changes and

120 RNA sequencing revealed that resistant cells express FGFR3-TACC3 fusion proteins, whi

121 In vitro, paclitaxel-resistant cells expressed higher SYK, and the ratio of p

122 e show that, aside from a finite fraction of resistant cell-free patients, the maximal response in su

123 a recombinant vaccinia virus to replicate in resistant cells from humans and other primates.

124 These results were confirmed in T-DM1-resistant cells from patient-derived HER2(+) samples.

125 IL-8 knockdown inhibits tamoxifen-resistant cell growth and invasion and partially attenua

126 mpairs cell survival and abolishes tamoxifen-resistant cell growth.

127 In resistant cells, GSN was highly expressed and CDDP faile

128 This relies on the assumption that resistant cells have impaired cellular fitness.

129 ents is a small preexisting subpopulation of resistant cells; however, little is known about the gene

130 so decreasing the proportion of chemotherapy-resistant cells identified by high ALDH activity.

131 Genotyping of resistant cells identified gene amplification of EGFR, K

132 g susceptible cells, drug tolerant, and drug resistant cells in less than 12h.

133 ents the formation of drug-tolerant and drug-resistant cells in Mtb cultures.

134 to hijack the biosynthetic rewiring of drug-resistant cells in response to antibiotics.

135 s the fitness disadvantage displayed by drug-resistant cells in the absence of the drug, forestalls t

136 tumor cells causes increased growth of drug-resistant cells in the population through a mechanism in

137 ding NB4 cells) and restores it in some ATRA-resistant cells (including NB4-LR1 cells).

138 vo Conversely, silencing their expression in resistant cells inhibited cell growth.

139 ed 14-3-3sigma expression in the gemcitabine-resistant cells is due to demethylation of the 14-3-3sig

140 Examples of putative treatment-resistant cells isolated in small topographical areas ar

141 bust tumor growth inhibition in a crizotinib-resistant cell line (H3122-L1196M).

142 er cell lines, and, importantly, a cisplatin resistant cell line EJ-R.

143 e was validated prospectively in a tamoxifen-resistant cell line generated by long-term drug treatmen

144 ellent inhibition of cell growth in the drug-resistant cell line H1975, without significantly affecti

145 lore the mechanism, we selected an erlotinib-resistant cell line in which the guanine nucleotide exch

146 2 or MDM4 by small interfering RNA in either resistant cell line induced p53 and restored p21 transac

147 We generated a broad panel of BRAF-mutant resistant cell line models across seven different clinic

148 in an acute myeloid leukemia (AML) sensitive/resistant cell line pair.

149 ell line CH1 and the intrinsically cisplatin resistant cell line SW480, with a set of four descriptor

150 lines and a better activity on one cisplatin-resistant cell line than cisplatin itself.

151 ance pathways in myeloma we generated an ATO-resistant cell line, 8226/S-ATOR05, with an IC50 that is

152 PSP94 is decreased in an ovarian cancer drug-resistant cell line, and plays an important role in the

153 cells, and compared the results with a drug resistant cell line, HCC1954.

154 CFT in antifolate resistance, a methotrexate-resistant cell line, M160-8, was selected from a HeLa su

155 cytotoxicity assay with NCI/ADR-RES, a drug resistant cell line, suggested that PEG5K-Fmoc-VE2 may h

156 reproducible classification of sensitive and resistant cell line-drug pairs, with 85% accuracy.

157 ing that was attenuated in the acquired drug resistant cell line.

158 s independent of reactivation of ERK in many resistant cell lines and clinical samples.

