ライフサイエンスコーパス: EGFR inhibitor

1 from 25 CRC patients receiving cetuximab (an EGFR inhibitor).

2 progresses during treatment with an initial EGFR inhibitor.

3 oursphere formation and improves efficacy of EGFR inhibitor.

4 n during previous treatment with an existing EGFR inhibitor.

5 treated in combination with the originating EGFR inhibitor.

6 Adverse events were those expected with an EGFR inhibitor.

7 kin toxicities in patients with mCRC for any EGFR inhibitor.

8 evelopment of T790M during treatment with an EGFR inhibitor.

9 s one strategy to address NSCLC resistant to EGFR inhibitors.

10 l746-750, T790M/L858R, and T790M/del746-750) EGFR inhibitors.

11 treatment of tumors resistant to traditional EGFR inhibitors.

12 f EGFR phosphorylation, and sensitization to EGFR inhibitors.

13 t in compromised autophagy when treated with EGFR inhibitors.

14 egarding the sensitivity of these tumours to EGFR inhibitors.

15 characteristics associated with response to EGFR inhibitors.

16 ved from Jak2/Tyk2 inhibitors into selective EGFR inhibitors.

17 been more evident than in the development of EGFR inhibitors.

18 ly for selecting patients for treatment with EGFR inhibitors.

19 enge of killing tumors that are resistant to EGFR inhibitors.

20 ncreased EGFR expression sensitized cells to EGFR inhibitors.

21 ategy may be useful in sensitizing HNSCCs to EGFR inhibitors.

22 d in the design of more potent and selective EGFR inhibitors.

23 clin D1 expression also causes resistance to EGFR inhibitors.

24 atients with colorectal cancer refractory to EGFR inhibitors.

25 ties are the most common adverse events with EGFR inhibitors.

26 iably predictive of therapeutic responses to EGFR inhibitors.

27 T) as a determinant of sensitivity of HCC to EGFR inhibitors.

28 de superior tumor control when combined with EGFR inhibitors.

29 n causes resistance against third-generation EGFR inhibitors.

30 dimerization, both of which are abolished by EGFR inhibitors.

31 tivity of the gold standard third-generation EGFR inhibitors.

32 ance exhibited by certain cancer patients to EGFR inhibitors.

33 tor, or an epidermal growth factor receptor (EGFR) inhibitor.

34 ghten therapeutic responses to EGF receptor (EGFR) inhibitors.

35 ponsive to epidermal growth factor receptor (EGFR) inhibitors.

36 (T790M/L858R and T790M/del746-750) selective EGFR inhibitor (2) as a starting point, activities again

37 Rociletinib (CO-1686) is an EGFR inhibitor active in preclinical models of EGFR-muta

38 itinib, an epidermal growth factor receptor (EGFR) inhibitor, added to, and in maintenance after, con

39 cells (PCSC) and its components using a pan-EGFR inhibitor afatinib in combination with gemcitabine.

40 ing is elevated in FLCN(-/-) tumours and the EGFR inhibitor afatinib suppresses the growth of human F

41 titatively contribute to the response of two EGFR inhibitors (afatinib and lapatinib).

42 heparin-bound (HB)-EGF inhibitor CRM 197, or EGFR inhibitor AG 1478.

43 ctor receptor (EGFR) in these cells, and the EGFR inhibitor AG1478 attenuated the increased SphK1 and

44 The EGFR inhibitor AG1478 blocked the subsequent effects of

45 this effect was blocked in MIN6 cells by the EGFR inhibitor AG1478 or the mTOR inhibitor rapamycin.

46 iferation in culture can be blocked with the EGFR inhibitor AG1478.

47 in, or the epidermal growth factor receptor (EGFR) inhibitor AG1478 blocks FXII-induced phosphorylati

48 atment with a COX-2 inhibitor (NS-398) or an EGFR inhibitor (AG1478) exacerbated Jo2-mediated liver i

49 nondiabetic (control) mice were treated with EGFR inhibitor (AG1478; 10 mg x kg(-1) x day(-1)) for 2

50 In the presence of EGFR inhibitor, AG1478, CS-induced histopathology and mo

51 ined potent activity in tumors refractory to EGFR inhibitor alone.

