ライフサイエンスコーパス: EGFR

1 EGFR activation has been recurrently identified in a set

2 EGFR activation kinetics, and consequently ERK signaling

3 EGFR-dependent activation of RhoA/Rock and PI3K-Akt sign

4 EGFR-mutant non-small-cell lung cancer (NSCLC) patients

5 The FDA AERS database contained 27,123 EGFR-TKI-associated AERs within the reporting period fro

6 We identified MET alterations (7%-24%), EGFR C797X (0%-29%), SCLC transformation (2%-15%), and o

7 f pre-treatment and PD tumor samples from 54 EGFR-mutant NSCLC patients.

8 other GBM cohorts (IDH wild-type [WT], 95%; EGFR amplified, approximately 50%), indicating that pati

9 required for SHIP1 recruitment, gB-activated EGFR mediated SHIP1 activation, underscoring the importa

10 s an EGFR-interacting protein that activates EGFR/ERK/Fos signaling to enhance neurite outgrowth and

11 e inhibitors (TKIs) in NSCLC with activating EGFR mutations is a critical limitation of this therapy.

12 enzyme) is responsible for producing active EGFR family ligands in the via ligand shedding.

13 Interestingly, the ADAM17-EGFR signaling axis coordinates neighboring cell migrati

14 ance often returns as a result of additional EGFR mutations.

15 In EGFR-mutated lung adenocarcinoma, EGFR-TKIs show enhanced efficacy in spheroid cultures.

16 an overview of important mutations affecting EGFR and Her2 and highlight their influence on the kinas

17 a stimulation and epigenetic control affects EGFR-TKI tolerance and cancer dissemination.

18 ulated by SOX2 and TGFbeta signaling affects EGFR-TKI tolerance and lung cancer dissemination.

19 t glutamine metabolism was upregulated after EGFR activation in a GDH1 (glutamate dehydrogenase 1)-de

20 , a monoclonal neutralizing antibody against EGFR, blocks HIV-associated exosome-enhanced KSHV infect

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

22 Here, we develop an allosteric EGFR degrader, DDC-01-163, which can selectively inhibit

23 tively, DDC-01-163 is a promising allosteric EGFR degrader with selective activity against various cl

24 cally advanced or metastatic, MET-amplified, EGFR mutation-positive non-small-cell lung cancer, who h

25 our activity in patients with MET-amplified, EGFR mutation-positive, advanced NSCLC, who had disease

26 bited by antibodies against amphiregulin, an EGFR ligand concentrated on these vesicles.

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

28 in patients with advanced NSCLC harboring an EGFR-sensitizing mutation and a performance status of 0

29 ally described in lung cancers harbouring an EGFR mutation, and was subsequently reported in multiple

30 proteins promoted apoptotic cell death in an EGFR inhibition-dependent manner.

31 these results demonstrate that sSORLA is an EGFR-interacting protein that activates EGFR/ERK/Fos sig

32 xpressing markers of pluripotency through an EGFR-ERK-EGR1-dependent axis.

33 evelopment of T790M during treatment with an EGFR inhibitor.

34 es consistent with the presence of IL-13 and EGFR/ERBB activation, with involvement of distinct EGFR

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

36 for example, NOTCH1, RAC1, PIK3CD, BCL2, and EGFR.

37 sistant NSCLC models with EGFR-dependent and EGFR-independent resistance mechanisms, IACS-13909, admi

38 ht the novel interaction between endocan and EGFR and new opportunities to effectively target endocan

39 on, these results demonstrate that FOXM1 and EGFR/ERBB2 pathways are key points of vulnerability for

40 riched transcripts for ST6GALNAC5, GJA1, and EGFR, all associated with brain metastasis.

41 Assessing HER3 and EGFR protein expression in combination may identify whic

42 -EGFR score outperformed individual HER3 and EGFR scores, with high HER3-EGFR score independently pre

43 nth) as best candidates to silence c-MET and EGFR genes and of two endogenous miRNAs (miR-15a and miR

44 that reciprocal cross-talk between STAT3 and EGFR pathways is a key molecular mechanism leading to re

45 icated dataset generated for this study) and EGFR inhibitory effect on cancer cell viability.

