ライフサイエンスコーパス: EGFR

1 EGFR and TfR were recruited to largely distinct clathrin

2 EGFR antibodies have shown promise in patients with adva

3 EGFR CNG was determined by fluorescent in situ hybridiza

4 EGFR expression on Th2 cells was TCR-signaling dependent

5 EGFR expression was also observed in circulating tumor c

6 EGFR is highly expressed in basal-like TNBC and is consi

7 EGFR signaling in macrophages may prove to be an effecti

8 EGFR-deficient myeloid cells in the colon of DSS-treated

9 ts with advanced EGFR-TKI-naive NSCLC and 15 EGFR-TKI-resistant patients to identify somatic SNVs, sm

10 Actionable genetic alterations included 25 EGFR mutations, 5 BRAF mutations, and 1 MET mutation, as

11 pression and mutations of EGFRs, or aberrant EGFR signaling are commonly associated with the developm

12 , virtually all patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs vi

13 n the plasma of NSCLC patients with acquired EGFR-TKI resistance than prior to EGFR-TKI therapy, and

14 in patients with NSCLC harbouring activating EGFR mutations.

15 In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection

16 our data suggest that a small pool of active EGFRs is sufficient to drive tumorigenesis by signaling

17 rst-line treatment of patients with advanced EGFR-mutation-positive non-small-cell lung cancer (NSCLC

18 scribe a total of 119 patients with advanced EGFR-TKI-naive NSCLC and 15 EGFR-TKI-resistant patients

19 line H1975, without significantly affecting EGFR wild-type cell lines.

20 rt how combining a select antioxidant and an EGFR-specific small molecule kinase inhibitor (SMKI) cou

21 irus ICOVIR-15K was engineered to express an EGFR-targeting BiTE (cBiTE) antibody under the control o

22 Erlotinib is an EGFR tyrosine kinase inhibitor that has shown a signific

23 ningeal metastases who had never received an EGFR tyrosine kinase inhibitor and patients with leptome

24 Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes

25 s who had progressed after treatment with an EGFR tyrosine kinase inhibitor received AZD3759 at 50 mg

26 l metastases who had been pretreated with an EGFR tyrosine kinase inhibitor.

27 ling complex between T1/ST2 (the IL-33R) and EGFR.

28 TP53 (n = 48), KRAS (n = 47) and EGFR (n = 15) were the most prevalent.

29 e of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab efficacy with th

30 ed here that the incidence of RAS, BRAF, and EGFR mutations is low in cSCC.

31 BiTEs bound specifically to both CD3(+) and EGFR(+) cells.

32 according to EGFR copy number gain (CNG) and EGFR, KRAS, BRAF, and PIK3CA mutation status.

33 ation (FISH) using prespecified criteria and EGFR FISH-positive status was defined as high polysomy o

34 essing esophageal adenocarcinomas (EACs) and EGFR overexpressing esophageal squamous cell carcinomas

35 rs of clathrin-mediated internalization; and EGFR activity was insensitive to Cbl overexpression.

36 rk where co-activation of Toll/NF-kappaB and EGFR signaling by ROS levels in the PSC/niche controls l

37 stic and predictive roles of TP53, KRAS, and EGFR in non-small-cell lung cancer (NSCLC).

38 ld-type [WT] and mutant) for TP53, KRAS, and EGFR were determined in blinded fashion in multiple labo

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

40 yrosine kinase inhibitor of VEGFR2, RET, and EGFR, all of which are in involved in the pathogenesis o

41 we demonstrate that co-targeting of ROS1 and EGFR could potentially offer an effective oral cancer th

42 ing and support continued evaluation of anti-EGFR antibodies in this subpopulation.

43 ossible explanation for the failures of anti-EGFR therapy in GBM and suggest a new approach to the tr

44 nity-modulated VH and VL regions of the anti-EGFR GA201 mAb were tested for selective targeting and e

45 ET pathways restores the sensitivity to anti-EGFR drugs, here we aimed at discovering the first compo

46 on as negative predictors of benefit to anti-EGFR monoclonal antibody therapies for targeted therapy

47 eading to resistance of cancer cells to anti-EGFR therapy.

48 rapy in patients with advanced NSCLC who are EGFR FISH-positive.

49 lating COP9 signalosome (CSN) in attenuating EGFR through an association between the Cops3 subunit of

50 FRET studies, we show that ENb-TRAIL blocks EGFR signalling via the binding of ENb to EGFR which in

51 derivatives that are dual inhibitors of both EGFR kinase and the NF-kappaB activity.

52 cription (STAT1), via an IFN-independent but EGFR- and integrin-dependent signaling pathway.

53 To evaluate associations by EGFR mutation status for lung adenocarcinoma risk among

54 SRS followed by EGFR-TKI resulted in the longest OS and allowed patients

55 tutional randomized trial of SRS followed by EGFR-TKI versus EGFR-TKI followed by SRS at intracranial

56 h SRS followed by EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followed by SRS or WBRT at intracr

57 Patients were treated with SRS followed by EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followe

58 changes upon tyrosine-221 phosphorylation by EGFR.

59 ovel proteins that are involved in cancerous EGFR signaling.

60 and MAPK pathway signaling under continuous EGFR inhibition in osimertinib-sensitive cells.

61 l results point to little benefit to current EGFR-targeted agents in an unselected patient population

62 non-small cell lung cancer (NSCLC) to detect EGFR mutations.

63 The recently discovered EGFR-C797S mutation causes resistance against third-gene

64 In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes

65 ither EGFR wild type or the mutant EGFRvIII, EGFR inhibition triggers a rapid adaptive response drive

66 show that in glioma cells expressing either EGFR wild type or the mutant EGFRvIII, EGFR inhibition t

67 cancer types which do not respond to either EGFR antagonist or DR agonist monotherapies.