52 owever, results from clinical trials testing EGFR inhibitors, alone or in combination with cytotoxic

53 reversible epidermal growth factor receptor (EGFR) inhibitors, alone or in combination with MET-kinas

54 atients with hypoxic tumors may benefit from EGFR inhibitors already available in the clinic.

55 Treatment with AG1478, an EGFR inhibitor, also significantly increased the number

56 tive cotreatment of lung tumor cells with an EGFR inhibitor and a BH3 mimetic eradicated early TKI-re

57 resistance and may benefit from a dual HER3-EGFR inhibitor and a PARP1 inhibitor.

58 This novel mechanism of pan-EGFR inhibitor and its ability to eradicate CSC may serv

59 deletion further sensitizes glioma cells to EGFR inhibitors and extends the lifespan of animals.

60 in the development of acquired resistance to EGFR inhibitors and offer preclinical proof-of-concept t

61 Monensin acts synergistically with EGFR inhibitors and oxaliplatin to inhibit cell prolifer

62 in the development of acquired resistance to EGFR inhibitors and prompt consideration to apply p53 re

63 eduling of treatment with the combination of EGFR inhibitors and radiation and suggest that EGFR inhi

64 indicate that p53 may enhance sensitivity to EGFR inhibitors and radiation via induction of cell-cycl

65 egies in future clinical trials that combine EGFR inhibitors and radiation.

66 and found a reduction in sensitivity to both EGFR inhibitors and radiation.

67 at of aminopyrimidine-based third-generation EGFR inhibitors and therefore constitutes a new set of i

68 mechanisms of lung cancer cell resistance to EGFR inhibitors and to assess effects of combined drug t

69 n and Raman signature of skin in the case of EGFR inhibitors and viable epidermis skin layer.

70 eated with epidermal growth factor receptor (EGFR) inhibitors and ALK inhibitors, respectively.

71 afatinib (epidermal growth factor receptor (EGFR) inhibitor) and YM155 (inhibitor of baculoviral inh

72 e and allowed to heal +/- Tyrphostin AG1478 (EGFR inhibitor), and assayed for EGFR activation and EGF

73 ted kinase switch that induces resistance to EGFR inhibitors, and identify a low ratio of MIG6 to miR

74 efficiency similar to metalloproteinase and EGFR inhibitors, and induced several markers of KC diffe

75 n HNSCC autophagy machinery that responds to EGFR inhibitors, and suggest potential combinatorial app

76 Third-generation EGFR inhibitors are generally preferred for patients wit

77 However, EGFR inhibitors are ineffective in these patients, and t

78 However, clinical responses to EGFR inhibitors are infrequent and short-lived.

79 ance inevitably develops, and more effective EGFR inhibitors are needed.

80 sms in EGFR and the toxicity and efficacy of EGFR inhibitors are warranted.

81 EGFR inhibitors are worthy of testing against ER-positiv

82 Because oncogene MET and EGF receptor (EGFR) inhibitors are in clinical development against sev

83 Epidermal growth factor receptor (EGFR) inhibitors are increasingly used in combination wi

84 oaches to attenuation of IL6 yielded AKT and EGFR inhibitors as enhancers of the inhibitory monoclona

85 n solution, to design novel and irreversible EGFR inhibitors based on a screening hit that was identi

86 Our findings suggest that treatment with an EGFR inhibitor before cisplatin would be antagonistic, a

87 EGF receptor (EGFR) inhibitors block osteolytic bone metastasis by tar

88 EGFR inhibitor blocked induction of phospho-ERK, showing

89 ransformants showed increased sensitivity to EGFR inhibitors both in vitro and in an in vivo xenograf

90 ules significantly increased the efficacy of EGFR inhibitors both in vitro and in vivo.