46 peptide inhibits SHP2 activity in vitro and EGFR and HER2 signaling in cells, suggesting inhibition

47 y combining two corresponding Tag-fused anti-EGFR single-chain Fvs (scFvs), which recognize different

48 that of bivalent AEC with two identical anti-EGFR scFvs at low concentrations of sEGFR, and met the c

49 anti-epidermal growth factor receptor (anti-EGFR) AEC worked efficiently as a sensing element; howev

50 The anti-EGFR bsAEC was successfully prepared by constructing glu

51 In addition to genetic alterations such as EGFR secondary mutation causing EGFR-TKI resistance, com

52 ensated by increases in HER3; thus, assaying EGFR and HER3 together may improve prognostic value.

53 e extracellular domain of EpCAM (EpEX) binds EGFR, activating both AKT and MAPK signaling to inhibit

54 We hypothesized that blocking EGFR palmitoylation, previously shown to inhibit EGFR ac

55 Both EGFR and BIRC5 are highly expressed in basal-like PDXs,

56 study shows that combined inhibition of both EGFR and STAT3 might overcome drug resistance encountere

57 nt; however, the combined inhibition of both EGFR and TGF-betaR1 signaling reduced inclusions by over

58 URF2 extends membrane retention of EGF-bound EGFR, whereas SMURF2 knockdown increases receptor sortin

59 g resistance and confirm its impact in BRAF, EGFR, HER2 and MEK1.

60 sed by acquired drug resistance conferred by EGFR-mutant variants.

61 I sensitivity in smokers with NSCLC carrying EGFR(WT) and that the combination of EGFR TKI and AMPK a

62 ions such as EGFR secondary mutation causing EGFR-TKI resistance, compensatory activation of signalin

63 Combined EGFR- and SOS1-inhibition markedly inhibited Raf/MEK/ERK

64 an HSP90-independent function in controlling EGFR trafficking through the ER.

65 olerance, whereas SMURF2 knockdown decreased EGFR steady-state levels and sensitized lung cancer cell

66 1 depletion with short hairpin RNA decreased EGFR degradation when activated by epidermal growth fact

67 RBB activation, with involvement of distinct EGFR ligands.

68 via direct binding and enhancing of the EGF-EGFR interaction and supported the growth of tumors driv

69 to AML-relevant signaling pathways like EGF/EGFR and Wnt/Hedgehog/Notch.

70 can is a novel and critical regulator of EGF/EGFR signaling and serves as an alternative target of EG

71 lastoma subtype and correlated with elevated EGFR levels.

72 opportunities to effectively target endocan-EGFR regulatory axis in patients with TKI-resistant NSCL

73 ive small-molecule inhibitor BGJ398 enhanced EGFR TKI sensitivity and promoted upregulation of BIM le

74 n of multiple parallel RTKs further enhances EGFR-TKI effectiveness.

75 YAP1, all deplete dormant cells by enhancing EGFR/MEK inhibition-induced apoptosis.

76 ed resistance mutations in CDK4, CDK6, ERK2, EGFR and HER2.

77 We explore EGFR-mutant glioma evolution in conditional mutant mice

78 Endocan facilitated EGFR signaling via direct binding and enhancing of the E

79 kinetic studies, and compound 6 is the first EGFR degrader suitable for in vivo efficacy studies.

80 that the compounds were highly selective for EGFR.

81 ept, we demonstrate a design of a sensor for EGFR tyrosine kinase-an important target in cancer resea

82 ) plus MET TKIs are a possible treatment for EGFR mutation-positive lung cancers with MET-driven acqu

83 ient dynamics of EGFR dimerization and found EGFR kinase activity to be essential for dimerization.

84 and ERalpha-associated genes, GATA3, FOXA1, EGFR, CDH1, DSP, KRT7, FBP1, MYB, RET, KRT8, MUC1, and E

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

86 ta catalytic subunit was recruited to the gB/EGFR complex despite p110delta being the primary PI3K is

87 n previously treated with a third-generation EGFR TKI (B1) and those who had not been previously trea

88 n previously treated with a third-generation EGFR TKI who were either Thr790Met negative (B2) or Thr7

89 in PI3K-Akt signaling pathway (such as GRB2, EGFR, EPHA2, GNB1, GNB2, 14-3-3 family, and Integrin fam

90 When ancestral clones harbor EGFR mutations, truncal mutation abundance significantly

91 BC patients, we analyzed the impact of HER3, EGFR, or combined HER3-EGFR protein expression in pre-tr

92 d the impact of HER3, EGFR, or combined HER3-EGFR protein expression in pre-treatment samples on brea

93 The combined HER3-EGFR score outperformed individual HER3 and EGFR scores,

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

95 ividual HER3 and EGFR scores, with high HER3-EGFR score independently predicting worse BCSS (Hazard R

