ライフサイエンスコーパス: resistant cell

1 elevated uptake of (3)H-monensin compared to resistant cells.

2 nzyme, was reduced by DNA CpG methylation in resistant cells.

3 d variant SCLC subtypes as well as cisplatin-resistant cells.

4 activity constitutively elevated in the drug-resistant cells.

5 usly identified NKX3.1(+) luminal castration-resistant cells.

6 eeded to design future therapies that target resistant cells.

7 driving effects of Indomethacin in cisplatin-resistant cells.

8 potent activity against chemotherapeutically resistant cells.

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

10 tive cells to exploit their competition with resistant cells.

11 TGER4) is upregulated after demethylation in resistant cells.

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

13 ability to inhibit the proliferation of CIBM resistant cells.

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

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

16 enhancing NK cell cytotoxicity to cisplatin-resistant cells.

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

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

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

20 anslocation of S6K1 for binding with MDM2 in resistant cells.

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

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

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

24 ilization enhances cytotoxicity to multidrug-resistant cells.

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

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

27 titumoral effects of PI3Kalpha inhibition in resistant cells.

28 7 cells, but remained relatively constant in resistant cells.

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

30 partially restored tamoxifen sensitivity of resistant cells.

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

32 ansform into permanent and irreversible drug-resistant cells.

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

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

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

36 her candidate antioxidant genes in cisplatin-resistant cells.

37 not observed in LCC9 USP11-KD, antiendocrine-resistant cells.

38 rogen-independent expression of CHPT1 in Enz-resistant cells.

39 fts in mice, including that of MET inhibitor-resistant cells.

40 luding castration-resistant and enzalutamide-resistant cells.

41 etitive barriers that may slow the growth of resistant cells.

42 e separation that is also elevated in taxane-resistant cells.

43 ination (HR) repair was not altered in CHK1i-resistant cells.

44 f miR-522-3p was downregulated in paclitaxel-resistant cells.

45 er and particularly in chemotherapeutic drug-resistant cells.

46 Akt activity remained unchanged in inhibitor-resistant cells.

47 MAD1/5 and p21 upregulation in anti-estrogen-resistant cells.

48 nhibitor PLX51107 and RNA sequencing of BETi-resistant cells.

49 se to reconstruct the GRNs for sensitive and resistant cells.

50 ker of sensitivity to combination therapy in resistant cells.

51 f the most upregulated genes in enzalutamide-resistant cells.

52 es could be comprised of metastatic and drug resistant cells.

53 cells and found additional mutations in the resistant cells.

54 e both highly upregulated in the mesenchymal-resistant cells.

55 ificantly reduced the survival of paclitaxel-resistant cells.

56 ing is a deregulated pathway in enzalutamide-resistant cells.

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

58 Following doxorubicin treatment, resistant cells accumulated in S phase, which partially

59 AI-resistant cells activate endogenous cholesterol biosynth

60 e the de novo regulation of RD3 synthesis in resistant cells after IMCT.

61 Resistant cells also co-opt developmental pathways and d

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

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

64 n acquired metabolic phenotype common in ARI-resistant cells and associated with perturbed glucose an

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

66 etabolism were altered between sensitive and resistant cells and between breast cancer tissues (avail

67 th linsitinib blocked Erk5 activation in SCH-resistant cells and decreased their growth in 3D spheroi

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

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

70 previously reported VCP inhibitor (CB-5083) resistant cells and found additional mutations in the re

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

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

73 peutic agents affirmed RD3 loss in surviving resistant cells and residual tumors.

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

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

76 ABCB1 was upregulated in ICEC0942-resistant cells and there was cross-resistance to THZ1.

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

78 NF-kappaB signaling were upregulated in BETi-resistant cells, and the transcription factor CEBPD cont

79 lation of membrane transport pathways in the resistant cells, and these pathways may contribute to re

80 he Rho(High) BRAFi-resistant cell lines, and resistant cells are more sensitive to inhibition of thes

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

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

83 However, PARPi-resistant cells are remarkably more sensitive to ATRi wh

84 nly used variation on this approach, wherein resistant cells are selected by immediately exposing can

85 We demonstrate that erlotinib-resistant cells are sensitive to MAPK pathway inhibition

86 breast cancer cells and show that these drug-resistant cells are specifically sensitive to PERK inhib

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

88 9, 10, and 13 were as effective in cisplatin-resistant cells as wild-type cells, signifying that they

89 Analyses revealed that therapy-resistant cells associated with a mesenchymal dedifferen

90 ead to very large preexisting populations of resistant cells at the initiation of treatment.

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

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

93 Further analyses indicate that in resistant cells c-Myc enhances the expression of EZH2 by

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

95 , the selection, growth and dissemination of resistant cells can ultimately be fatal.