91 tor receptor (EGFR) is sensitive to approved EGFR inhibitors, but resistance develops, mediated by th

92 Here we identify a covalent pyrimidine EGFR inhibitor by screening an irreversible kinase inhib

93 e binding motif as a new structural class of EGFR inhibitors by a target hopping approach from p38alp

94 ation by IGFBP-3-Fc enhances the activity of EGFR inhibitors by decreasing cell survival and inhibiti

95 c lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual dis

96 et or a fast-food diet (FFD) with or without EGFR inhibitor (canertinib) for 2 months.

97 F mutations in predicting sensitivity to the EGFR inhibitor cetuximab.

98 py and the epidermal growth factor receptor (EGFR) inhibitor cetuximab improves clinical outcome in c

99 py and the epidermal growth factor receptor (EGFR) inhibitor cetuximab shows an improved response in

100 at higher concentrations of the irreversible EGFR inhibitor CL-387,785 are required to inhibit EGFR p

101 ationale for clinical trials testing Akt and EGFR inhibitor co-treatment in patients with elevated ph

102 The OSU-03012/EGFR inhibitor combination induced pronounced apoptosis

103 kt and ER stress pathways with the OSU-03012/EGFR inhibitor combination represents a unique approach

104 In keratinocytes treated solely with the EGFR inhibitor, complement activation was dependent on s

105 reversible epidermal growth factor receptor (EGFR) inhibitors contain a reactive warhead which covale

106 tment with epidermal growth factor receptor (EGFR) inhibitors continues to grow.

107 Importantly, attenuation of BTIC growth by EGFR inhibitors could be overcome by activation of neuro

108 found that MEHD7945A, but not single target EGFR inhibitors, could inhibit tumor growth and cell-cyc

109 hypomethylated EGFR status may benefit from EGFR inhibitors currently used in the clinic.

110 For MEK and EGFR inhibitors, discriminative power was more than 90%

111 how a novel link between erlotinib, a potent EGFR inhibitor, DNA damage, and homology-directed recomb

112 as well as primary resistance to reversible EGFR inhibitors driven by a subset of EGFR mutations, wi

113 glioblastoma following administration of the EGFR inhibitor drug of Erlotinib.

114 milar to the rash seen in patients receiving EGFR inhibitor drugs.

115 istance compromises the clinical efficacy of EGFR inhibitors during long-term treatment.

116 cation of anti-dynorphin, KOR antagonist, or EGFR inhibitor effectively reduces axon extension of DRG

117 wer in KOR-null (KOR(-/-)) spinal cords, and EGFR inhibitors effectively reduce the levels of KOR, GA

118 is minimal, and known predictive factors for EGFR inhibitor efficacy are infrequent in this disease.

119 ivation of the EGFR pathway is predictive of EGFR inhibitor efficacy.

120 ss of tyrosine kinase inhibitors such as the EGFR inhibitor (EGFRi), osimertinib, in non-small cell l

121 mination of MET and EGFR signaling [MET KO + EGFR inhibitor (EGFRi)], but not individual disruption,

122 ny patients with HNSCC respond poorly to the EGFR inhibitors (EGFRI) cetuximab and erlotinib, despite

123 R-activating mutations respond clinically to EGFR inhibitors (EGFRIs), suggests that responsive tumor

124 Erlotinib, a selective EGFR inhibitor, enhanced AQP2 apical membrane expression

125 rthermore, we show that a single dose of the EGFR inhibitor erlotinib delivered prior to DEN-induced

126 atment of Vil-Cre;Nf2(lox/lox) mice with the EGFR inhibitor erlotinib halted the proliferation of tum

127 (ELP) complex mediates insensitivity to the EGFR inhibitor erlotinib in TNBC cells by promoting the

128 d SQ20B cells to cell killing induced by the EGFR inhibitor Erlotinib in vitro.

129 n waved-2 mutant mice) or treatment with the EGFR inhibitor erlotinib increased mobilization.

130 or intravitreal injection of TIMP3 or of the EGFR inhibitor erlotinib influenced the outcome of OIR.

131 stance, we undertook a phase II trial of the EGFR inhibitor erlotinib with whole-brain radiation ther

132 ion of some identified molecular ions of the EGFR inhibitor erlotinib, a phosphatidylcholine lipid, a

133 YAP sensitizes non-small cell lung cancer to EGFR inhibitor Erlotinib.

134 gic airway disease and then treated with the EGFR inhibitor Erlotinib.