96 TNBCs with high HER3-EGFR scores exhibited significantly suppressed ATM signa

97 ant melanomas, but little is known about how EGFR, or possibly other receptor tyrosine kinases, becom

98 p12 amplification, including the genes HUS1, EGFR, ABCA13, and IKZF1, predicted nonresponse in patien

99 machine learning model was able to identify EGFR-mutant patients in multiple validation sets with gl

100 In EGFR (HER1) and EGFR2 (HER2) signaling, SHP2 increases t

101 In EGFR-mutant osimertinib-resistant NSCLC models with EGFR

102 In EGFR-mutated lung adenocarcinoma, EGFR-TKIs show enhance

103 g model, which demonstrates high accuracy in EGFR mutation status prediction across patient cohorts f

104 for upstream mutations in cancer, such as in EGFR.

105 potential of SOX2 as a prognostic marker in EGFR-mutant lung cancer, as SOX2-mediated cell plasticit

106 Driver mutations in EGFR, KRAS, MET, PIK3CA, and EML4-ALK fusion were mostly

107 iated largely through secondary mutations in EGFR-either C797S or L718V/Q.

108 nted the emergence of secondary mutations in EGFR.

109 residues N-terminal to the substrate pTyr in EGFR and HER2 mediate specific binding by the SHP2 activ

110 rotein concentrations play critical roles in EGFR signaling.

111 how that the phosphorylation of this site in EGFR regulates metastasis.

112 Also, increased EGFR expression sensitized cells to EGFR inhibitors.

113 ion between AEBP1 upregulation and increased EGFR expression in primary glioma, and employ a glioma c

114 ivated by epidermal growth factor, increased EGFR protein expression, and conferred resistance to BRA

115 cell lines, SMURF2 overexpression increased EGFR levels, improving TKI tolerance, whereas SMURF2 kno

116 th AMPK activators synergistically increases EGFR TKI sensitivity.

117 GFR in vitro, and sSORLA treatment increases EGFR Y1173 phosphorylation, which is involved in ERK act

118 t affect the stability of ligand-independent EGFR oligomers.

119 nockdown of FGFR1 attenuated hypoxia-induced EGFR TKI resistance in each line.

120 rapy with antineoplastic agents that inhibit EGFR and MEK is frequently limited by cutaneous adverse

121 palmitoylation, previously shown to inhibit EGFR activity, might alter downstream signaling in the K

122 erations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been developed for the treatment of patie

123 the phosphorylation patterns of full-length EGFR.

124 We propose Sym004 cross-links EGFR physically triggering EGFR endocytosis and incorpor

125 adenocarcinoma component of PSC showed lower EGFR incidence.

126 le-molecule imaging of a model tumor marker (EGFR) on a panel of living cancer cells.

127 panitumumab, and trastuzumab to monitor MET, EGFR, and HER2 protein levels, respectively, during trea

128 lterations in these gliomas including mutant EGFR amplifications and Sub1, Trp53, and Tead2 loss-of-f

129 orted the growth of tumors driven by mutated EGFR.

130 ere we report that the inhibition of mutated EGFR promotes the secretion of a potent vasoconstrictor,

131 lung cancer (NSCLC) population with mutated EGFR receiving TKIs and CRT.

132 overexpression of EDN1 in cells with mutated EGFR resulted in poor drug delivery and retarded growth

133 nesis in vivo identifies 281 known and novel EGFR-cooperating driver genes, including Cdkn2a, Nf1, Sp

134 The LIFR is upregulated by nuclear EGFR, which acts as a transcriptional regulator, directl

135 Notably, selective abrogation of EGFR signaling in myeloid cells was sufficient to protec

136 In the absence of EGFR-mediated phosphorylation, STING rapidly transits in

137 Activation of EGFR signaling in the ALA neuron has previously been sug

138 low TXN activity, resulting in activation of EGFR, PARP1, and caspases and inhibition of p53 and NFka

139 y mediators and suppressed the activation of EGFR, protease-activated receptor 2, nucleotide-binding

140 tion between the tyrosine kinase activity of EGFR and innate immune functions of STING and suggest ne

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

142 lity analysis of the adverse events (AEs) of EGFR-TKIs (gefitinib, erlotinib, afatinib, osimertinib)

143 palmitoylation increased the association of EGFR with the MAPK adaptor Grb2 and decreased that with

144 arrying EGFR(WT) and that the combination of EGFR TKI and AMPK activator may be a potentially effecti

145 signaling, where a subsequent combination of EGFR TKI with FGFR1 inhibitors or MEK inhibitors reverse

146 Conditional deletion of EGFR in hematopoietic stem and progenitor cells (HSPCs)

147 ovel bypass mechanism for the development of EGFR-TKI resistance.