159 ian cancer, A2780 and the related paclitaxel-resistant cell lines and did not cause cytotoxicity, as

160 be equipotent on chloroquine-sensitive and -resistant cell lines and on both blood and liver stage f

161 Upregulation of EGFR was observed in BRAFi-resistant cell lines and patient tumors because of demet

162 imulate VSV replication and oncolysis in all resistant cell lines but only partially improve the susc

163 Interestingly, analysis of signaling in resistant cell lines demonstrated that FGFR3-TACC3 fusio

164 ighly responsive to FLT3 inhibitors, whereas resistant cell lines display resistance to multiple FLT3

165 All ALK inhibitor resistant cell lines displayed significant cross-resista

166 Tubulin-binding agent-resistant cell lines displayed the highest flubendazole

167 ed by normalization of p53 stability in both resistant cell lines grown at the permissive temperature

168 phenotype (p = 0.036, Chi square test), and resistant cell lines harbored methylation of the ALPi pr

169 Investigating the mechanistic anomalies in resistant cell lines is of therapeutic significance and

170 the P-glycoprotein-overexpressing multi-drug-resistant cell lines NCI/ADR-RES and Messa/Dx5.

171 ay in this system, while most BRAF inhibitor-resistant cell lines showed intact MAPK pathway activity

172 14a revealed that potency against multidrug-resistant cell lines was compromised by increased polari

173 against the sensitive and Pgp overexpressing resistant cell lines was found to correlate directly wit

174 Resistant cell lines were significantly enriched for tho

175 as not significantly changed in several drug-resistant cell lines with activated P-glycoprotein drug

176 whereas this combination was ineffective in resistant cell lines with low OxPhos.

177 rmacology and its activity against multidrug-resistant cell lines, 23r was identified as a potential

178 lting approximately 10-fold more vemurafenib-resistant cell lines, A375rVem and D443rVem, had higher

179 artially overcome resistance in several drug-resistant cell lines, and they were not substrates for t

180 Gene expression analysis of sensitive and resistant cell lines, as well as of blasts from patients

181 cytarabine in order to establish equivalent resistant cell lines, HL-60(R) and KG-1(R).

182 n induced ALPi promoter-reporter activity in resistant cell lines, KLF5 knockdown attenuated butyrate

183 hrough microarray profiling of sensitive and resistant cell lines, we identified KLF5 to be both basa

184 Through characterization of novel K5I-resistant cell lines, we unveil an Eg5 motility-independ

185 t of candidate therapies across the panel of resistant cell lines.

186 of FLT3 signaling by sorafenib in otherwise resistant cell lines.

187 s-of-function mutations in Dck in both Ara-C resistant cell lines.

188 mutant drug-sensitive and five matched drug-resistant cell lines.

189 ssion, and a series of naturally gemcitabine-resistant cell lines.

190 ed its cytotoxic potential in the bortezomib resistant cell lines.

191 ntial against Triapine-sensitive as well as -resistant cell lines.

192 nd tumor formation, and induced apoptosis in resistant cell lines.

193 differed in estrogen-sensitive and estrogen-resistant cell lines.

194 3 (VLN) and doxorubicin (Dox) on K562R (dox-resistant) cell lines.

195 ranging from 5 to 10 nM) including all drug resistant cell-lines.

196 show that, following irradiation, apoptosis-resistant cells lose their identity and translocate to a

197 Finally, we demonstrated that vemurafenib-resistant cells maintain their addiction to the MAPK pat

198 NT reversed the characteristics of cisplatin-resistant cells, making these cells cisplatin-sensitive,

199 These data highlight the concept that drug-resistant cells may also display drug dependency, such t

200 In ABT-737-resistant cells, Mcl-1 co-immunoprecipitated with BAG3,

201 f signaling network activity observed in the resistant cells mirrored the patterns of response to sev

202 We found cisplatin-resistant cells more resistant to NK cell cytotoxicity t

203 l division, and the metabolic phenotype made resistant cells more sensitive to hydrogen peroxide and

204 oreover, CXCL8 and CXCL1 gene silencing made resistant cells more sensitive to OXA through the inhibi

205 Although gossypol was effective only in resistant cells, obatoclax induced cell death in both pa

206 cated both radiation-sensitive and radiation-resistant cells of the joint tissue in the proarthritic

207 ddition, silencing MUC1-C in the trastuzumab-resistant cells or treatment with GO-203 decreased p-HER

208 In BRAFi-resistant cells, PAKs phosphorylate CRAF and MEK to reac

209 of oestrogen receptors alpha (ERalpha) in AI-resistant cells, partly via the biosynthesis of 27-hydro

210 Proliferation of newly derived CaCCinh-A01-resistant cell pools was not affected by CaCCinh-A01 as

211 s that generate tumor heterogeneity and drug-resistant cell population are still unfolding.