135 F receptor (EGFR) expression or by using the EGFR inhibitor erlotinib.

136 EGFR levels at the plasma membrane, and the EGFR inhibitors erlotinib and AG1478, as well as Akt and

137 xenografted at surgery were treated with the EGFR inhibitors erlotinib and cetuximab and analyzed for

138 KRAS mutation and radiosensitization by the EGFR inhibitors erlotinib and cetuximab.

139 correlated with impressive responses to the EGFR inhibitors erlotinib and gefitinib in nonsmall cell

140 r findings indicate the possibility of using EGFR inhibitors erlotinib and lapatinib to counter the p

141 associated with cancer progression, and the EGFR inhibitors erlotinib/tarceva and tyrphostin/AG-1478

142 udy of the epidermal growth factor receptor (EGFR) inhibitor erlotinib as a single agent and in combi

143 The epidermal growth factor receptor (EGFR) inhibitor erlotinib blocked ERK1/2 phosphorylation

144 The epidermal growth factor receptor (EGFR) inhibitor erlotinib is approved for treatment of p

145 re examined the effects of the EGF receptor (EGFR) inhibitor erlotinib on liver fibrogenesis and hepa

146 l antibody, cetuximab, or the small molecule EGFR inhibitor, erlotinib, effectively impaired tumorige

147 The EGFR inhibitor, erlotinib, neutralized ST6Gal-I-dependen

148 We show that combining IFN-alpha with the EGFR inhibitor, erlotinib, potentiates the antiviral eff

149 nstitutional phase I/II study we combined an EGFR inhibitor, erlotinib, with an anti-VEGF antibody, b

150 Using clinically relevant EGFR inhibitors, erlotinib and lapatinib, we found that

151 nse to the epidermal growth factor receptor (EGFR) inhibitor, erlotinib, in Non-Small Cell Lung Cance

152 e a useful target for treating resistance to EGFR inhibitors, especially EMT-driven resistance.

153 LI1 as they became resistant after long-term EGFR inhibitor exposure.

154 esults herein offer an explanation as to why EGFR inhibitors failed TNBC patients and support how com

155 y, through combined treatment with STAT3 and EGFR inhibitors, for pancreatic cancer patients.

156 The EGFR inhibitor gefitinib (Iressa) and the phosphatidylin

157 Cell treatment with the EGFR inhibitor gefitinib abolished upregulation of the E

158 netic/pharmacodynamic characteristics of the EGFR inhibitor gefitinib in mice with intracerebral tumo

159 rug discovery industry, such as the marketed EGFR inhibitor gefitinib, a quinolinecarbonitrile Src ty

160 common mutation conferring resistance to the EGFR inhibitor gefitinib, also preexists in cancer cells

161 biting de novo or acquired resistance to the EGFR inhibitor gefitinib, MEK inhibition enhanced the se

162 ed by ACK1 inhibition can be reversed by the EGFR inhibitor gefitinib.

163 vement in response to HS-173 with reversible EGFR inhibitor gefitinib.

164 ibility to apoptosis after treatment with an EGFR inhibitor, gefitinib.

165 tic growth inhibition when combined with the EGFR inhibitors, gefitinib and AZD8931.

166 nterestingly, mesenchymal cells resistant to EGFR inhibitors had increased AKT and signal transducer

167 (EGFR)-mutant non-small-cell lung cancers to EGFR inhibitors have been identified, little is known ab

168 the past decade, first and second generation EGFR inhibitors have significantly improved outcomes for

169 ired for tumor maintenance in animal models, EGFR inhibitors have thus far failed to deliver signific

170 Epidermal growth factor receptor (EGFR) inhibitors have been used clinically in the treatm

171 R kinase domain, which confers resistance to EGFR inhibitors (i.e., gefitinib).

172 tory to previous standard therapy, including EGFR inhibitors if KRAS wild-type, were enrolled.

173 macodynamic effect of a radionuclide-labeled EGFR inhibitor in situ.