148 Cell surface display of EGFR is essential for cellular responses to its ligands.

149 1 partner, RUSC2, in cell surface display of EGFR.

150 he DrBpP-PCM with the cytoplasmic domains of EGFR and FGFR1.

151 While the signal transduction downstream of EGFR has been extensively investigated, our knowledge of

152 bserved time-dependent transient dynamics of EGFR dimerization and found EGFR kinase activity to be e

153 detection range of the soluble ectodomain of EGFR (sEGFR).

154 the key obstacle to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

155 might be connected to the low expression of EGFR in PSW which may affect epithelial function and con

156 mers of fluorescent protein-labeled forms of EGFR and its paralog, human epidermal growth factor rece

157 Although new generations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been dev

158 SOS1 was required for 3D spheroid growth of EGFR-mutated NSCLC cells.

159 duced lysosomal degradation independently of EGFR ubiquitylation but dependent upon Hrs/Tsg101 that a

160 Induction of EGFR under hypoxia led to an increase in AKT, ERK, and R

161 g cancer cells to survive dual inhibition of EGFR and MEK.

162 e mechanistic study showed the inhibition of EGFR caused nuclear translocation of S6K1 for binding wi

163 of KSHV infection and that the inhibition of EGFR serves as a novel strategy for preventing KSHV infe

164 Inhibition of EGFR signaling prevented expansion of the NSC population

165 ent with lapatinib [dual kinase inhibitor of EGFR (ERBB1) and ERBB2] and thiostrepton (FOXM1 inhibito

166 k elucidates functional driver landscapes of EGFR-mutant gliomas, uncovering potential therapeutic st

167 owledge of the initiation and maintenance of EGFR signaling during cell migration remains limited.

168 to osimertinib in transgenic mouse models of EGFR(L858R) -induced lung adenocarcinoma and found that

169 n of p120ctn combined with overexpression of EGFR induces a signaling cascade that leads to hyperacti

170 tumorspheres by reducing phosphorylation of EGFR family proteins, ERK, FAK, and CSC markers.

171 Preselection of EGFR-mutant lung cancer cells with the mesenchymal pheno

172 ancer cells, when exposed to the pressure of EGFR- and BRAF-targeted therapies, transiently alter the

173 in that interacts and activates promoters of EGFR, c-MET, and their signaling molecules.

174 nvasive method for precise quantification of EGFR mutation status in NSCLC patients, which is promisi

175 enhanced transcription and up-regulation of EGFR and MET.

176 ying cellular localization and regulation of EGFR in tissues.

177 90 co-chaperone CHP-1 acts as a regulator of EGFR trafficking in C. elegans.

178 Crucial for stabilization of EGFR asymmetric dimer is a "latch" formed between kinase

179 resistance mechanism inherent to a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor

180 aling and serves as an alternative target of EGFR-TKI resistance in NSCLC.

181 tease responsible for the transactivation of EGFR by LPA in ovarian cancer cells.

182 Moreover, combined treatment of EGFR TKI with AMPK activators synergistically increases

183 elementary bodies and diminished turnover of EGFR.

184 e counteracting Matriptase effects depend on EGFR and the newly identified mediator phospholipase D (

185 mall-cell lung cancer, who had progressed on EGFR TKIs.

186 lectively recognizes RasGAP-binding sites on EGFR and HER2.

187 low- and high-affinity ligands and oncogenic EGFR mutants.

188 val in the elevated lactate dehydrogenase or EGFR and ALK wild-type populations.

189 DA approved drugs, afatinib and palbociclib (EGFR and CDK4/6 inhibitors, respectively) demonstrated s

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

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

192 of expression of oncogenes involved in PDGF, EGFR, VEGF, insulin/IGF/MAPKK, FGF, Hedgehog, TGFbeta, a

193 gers ERK activation, whereas pharmacological EGFR or ERK inhibition reverses sSORLA-dependent enhance

194 tudy shows that HUNK directly phosphorylates EGFR at T654 to promote metastasis and is the first stud

195 Our studies show that HUNK phosphorylates EGFR at T654, enhancing receptor stability and downstrea

196 ey signaling pathways associated with ER/PR, EGFR, PI(3)K, Hippo, and Wnt in cancer.

