ライフサイエンスコーパス: EGFR inhibitor

1 e COX-2 inhibitor) or erlotinib (Tarceva, an EGFR inhibitor).

2 Adverse events were those expected with an EGFR inhibitor.

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

4 rikingly enhanced apoptosis by gefitinib, an EGFR inhibitor.

5 progresses during treatment with an initial EGFR inhibitor.

6 oursphere formation and improves efficacy of EGFR inhibitor.

7 n during previous treatment with an existing EGFR inhibitor.

8 treated in combination with the originating EGFR inhibitor.

9 characteristics associated with response to EGFR inhibitors.

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

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

12 ly for selecting patients for treatment with EGFR inhibitors.

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

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

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

16 atients with colorectal cancer refractory to EGFR inhibitors.

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

18 iably predictive of therapeutic responses to EGFR inhibitors.

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

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

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

22 ued proliferation that is halted by specific EGFR inhibitors.

23 ct sensitivity of recurrent glioblastomas to EGFR inhibitors.

24 c target to improve the clinical response to EGFR inhibitors.

25 ance exhibited by certain cancer patients to EGFR inhibitors.

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

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

28 n causes resistance against third-generation EGFR inhibitors.

29 treatment of tumors resistant to traditional EGFR inhibitors.

30 f EGFR phosphorylation, and sensitization to EGFR inhibitors.

31 t in compromised autophagy when treated with EGFR inhibitors.

32 egarding the sensitivity of these tumours to EGFR inhibitors.

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

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

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

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

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

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

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

40 timulated proliferation was inhibited by the EGFR inhibitor AG1478 and the MEK inhibitor U0126 in rat

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

42 The EGFR inhibitor AG1478 blocked the subsequent effects of

43 s activated following TBHP exposure, and the EGFR inhibitor AG1478 blocked the up-regulation of PGC-1

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

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

46 nterfering RNA or pretreatment of cells with EGFR inhibitors AG1478 and PD158780 almost completely bl

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 cells in a manner that was inhibitable by an EGFR inhibitor, AG1478.

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

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

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

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 ative agents showed that both an alternative EGFR inhibitor and a cyclin-dependent kinase 4 inhibitor

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

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

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

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

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

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

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

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

66 tations mediating resistance to irreversible EGFR inhibitors and reveal alternative strategies to ove

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

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

73 e exploration of combination of gemcitabine, EGFR inhibitors, and radiation.

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

75 Recent studies showed that EGFR inhibitors are effective for patients with HNSCC.

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 However, EGFR inhibitors as monotherapy have yielded only modest

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 uced epidermal hyperplasia, and suggest that EGFR inhibitors can mitigate retinoid-induced scaling.

95 phosphorylation; inhibiting this effect with EGFR inhibitors can potentiate cytotoxicity and radiosen

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

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

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

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

100 istant to both erlotinib and an irreversible EGFR inhibitor (CL-387,785) but sensitive to a multikina

101 apoptosis when treated with the irreversible EGFR inhibitor, CL-387,785.

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

103 Furthermore, the OSU-03012/EGFR inhibitor combination induced GADD153-mediated up-r

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

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

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

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

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

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

110 EGFR inhibitors could therefore be useful for the contro

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

112 re at least two separate mechanisms by which EGFR inhibitors decrease VEGF expression.

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

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

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

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

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

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

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

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

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

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 differing in PTEN status, treating with the EGFR inhibitor erlotinib and a novel dual inhibitor of P

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

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

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 PDK1 augmented the antitumor effects of the EGFR inhibitor erlotinib, indicating PDK1 as a therapeut

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 f the oral epidermal growth factor receptor (EGFR) inhibitor erlotinib in patients with gastroesophag

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

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

147 reversible epidermal growth factor receptor (EGFR) inhibitor erlotinib, resembling the resistant phen

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

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

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

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

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

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

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

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

156 research in cancer cell biology, a series of EGFR inhibitors from both the monoclonal antibody (mAb)

157 The EGFR inhibitor gefitinib (Iressa) and the phosphatidylin

158 nce of human squamous cell carcinomas to the EGFR inhibitor gefitinib (see the related article beginn

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

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

161 The EGFR inhibitor gefitinib potentiates chemotherapy and ra

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

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

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

165 plified in lung adenocarcinomas sensitive to EGFR inhibitors gefitinib and erlotinib.