174 natorial treatment with CDK4/6 inhibitor and EGFR inhibitor in vitro and in vivo.

175 , and KRAS G13D-mutated cells can respond to EGFR inhibitors in a neurofibromin-dependent manner.

176 Hypoxia sensitizes breast cancer cells to EGFR inhibitors in an HIF1alpha- and a methylation-speci

177 athways also promoted acquired resistance to EGFR inhibitors in basal-type UCB.

178 resistance to targeted therapies, including EGFR inhibitors in colorectal cancer (CRC).

179 m patients who have progressed on current or EGFR inhibitors in development may support subsequent tr

180 al data support the combined use of PI3K and EGFR inhibitors in HNSCC, in-human studies have displaye

181 the EGFR pathway predicts susceptibility to EGFR inhibitors in pancreatic cancer.

182 ental rationale for investigating the use of EGFR inhibitors in pemphigus.

183 nd rationalize consideration of irreversible EGFR inhibitors in the therapy of these tumors.

184 erapies, and the mechanism for resistance to EGFR inhibitors in this setting is not fully understood.

185 ed by the ELP complex and that resistance to EGFR inhibitors in TNBC might be overcome by cotargeting

186 on of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individual

187 ainst wild-type EGFR, than quinazoline-based EGFR inhibitors in vitro.

188 al role of epidermal growth factor receptor (EGFR) inhibitors in advanced EGFR-mutant non-small-cell

189 HER2, and HER4, with erlotinib, a reversible EGFR inhibitor, in patients with advanced non-small-cell

190 nd multikinase inhibitor, with erlotinib, an EGFR inhibitor, in patients with advanced non-small-cell

191 hose disease has progressed on their initial EGFR inhibitor, including therapies targeting both T790M

192 er whose disease progresses on their initial EGFR inhibitor, including those with T790M and other typ

193 ll lines to various combinations of PI3K and EGFR inhibitors, including EGFR agents with varying spec

194 EGFR inhibitors, including monoclonal antibodies and tyr

195 Irreversible EGFR inhibitors, including PF00299804, are effective in

196 sistance include the use of mutant selective EGFR inhibitors, including WZ4002, or the use of high co

197 d protein kinase kinase) inhibition enhances EGFR inhibitor-induced apoptosis and cell cycle arrest,

198 on through p73 represents a new mechanism of EGFR inhibitor-induced apoptosis, and provide potential

199 Despite its growth-inhibiting effect, EGFR inhibitor-induced ZEB1 strongly promotes EMT-depend

200 EGFR receptor in the presence or absence of EGFR inhibitors is investigated.

201 Resistance to targeted EGFR inhibitors is likely to develop in EGFR-mutant lung

202 -C: elevated EGFR signalling, sensitivity to EGFR inhibitors; (iv) CRIS-D: WNT activation, IGF2 gene

203 effective epidermal growth factor receptor (EGFR) inhibitors (kinact/Ki in the range 10(5)-10(7) M(-

204 istance to epidermal growth factor receptor (EGFR) inhibitors limits their clinical usefulness in pat

205 aling suppresses the ST phenotype, therefore EGFR inhibitors may be potential treatments for COPD-rel

206 Furthermore, they suggest that EGFR inhibitors may protect quiescent tumor cells, where

207 gesting that the combination of both ALK and EGFR inhibitors may represent an effective therapy for t

208 These potent mutant EGFR inhibitors may serve as a basis for the development

209 ine panels to identify genomic biomarkers of EGFR inhibitor-mediated radiosensitization.

210 wn about the effects of cell cycle status on EGFR inhibitor-mediated radiosensitization.

211 G1 promotes EGFR down-regulation through the EGFR inhibitor MIG6, which leads to late endosomal/lysos

212 FR inhibitors and radiation and suggest that EGFR inhibitors might best be given after radiation in o

213 mplete ERK pathway inhibition in response to EGFR inhibitor monotherapy.