197 s that LKB1 may serve as a marker to predict EGFR TKI sensitivity in smokers with NSCLC carrying EGFR

198 ng pathway by binding to EGFR and preventing EGFR internalization.

199 C, who had disease progression on a previous EGFR TKI.

200 ndicate that vertical inhibition of proximal EGFR signaling should be pursued as a potential therapy

201 nt studies have identified the EGF receptor (EGFR) ligand amphiregulin (AREG) as an important mediato

202 Because Rho, EGF receptor (EGFR), and E-cad are associated with colorectal cancer i

203 ailed anti-epidermal growth factor receptor (EGFR) affibody was employed to easily synthesize the hig

204 Epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3

205 e cellular epidermal growth factor receptor (EGFR) and integrin beta1, respectively, to reshape canon

206 ns such as epidermal growth factor receptor (EGFR) and MYC can suppress proliferation of cancer cells

207 the RTKs, epidermal growth factor receptor (EGFR) and proto-oncogene c-Met (MET), and shunts their t

208 s model to epidermal growth factor receptor (EGFR) antibodies and find that the activity of antibody

209 ing by the epidermal growth factor receptor (EGFR) family (EGFR1-4 or the human homologs HER1-4).

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

211 rmation of epidermal growth factor receptor (EGFR) is crucial for EGF-induced receptor activation.

212 ING by the epidermal growth factor receptor (EGFR) is required for directing STING to endosomes, wher

213 istance in epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer is a persistent

214 tology and epidermal growth factor receptor (EGFR) mutations.

215 ons in the epidermal growth factor receptor (EGFR) or the guanosine triphosphatase KRAS.

216 eport that epidermal growth factor receptor (EGFR) regulates DNA repair in HSCs following irradiation

217 The epidermal growth factor receptor (EGFR) signaling cascade is known to drive cell migration

218 nes of the epidermal growth factor receptor (EGFR) signaling pathway are expressed in RIS.

219 L-6R), and epidermal growth factor receptor (EGFR) signaling.

220 Targeting epidermal growth factor receptor (EGFR) through an allosteric mechanism provides a potenti

221 Several epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and

222 ctivity of epidermal growth factor receptor (EGFR), a known EMT driver.

223 luding the epidermal growth factor receptor (EGFR), and activates cellular signaling cascades for hos

224 tor (MET), epidermal growth factor receptor (EGFR), and human epidermal growth factor receptor 2 (HER

225 ession of epithelial growth factor receptor (EGFR), IL-33 and receptor ST2 were investigated in bronc

226 uch as the epidermal growth factor receptor (EGFR), locally increases the abundance of reactive oxyge

227 se (PARP), epidermal growth factor receptor (EGFR), Vascular endothelial growth factor (VEGF), etc.

228 umorigenic Epidermal Growth Factor Receptor (EGFR)-Akt axis, and finally cell death.

229 c model of epidermal growth factor receptor (EGFR)-driven tumorigenesis similarly relies on the inter

230 y p53- and epidermal growth factor receptor (EGFR)-mediated DNA repair.

231 essing the epidermal growth factor receptor (EGFR).

232 hrough the epidermal growth factor receptor (EGFR).

233 ion of the epidermal growth factor receptor (EGFR).

234 arget, the epidermal growth factor receptor (EGFR).

235 first-in-class E3 ligase cereblon-recruiting EGFR degrader, MS154 (compound 10), using the proteolysi

236 novel E3 ligase von Hippel-Lindau-recruiting EGFR degrader, MS39 (compound 6), and a first-in-class E

237 e development of DHHC20 inhibitors to reduce EGFR-PI3K signaling could be beneficial to patients with

238 Reduced EGFR levels can be compensated by increases in HER3; thu

239 We found that YM155 reduces EGFR expression in TNBC cells, shedding light on its pot

240 activity against various clinically relevant EGFR mutants as a single agent and when combined with an

241 of inhibitors that target the drug resistant EGFR(L858R/T790M/C797S) mutant with nanomolar potencies

242 rapeutic strategy to overcome drug-resistant EGFR mutations that emerge within the ATP binding site.

243 Our findings unveil a new AURKA-SDCBP-EGFR axis that is involved in ESCC progression and provi

244 Another group has shown EGFR and MDM2/MDM4 amplifications in patients with HPD.

245 ed, at least in part, by alpha2-6-sialylated EGFR.

246 tion, and in mice with myeloid cell-specific EGFR deficiency.