166 l-molecule epidermal growth factor receptor (EGFR) inhibitor gefitinib (ZD1839, Iressa) blocked cell

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

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

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

170 EGFR) in cancer development and progression, EGFR inhibitors have emerged as promising novel therapie

171 Several EGFR inhibitors have recently gained US Food and Drug Ad

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

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

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

175 Treatment with an irreversible EGFR inhibitor, HKI-272, dramatically reduced the size o

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

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

178 To summarize the current status of EGFR inhibitors in aerodigestive carcinomas (ADCs), high

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

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

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

182 g of the EGFR pathway may improve the use of EGFR inhibitors in HNSCC.

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

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

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

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

187 ization of epidermal growth factor receptor (EGFR) inhibitors in the treatment of nonsmall-cell lung

188 l-molecule epidermal growth factor receptor (EGFR) inhibitors in treating advanced non-small cell lun

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 EGFR inhibitors, including monoclonal antibodies and tyr

194 Irreversible EGFR inhibitors, including PF00299804, are effective in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 vestigated whether neoadjuvant gefitinib, an EGFR inhibitor, might overcome biologic and clinical res

211 -April 2007) performed using the terms EGFR, EGFR inhibitors, monoclonal antibodies, tyrosine kinase

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

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

214 Treatment of cell lines with either an EGFR inhibitor or an src kinase inhibitor had no effect

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

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

217 kinase inhibitors in combination with either EGFR inhibitors or standard chemotherapeutics might repr

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

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

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

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

222 EGFR inhibitor PD153035 suppressed regeneration of 50% g

223 effects could be partially abolished by the EGFR inhibitor PD153035.

224 The EGFR inhibitor PD168393 and the metalloprotease inhibito

225 All current EGFR inhibitors possess a structurally related quinazoli

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

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

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

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

230 Resistance to EGFR inhibitors reportedly involves activation of signal

231 Resistance to EGFR inhibitors reportedly involves SRC activation and i

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

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

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

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

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

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

238 cept that MEHD7945A can effectively overcome EGFR inhibitor resistance.

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

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

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

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

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

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

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

246 858R) and KRAS(G12V) chimeric models with an EGFR inhibitor resulted in near complete tumor regressio

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

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

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

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

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

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

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

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

255 Irreversible EGFR inhibitors such as CL-387,785 can overcome resistan

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

257 ivated EGFR can be effectively targeted with EGFR inhibitors such as erlotinib.

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

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

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

261 Most EGFR inhibitors target the extracellular, growth factor-

262 The EGFR inhibitors tested had varying effectiveness at prev

263 16 is a novel, irreversible mutant-selective EGFR inhibitor that specifically targets EGFR-activating

264 s, there is a clinical need to develop novel EGFR inhibitors that can effectively inactivate T790M-co

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

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

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

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

269 e biologic significance and implications for EGFR inhibitor therapies in HNSCC.

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

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

272 Those with prior EGFR inhibitor therapy were excluded.

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

274 the optimal sequencing of these agents with EGFR inhibitors to provide better guidance for clinical

275 EGFR inhibitors toxicities include rash, diarrhea, and h

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

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

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

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

280 Five EGFR inhibitors, two monoclonal antibodies and three TKI

281 ence of an epidermal growth factor receptor (EGFR) inhibitor (tyrphostin AG1478), a matrix metallopro

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

283 file and long half-life of this irreversible EGFR inhibitor warrant its further evaluation as a singl

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

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

286 Such resistance to first-generation EGFR inhibitors was frequently linked to an acquired T79

287 lopment of epidermal growth factor receptor (EGFR) inhibitors was greeted with tremendous enthusiasm

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

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

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

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

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

293 EGFR inhibitors were used to determine whether EGFR sign

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

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

296 particularly with regard to how best combine EGFR inhibitors with conventional cancer therapies, and

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

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

299 metastatic (R/M) disease, the combination of EGFR inhibitors with other therapeutic strategies will b

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