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

97 d cell proliferation and migration of CB-839-resistant cells compared with single inhibition of each

98 d genetic/molecular rearrangement in therapy-resistant cells contributes to tumor relapse.

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

100 due to detrimental effects of antibiotics on resistant cells, coupled with the inherently stochastic

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

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

103 ensitive cells increasing but growth of drug-resistant cells decreasing effective drug inhibition.

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

105 loss of RD3 mRNA and protein was observed in resistant cells derived from patients with PD after IMCT

106 Reconstitution of miR-3613-3p in resistant cells downregulated CDC7 expression and reduce

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

108 chemotherapy has not been effective as drug-resistant cells escape lethal DNA damage effects by indu

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

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

111 Our results demonstrated that Vemurafenib-resistant cells exhibited a persistent expression of CDC

112 y demonstrated the competing effects of drug-resistant cell expansion versus overall tumor regression

113 Intrinsically resistant cells exploited an integrated stress response,

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

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

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

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

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

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

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

121 In addition, the extent to which resistant cells harbor additional mutations in other gen

122 ing resistance plasmids, we show that single resistant cells have <5% probability of detectable outgr

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

124 Cisplatin-resistant cells, however, can demonstrate increased bind

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

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

127 ces the viability of prostate cancer-therapy-resistant cells in both CSCs and non-CSC populations.

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

129 cies were significantly up-regulated in 5-FU-resistant cells in MALDI-TOF analysis.

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

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

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

133 enin showed synergistic suppression of PARPi-resistant cells in vitro and in vivo in a xenograft EOC

134 d DNA damage were significantly lower in the resistant cells, indicating that decreased damage format

135 The decreased growth of drug-resistant cells induced by these nanoparticles was assoc

136 M metallopeptidase domain 10 (ADAM10) in the resistant cells induces an exclusive reduction in cleave

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

138 that the decreased Erk1/2 activation in SCH-resistant cells involved reduced expression and function

139 Survival of resistant cells is myosin II dependent, regardless of th

140 ntly, elevated c-Myc-miR-137-EZH2 pathway in resistant cells is sustained by dual oxidase maturation

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

142 c reprogramming in aromatase inhibitors (AI)-resistant cells, leading to Keratin-80 (KRT80) upregulat

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

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

145 2 or MDM4 by small interfering RNA in either resistant cell line induced p53 and restored p21 transac

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

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

148 other rhenium anticancer agents in the TRIP-resistant cell line were determined.

149 We developed the first Tsc2-null rapamycin-resistant cell line, ELT3-245, which is highly tumorigen

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

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

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

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

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

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

156 s dispensable for MYC expression in the most resistant cell lines and that MYC RNAi + BET bromodomain

157 pression of HER2 and beta-catenin pathway in resistant cell lines as compared to parent cells.

158 expression analyses of HER2 kinase inhibitor-resistant cell lines as compared to their drug-sensitive

159 ion and inhibited proliferation of tamoxifen-resistant cell lines as well as ex vivo-cultured ERalpha

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

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

162 was altered in adriamycin- and mitoxantrone-resistant cell lines demonstrating ABC-transporter upreg

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

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

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

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

167 d genetics strategy, we identified benzamide-resistant cell lines harboring a Thr238Ala mutation in b

168 analysis of BBDI responses in sensitive and resistant cell lines highlight significant heterogeneity

169 l ovarian carcinoma cisplatin-sensitive and -resistant cell lines identified eight analogues displayi

170 RNA-seq analysis of the anti-androgen resistant cell lines identified hyper-activation of the

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

172 aring expression profiles from sensitive and resistant cell lines revealed a TGFBR2 signaling axis th

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

174 Paclitaxel-resistant cell lines were established using two ovarian

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

176 d YAP1, are activated in the Rho(High) BRAFi-resistant cell lines, and resistant cells are more sensi

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

178 Thus, we also detail development of DTA-resistant cell lines, engineered through CRISPR/Cas9-med

179 sion levels are elevated in two enzalutamide-resistant cell lines, MR49F and C4-2R, indicating NOTCH

180 itive cell lines, and in 62.5%, 0% and 0% of resistant cell lines, respectively.

181 Mechanistic studies in endocrine resistant cell lines, suggest an ER-independent function

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

183 to additive anti-tumor activity in the most resistant cell lines.

184 viability in B-Raf inhibitor-sensitive and -resistant cell lines.

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

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

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

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

189 a DNA damage response in both sensitive and resistant cell lines; however, sensitive cell lines were

190 3 (VLN) and doxorubicin (Dox) on K562R (dox-resistant) cell lines.

191 We found that KA-resistant cells lose the WE but continue to conduct glyc

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

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

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

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

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

197 Under the assumption of only preexisting resistant cells or only persister evolution, it is not p

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

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

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

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

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

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

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

205 llenges to overcome treatment failure due to resistant cell populations.