247 Because of cellular stress, EGFR directly activates RIS.

248 found that increased phosphorylation of T654 EGFR correlates with increased epithelial to mesenchymal

249 eloping next generation inhibitors targeting EGFR in non-small-cell lung cancer.

250 We found that EGFR activation is a main cause for resistance to STAT3

251 We found that EGFR is predominantly phosphorylated at multiple sites,

252 kinase substrate screen and identified that EGFR is phosphorylated by HUNK.

253 Collectively, our findings indicate that EGFR phosphorylates ELK1 to activate GDH1 transcription

254 Much evidence indicates that EGFR/ERBB1 also forms oligomers in the absence of ligand

255 Preclinical data suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are

256 The EGFR monoclonal antibody cetuximab is generally used in

257 The EGFR-sfGFP fly is an exciting new resource for studying

258 nistic studies show that SDCBP activates the EGFR-PI3K-Akt signaling pathway by binding to EGFR and p

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

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

261 cells to EGF stimulation is attenuated, the EGFR accumulates in the ER and ERK2 activity decreases.

262 of epithelial cells and stimulated both the EGFR and TGF-beta signaling pathways.

263 Inhibition of either the EGFR or TGF-betaR1 signaling substantially reduced inclu

264 this study was to determine the role of the EGFR ligand heparin-binding EGF-like growth factor (HB-E

265 enhanced autocrine/paracrine release of the EGFR ligand transforming growth factor alpha in a TACE-d

266 terestingly, the spatial localization of the EGFR to the apical side of the FCs at early stages depen

267 Thus, the EGFR-DLS provides a non-invasive method for precise quan

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

269 moderate hypoxia promotes resistance to the EGFR TKI osimertinib (AZD9291) in the non-small cell lun

270 whose signaling pathway synergizes with the EGFR cascade, but its role in infectivity, inclusions, a

271 Thus, EGFR-mediated FUS phosphorylation regulates FUS nuclear

272 In addition, tissue EGFR expression was significantly reduced in PSW and cor

273 GFR-PI3K-Akt signaling pathway by binding to EGFR and preventing EGFR internalization.

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

275 ncreased EGFR expression sensitized cells to EGFR inhibitors.

276 ested that cetuximab is bound differently to EGFR in the stroma-rich area than in stroma-poor regions

277 t evidence for the reversal of resistance to EGFR TKI by the addition of small molecule S6K1/MDM2 ant

278 Hypoxia-induced resistance to EGFR TKI is driven by overexpression of FGFR1 to sustain

279 1 as a candidate mechanism for resistance to EGFR TKI therapy was investigated by interrogation of pu

280 The development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with act

281 sing to identify NSCLC patients sensitive to EGFR-TKI or ICI-treatments.

282 d be pursued as a potential therapy to treat EGFR-mutated tumors.

283 ym004 cross-links EGFR physically triggering EGFR endocytosis and incorporation onto ILVs and so Sym0

284 UC4, MUC5AC, MUC6, Das-1, STMN1, TSP1, TSP2, EGFR, EpCAM, GPC1, WNT-2, EphA2, S100A4, PSCA, MUC13, ZE

285 r (NSCLC) cell line H1975, which harbors two EGFR mutations including T790M.

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

287 ing total body irradiation is dependent upon EGFR-mediated repair of DNA damage via activation of DNA

288 provides a mechanism whereby ADT upregulates EGFR-LIFR signaling that activates SUCLG2, which subsequ

289 T) mutant Ba/F3 cells while leaving wildtype EGFR Ba/F3 cells unaffected.

290 at when NFkB is hyperactivated in cells with EGFR overexpression and p120ctn inactivation, Twist2 is

291 sSORLA coprecipitates with EGFR in vitro, and sSORLA treatment increases EGFR Y1173

292 ation of cisplatin responses correlated with EGFR surface expression in head and neck cancer cells.

293 Vs and so Sym004 sensitivity correlates with EGFR numbers available for binding, rather than specific

294 tant osimertinib-resistant NSCLC models with EGFR-dependent and EGFR-independent resistance mechanism

295 tive therapeutic strategy against NSCLC with EGFR(WT).

296 with non-small cell lung cancer (NSCLC) with EGFR-mutant tumors, TKI resistance often returns as a re

297 characteristics of early stage patients with EGFR mutations.

298 Patients with EGFR-mutant NSCLC without prior treatment of advanced di

299 ly develop drug resistance when treated with EGFR tyrosine kinase inhibitors (TKIs).

300 equent gefitinib accumulation in xenografted EGFR-mutant tumors.