214 : VEGF inhibitors or anti-angiogenic agents, EGFR inhibitors, mTOR inhibitors, CTLA-4 inhibitors, or

215 ns tend to develop resistance to therapeutic EGFR inhibitors, often due to secondary mutation EGFR(T7

216 gely obscure if sensitivity or resistance to EGFR inhibitors operates in cancer stem cells.

217 C12 myotubes with EGF-neutralizing antibody, EGFR inhibitor or an EGFR-silencing RNA added.

218 pe mice, or in infected cells incubated with EGFR inhibitors or deficient in EGFR.

219 cells was sufficient to resensitize them to EGFR inhibitors or radiation in vitro and in vivo.

220 When combined with an ATP-site EGFR inhibitor, osimertinib, the anti-proliferative acti

221 up-regulation in the presence and absence of EGFR inhibitor, p38 MAPK inhibitor, NFkappaB inhibitor,

222 ation, may be associated with the use of the EGFR inhibitors panitumumab and erlotinib.

223 ect of the epidermal growth factor receptor (EGFR) inhibitor panitumumab on cell lines expressing wil

224 trongly promotes EMT-dependent resistance to EGFR inhibitors partially through NOTCH1, suggesting a m

225 EGFR inhibitor PD153035 suppressed regeneration of 50% g

226 The EGFR inhibitor PD168393 and the metalloprotease inhibito

227 All current EGFR inhibitors possess a structurally related quinazoli

228 of cyclin-dependent kinase 4/6 (CDK4/6) and EGFR inhibitors prevents the emergence of resistance in

229 Reversible epidermal growth factor receptor (EGFR) inhibitors prompt a beneficial clinical response i

230 ltiple targeted therapies, including BRAF or EGFR inhibitors, rapidly deplete the pro-apoptotic facto

231 istance to epidermal growth factor receptor (EGFR) inhibitors remains a major challenge in non-small

232 usion, although TNBC clinical trials testing EGFR inhibitors reported lack of benefit, our results of

233 Resistance to EGFR inhibitors reportedly involves activation of signal

234 Resistance to EGFR inhibitors reportedly involves SRC activation and i

235 sease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activit

236 approaches that have been employed to study EGFR inhibitor resistance and review the oncogene and no

237 These include genes already known to mediate EGFR inhibitor resistance as well as many TSGs not previ

238 n represents a unique approach to overcoming EGFR inhibitor resistance in NSCLC and perhaps other typ

239 patritumab can overcome heregulin-dependent EGFR inhibitor resistance in NSCLC in vitro and in vivo

240 EGFR/ERBB family, is known to contribute to EGFR inhibitor resistance in other cancers, its function

241 lecoxib-derived antitumor agent, to overcome EGFR inhibitor resistance in three NSCLC cell lines, H11

242 cept that MEHD7945A can effectively overcome EGFR inhibitor resistance.

243 that this combination may overcome intrinsic EGFR-inhibitor resistance in patients with CRIPTO1-posit

244 PAWI-2 also overcame erlotinib (an EGFR inhibitor) resistance in FGbeta(3) cells more poten

245 lso limited cross-resistance to radiation in EGFR inhibitor-resistant cells by modulating cell-cycle

246 Conversely, restoration of functional p53 in EGFR inhibitor-resistant cells was sufficient to resensi

247 investigate these mechanisms, we established EGFR inhibitor-resistant clones from non-small cell lung

248 indings using cultures derived directly from EGFR inhibitor-resistant patient tumors.

249 am, increasing the magnitude and duration of EGFR inhibitor response in preclinical models.

250 We defined new pathways limiting EGFR-inhibitor response, including WNT/beta-catenin alte

251 peratively promote tumor metastasis or limit EGFR-inhibitor response.

252 858R) and KRAS(G12V) chimeric models with an EGFR inhibitor resulted in near complete tumor regressio

253 associated carcinoma cells with irreversible EGFR inhibitors resulted in inactivation of EGFR signali

254 generation epidermal growth factor receptor (EGFR) inhibitor rociletinib.

255 EGFR inhibitor-sensitive cells exhibited decreased activ

256 h the IGF1R inhibitor, BMS 536924, restoring EGFR inhibitor sensitivity.