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

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

208 Populations containing only resistant cells rapidly escape the threshold density, bu

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

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

211 Gboxin-resistant cells require a functional mitochondrial perme

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

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

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

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

216 f HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulati

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

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

219 estored expression impaired survival of drug-resistant cells, sensitized them to TKIs in vitro, and m

220 MEKi-resistant cells showed cross-resistance to the structura

221 TAE684-resistant cells showed greater sensitivity to HSP90 inhi

222 The paclitaxel-resistant cells showed stronger E2F2 expression than the

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

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

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

226 ncer function as important modulators of the resistant cell state.

227 or heterogeneity and lack of knowledge about resistant cell states remain a barrier to targeted cance

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

229 ressed in the chemotherapy- and radiotherapy-resistant cell subpopulations of many different cancer t

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

231 While therapeutic approaches targeting fully resistant cells, such as those harboring an EGFR(T790M)

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

233 sitivities, absent in therapy naive or fully resistant cells, suggesting the potential for new therap

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

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

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

237 y reported that some, but not all, multidrug-resistant cells that overexpressed various drug-resistan

238 pancreatic cancer stem cells, highly therapy-resistant cells that preferentially drive tumorigenesis

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

240 Notably, in enzalutamide-resistant cells, the expressions of both KDM8 and EZH2 a

241 tions that are genetically or phenotypically resistant cells, the latter known as persisters.

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

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

244 conversely, knockdown of SMARCA4 sensitized resistant cells to BETi.

245 Furthermore, exposure of enzalutamide-resistant cells to both PF-03084014 and enzalutamide inc

246 locks pathway reactivation, and resensitizes resistant cells to BRAF/MEK inhibitors, whereas expressi

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

248 er, we find that A3B knockdown re-sensitises resistant cells to cisplatin, and A3B knockout enhances

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

250 of c-Myc-miR-137-EZH2 pathway re-sensitizes resistant cells to cisplatin.

251 d H3K9me3 and H3K36me3 levels and sensitized resistant cells to CP.

252 Therefore, CHK1i sensitizes CHK1i-resistant cells to DNA damaging agents such as gemcitabi

253 nhibition of NOTCH signaling can resensitize resistant cells to enzalutamide.

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

255 ly, inhibiting c-Myc sensitizes enzalutamide-resistant cells to growth inhibition by enzalutamide.

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

257 n of HGF or MET restored sensitivity of MEKi-resistant cells to MEKi.

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

259 The restoration of miR-522-3p sensitized the resistant cells to paclitaxel, and its downregulation de

260 cells, while E2F2 inhibition sensitized the resistant cells to paclitaxel.

261 nhibition of the Wnt/beta-catenin sensitizes resistant cells to PARPi.

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

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

264 n of FOXO3 can reduce the sensitivity of the resistant cells to the PERK inhibitor GSK2606414, while

265 mitochondrial activity, sensitizing therapy-resistant cells to TKIs.

266 rations of CDC7 inhibitor TAK-931 sensitized resistant cells to Vemurafenib and reduced the number of

267 Suppressing PHGDH in MEKi-resistant cells together with MEKi treatment decreased o

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

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

270 mors share a common chromatin signature with resistant cells, undetectable using bulk approaches.

271 (2020) show that MEKi-resistant cells upregulate phosphoglycerate dehydrogenas

272 THZ1-resistant cells upregulated ABCG2 but remained sensitive

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

274 ROCK-myosin II ablation specifically kills resistant cells via intrinsic lethal reactive oxygen spe

275 4-5p and miR-211-5p occurring in vemurafenib-resistant cells was determined to impact vemurafenib res

276 2 inhibitors alone can activate p53 in these resistant cells was investigated with the goal to establ

277 AXL activation in resistant cells was mediated through increased expressio

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

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

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

281 By RNAi and RNA-seq in resistant cells, we found that the AS programs controlle

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

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

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

285 The ERKi-resistant cells were also resistant to vemurafenib (VMF)

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

287 Compared with sensitive cells, resistant cells were less glutaminolytic and, upon CB-83

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

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

290 fied schedules on the basis of the number of resistant cells where drug interactions and pharmacokine

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

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

293 time course experiments showed that the drug-resistant cells, which express lower expression and high

294 t differentiation-state aggregations of drug-resistant cells, which may be fundamental to the design

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

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

297 01-163 is also effective against osimertinib-resistant cells with L/T/C797S and L/T/L718Q EGFR mutati

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

299 Treatment of resistant cells with these thiosemicarbazones resulted i

300 several JMJD2 family genes upregulated in CP-resistant cells, with JMJD2B expression being upregulate