212 g pathways blunted the outgrowth of the drug-resistant cell population in BRAF mutant human melanoma,

213 sient generation of an anti-androgen therapy-resistant cell population, suggesting that ERG may have

214 ease and identify T2M cells as a new steroid-resistant cell population.

215 of localized environmental niches where drug-resistant cell populations can evolve and survive.

216 Compared with parental cells, a number of resistant cell populations were more sensitive to inhibi

217 tion of intratumor heterogeneity and disease-resistant cell populations, that may ultimately unveil n

218 elps drive the selection for diverse therapy-resistant cell populations.

219 henotype, despite the latter contributing to resistant cells' proliferation.

220 Despite the lack of BRCA1, PARPi-resistant cells regain RAD51 loading to DNA double-stran

221 We determined that intrinsically resistant cells rely on the genes encoding TFAM, which c

222 ated with PKM2 overexpression, and cisplatin-resistant cells respond sensitively to shikonin.

223 f FGFR1 and downstream MAPK effectors; these resistant cells responded synergistically to combinatori

224 t signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness.

225 RNA-mediated knockdown of isoform 2 in BRAFi resistant cells restored sensitivity to BRAFi compared w

226 inhibition, whereas its suppression in drug-resistant cells restores partial sensitivity, a correlat

227 Use of the anti-Gli1 shRNA in cisplatin-resistant cells resulted in a block of the cell's abilit

228 NAi-mediated depletion of SMO or GLI1 in the resistant cells resulted in reduced proliferation, clono

229 alteration acquired upon drug pressure, most resistant cells retained sensitivity to vertical MAPK pa

230 Protein synthesis was increased in drug-resistant cells, secondary to a Pim-mediated increase in

231 els below the viability threshold, and kills resistant cells selectively over cells that lack ABCG2 t

232 The 5th and 10th PDT-resistant cells showed an amplicon in 5q11.2 MAP3K1, whi

233 TAE684-resistant cells showed greater sensitivity to HSP90 inhi

234 t cancer cells in a high mesenchymal therapy-resistant cell state are dependent on the lipid hydroper

235 cular basis for this 'alternative' treatment-resistant cell state remain incompletely understood.

236 Here we show that a similar therapy-resistant cell state underlies the behaviour of persiste

237 he most tumorigenic, metastatic, and therapy-resistant cell subpopulation within human tumors, curren

238 tered in combination to prevent emergence of resistant cell subpopulations.

239 f DDX18 directly affects growth of tamoxifen-resistant cells, suggesting that it may be a critical do

240 Given SGK3 inhibition reduces AI-resistant cell survival by eliciting excessive EnR stres

241 shown to induce greater cytotoxicity against resistant cells than their nonresistant counterparts.

242 ical contributor to the tolerance of therapy-resistant cells that arise as a consequence of transient

243 neously arising resistance mechanisms occur: resistant cells that cannot become infected and resistan

244 ces a strategy to kill selectively multidrug-resistant cells that express the ABCG2 transporter (also

245 C-chemokines, CXCL8, CXCL1 and CXCL2, in the resistant cells that were more efficiently down-regulate

246 show a consistent pattern in populations of resistant cells, there were several cases where exposure

247 induced PI3K/AKT pathway activation in BRAFi-resistant cells through epigenetic regulation.

248 GSH levels, and that GO-203 resensitizes BTZ-resistant cells to BTZ treatment by synergistically down

249 and to restore the sensitivity of ribociclib-resistant cells to CDK4/6 inhibitors.

250 targeting this pathway could sensitize drug-resistant cells to chemotherapy.

251 NT, resulting in the resensitization of drug-resistant cells to cisplatin, was observed.

252 nced Bax activation and sensitized otherwise resistant cells to cisplatin-induced apoptosis.

253 We used antiestrogen-sensitive and -resistant cells to determine the effect of antiestrogens

254 mRNA degradation); it sensitized doxorubicin-resistant cells to doxorubicin (as shown by reduced prol

255 nhibitor, or STAT3-specific siRNA sensitized resistant cells to gefitinib.