257 t for patients who progress on their initial EGFR inhibitor should be tailored to identified resistan

258 and combination approaches with cisplatin or EGFR inhibitors should be explored.

259 Further study of irreversible EGFR inhibitors should be restricted to patients with ac

260 Lapatinib, a clinically active EGFR inhibitor, significantly reversed the epidermal gro

261 ompted us to determine whether EGF receptor (EGFR) inhibitors stimulate AQP2 trafficking and reduce u

262 Using RMS cells, we showed that EGFR inhibitors successfully antagonized RMS RD cells, w

263 tant lung cancer benefit from treatment with EGFR inhibitors such as erlotinib, gefitinib, and afatin

264 h concentrations of irreversible quinazoline EGFR inhibitors such as PF299804.

265 argeting of GSCs by CBL0137 and synergy with EGFR inhibitors support the development of clinical tria

266 Combination treatment with PQIP and EGFR inhibitor Tarceva resulted in synergistic effects a

267 Most EGFR inhibitors target the extracellular, growth factor-

268 The EGFR inhibitors tested had varying effectiveness at prev

269 In vitro MGG70R-GSC was more sensitive to EGFR inhibitors than MGG70RR-GSC.

270 16 is a novel, irreversible mutant-selective EGFR inhibitor that specifically targets EGFR-activating

271 of a series of covalent and mutant-selective EGFR inhibitors that effectively target the T790M mutant

272 described complement the covalent pan-mutant EGFR inhibitors that have shown encouraging results in r

273 ished apoptotic response to third-generation EGFR inhibitors that target EGFR(T790M); treatment with

274 istance to epidermal growth factor receptor (EGFR) inhibitors that are now being used widely in the t

275 s associated with both primary resistance to EGFR inhibitor therapy and with the development of metas

276 shortened overall survival and resistance to EGFR inhibitor therapy in GBM patients and plays an acti

277 Those with prior EGFR inhibitor therapy were excluded.

278 concurrent epidermal growth factor receptor (EGFR) inhibitor therapy with cetuximab, indicating the n

279 ities in HNSCC and support combining MEK and EGFR inhibitors to enhance clinical efficacy in HNSCC.

280 Furthermore, we find that EGFR inhibitor treatment, which inhibits the growth of E

281 on could be visualized after radiotherapy or EGFR inhibitor treatment.

282 get its mutant-protein product (for example, EGFR-inhibitor treatment in EGFR-mutant lung cancers).

283 Tumor genomic complexity increases with EGFR-inhibitor treatment, and co-occurring alterations i

284 Five EGFR inhibitors, two monoclonal antibodies and three TKI

285 lly developed resistance to first-generation EGFR inhibitors via cMET activation.

286 Treatment of EGFR inhibitor was effective in BRAFi-resistant melanoma

287 nalysis revealed that acquired resistance to EGFR inhibitors was associated consistently with the los

288 e CDK4/6 inhibitor) given with cetuximab (an EGFR inhibitor) was safe.

289 itinib (an epidermal growth factor receptor [EGFR] inhibitor), was rescinded after a randomized trial

290 Erlotinib, a selective EGFR inhibitor, was combined with temozolomide (TMZ) and

291 r receptor (EGFR) signaling, and efficacy of EGFR inhibitors, we performed a phase I trial combining

292 to EGFR variants associated with response to EGFR inhibitors, we suggest that IGF signaling achieves

293 pression when combinations of ERK, BRAF, and EGFR inhibitors were applied.

294 EGFR inhibitors were used to determine whether EGFR sign

295 of resistance to chemotherapy agents and the EGFR inhibitors, which results in recurrence of highly a

296 reports about resistance to third-generation EGFR inhibitors will lay the groundwork for overcoming t

297 artinib), a novel, covalent mutant-selective EGFR inhibitor with equipotent activity on both oncogeni

298 g hit (7) into a number of targeted covalent EGFR inhibitors with equipotent activity across mutants

299 potential to overcome acquired resistance to EGFR inhibitors with MEHD7945A, a monoclonal antibody th

300 redicted sensitivity of alternative ERK2 and EGFR inhibitors, with a particular highlight of two mole