256 sing ST6Gal-I activity sensitizes inherently resistant cells to gemcitabine.

257 rmore, we can estimate the time required for resistant cells to grow to detectable levels.

258 The response of resistant cells to high concentrations of cisplatin reve

259 served increased susceptibility of cisplatin-resistant cells to NK cell cytotoxicity when neutralizin

260 of CREB1 phosphorylation potently sensitized resistant cells to platinum therapy and was effective in

261 ia, is a cooperative behavior that can allow resistant cells to protect sensitive cells from antibiot

262 ific inhibitors significantly sensitized the resistant cells to the IGF1R antibody.

263 axis restored the sensitivity of vemurafenib-resistant cells to vemurafenib.

264 ear accumulation and less drug efflux in the resistant cells treated by DLMC+US than those treated by

265 eduction of P-glycoprotein expression in the resistant cells treated with DLMC+US compared with the c

266 h it is unnecessary to invoke special damage-resistant cell types such as stem cells.

267 ncer agents for collateral sensitivity among resistant cells, uncovering possibilities for further tr

268 E requires activation of IL-1R1 on radiation-resistant cells via IL-1beta secreted by bone marrow-der

269 wed how after pretreatment only species with resistant cell walls, such as diatoms, continued to be p

270 of Platin-M and its targeted-NP in cisplatin-resistant cells was correlated with the hyperpolarizatio

271 4-5p and miR-211-5p occurring in vemurafenib-resistant cells was determined to impact vemurafenib res

272 AXL activation in resistant cells was mediated through increased expressio

273 nes, and knockdown of HOXB7 and HOXA9 in the resistant cells was sufficient to improve sensitivity to

274 RNA sequencing of the resistant cells was used to examine (i) emergence of gen

275 To generate cetuximab-resistant cells, we exposed cetuximab-sensitive colorect

276 iments with inhibitor-sensitive or inhibitor-resistant cells, we uncover Midasin's role in assembling

277 the impedance change between susceptible and resistant cells were 8971+/-1515 Omega and 3281+/-429 Om

278 Resistant cells were able to maintain a high level of H3

279 ent mice showed that the tumors generated by resistant cells were bigger than those induced by parent

280 o mesenchymal transition properties of BRAFi-resistant cells were enhanced significantly.

281 Resistant cells were exquisitely sensitive to MEK inhibi

282 to cisplatin treatment of both sensitive and resistant cells were minimal, indicating the importance

283 on Th17 cells and LTbetaR on meningeal radio-resistant cells were necessary for the propagation of de

284 The resistant cells were potentially incapable of developing

285 an unexpected secondary NRAS Q61K mutation; resistant cells were sensitive to concurrent EGFR and ME

286 tment effectively blocked FLT3 activation in resistant cells, whereas it was unable to block colony f

287 human cancer cell lines, including cisplatin-resistant cells, whereas it was up to 100-fold less acti

288 Chromatin-bound BRD4 is globally reduced in resistant cells, whereas the expression of key target ge

289 IR-resistant cells, which are efficient at DSB repair, cont

290 utive and immunoproteasome were increased in resistant cells, which correlated to an increase in subu

291 that phosphorylation of BMK1 was enhanced in resistant cells, which suggested an association of BMK1

292 s silenced in plasmid-containing, antibiotic-resistant cells, while part of the population undergoes

293 ysplasia and carcinoma, as well as apoptosis-resistant cells with DNA damage.

294 Notably, all selumetinib-resistant cells with elevated OxPhos could be resensitiz

295 Comparing resistant cells with parental counterparts, 18-91 coding

296 Notably, treatment of resistant cells with PI3K inhibitors decreased SMO and G

297 Treatment of vemurafenib-resistant cells with the GLI1/GLI2 inhibitor Gant61 led

298 Treatment of resistant cells with the HSP90 inhibitor 17-dimethylamin

299 Treatment of resistant cells with these thiosemicarbazones resulted i

300 l damage and subsequent cytotoxicity in drug-resistant cells, with Dp44mT being demonstrated to be a