68 tion, poor prognosis; (iii) CRIS-C: elevated EGFR signalling, sensitivity to EGFR inhibitors; (iv) CR

69 used in the DS-GPA index plus 2 new factors: EGFR and ALK alterations in patients with adenocarcinoma

70 bly underwent NRP2 loss, a step required for EGFR upregulation.

71 esistance by preferentially substituting for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signal

72 We screened human colorectal tumors for EGFR-positive myeloid cells and investigated their assoc

73 Furthermore, EGFR activation in epithelial cells promoted the prolife

74 imaging features and mutation status (e.g., EGFR-positive [EGFR+] vs. EGFR-negative) was assessed us

75 n causes resistance against third-generation EGFR inhibitors.

76 treated with osimertinib, a third-generation EGFR TKI, after previous treatment failure with one or m

77 nd patient-derived glioma stem cells (GSCs), EGFR signaling promotes H3K23 acetylation and associatio

78 n resistance to a previous EGFR TKI, and had EGFR-activating mutations and acquired Thr790Met mutatio

79 Hence EGFR elicits PLCgamma1-calcium signals to facilitate for

80 more, a significant correlation between high EGFR activity in tumour cells and macrophage-tumour cell

81 ERBB3) and its catalytically active homologs EGFR and HER2 are essential for their signaling.

82 /or number, we studied mice expressing human EGFR in SCs and SCP in the context of mice that form neu

83 ongly interacted with oncogenic, hyperactive EGFR variants.

84 To test if EGFR activity affects neurofibroma initiation, size, and

85 inhibition of integrin linked kinase (ILK), EGFR and NF-kappaB, as well as transfection of a dominan

86 alt of cell proliferation, severely impaired EGFR signaling and the onset of cellular senescence.

87 ese evanescent fields reflect the changes in EGFR kinase domain polarization upon ligand binding.

88 g small-molecule inhibitors have efficacy in EGFR-amplified oesophageal squamous cell carcinoma (ESCC

89 ccount for the intratumoral heterogeneity in EGFR activity observed.

90 cant degree of intratumoral heterogeneity in EGFR activity, as well as the pharmacodynamic effect of

91 in a significant, dose-dependent increase in EGFR tyrosine phosphorylation, particularly of sites cor

92 Insertion mutations in EGFR and HER2 both occur at analogous positions in exon

93 Mutations in EGFR drive tumor growth but render tumor cells sensitive

94 a novel mechanism of acquired resistance in EGFR-dependent cancers of multiple cell lineages.

95 s not known how K-Ras activation inactivates EGFR, leading to resistance of cancer cells to anti-EGFR

96 samples for resistance mechanisms, including EGFR-activating, Thr790Met, and Cys797Ser mutations, and

97 or tyrosine kinase/Ras/Raf pathway including EGFR and KRAS were not significantly different between p

98 iptional derepression of EGFR, and increased EGFR pathway output.

99 lusively in EBs and newborn ECs that inherit EGFR and active MAPK from fast-dividing progenitors.

100 side and delphinidin-3-O-glucoside inhibited EGFR (IC50=0.10 and 2.37microM, respectively).

101 rther showed that knockout of RCN2 inhibited EGFR phosphorylation, Ki-67 expression and tumor growth

102 om ubiquitination to neddylation, inhibiting EGFR dynamics in response to an acute ligand stimulus.

103 nguish between cell-surface and internalized EGFR on the basis of the addition of red or blue fluorog

104 ucomatous damage, a process that may involve EGFR signaling and other immune responses in the optic n

105 r receptor/mitogen-activated protein kinase (EGFR/MAPK) signalling triggers Drosophila intestinal ste

106 , and ALK inhibition in BRAF-, NRAS-, KRAS-, EGFR-, and ALK-mutant lung cancer cells.

107 The fluorescent color of the aptamer-labeled EGFR can be switched between blue and red in situ simply

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

109 We performed experiments in mice lacking EGFR in intestinal epithelial cells (Villin-Cre; Egfr(f/

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

111 Lnc-EGFR links an immunosuppressive state to cancer by promo

112 ration and RANK expression while maintaining EGFR expression.

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

114 is a key ERK phosphorylation site mediating EGFR-induced sensitization of the channel to stimulate s

115 2/NRF2, modulated the response to BRAF, MEK, EGFR, and ALK inhibition in BRAF-, NRAS-, KRAS-, EGFR-,

116 n kinase C- and Gbetagamma-metalloproteinase/EGFR-dependent MAPK/ERK signaling cascades.

117 assay might be an optional method to monitor EGFR-TKI resistance and to discover mechanisms of drug r

118 Moreover, EGFR(+) oligodendrocyte progenitors, but not neuroblasts

119 nd synergistic growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell

120 ucial GBM signaling involving FAK and mutant EGFR, EGFRvIII, and abrogated gains in secreted protease

121 of interaction partners that bind to mutated EGFR can help identify novel targets for drug discovery.

122 On soft surfaces, neither EGFR inhibition nor EGF stimulation have any effect on c

123 known oncogenes, including BRAF, NRAS, NF1, EGFR, ALK, TERT, and APC.

124 AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to p

125 High expression and activation of EGFR and/or ErbB2 were recently demonstrated in biliary

126 EREG-mediated activation of EGFR enhanced nociception through a mechanism involving

127 nitive evidence that sustained activation of EGFR in proximal epithelia is sufficient to cause sponta

128 Concurrent amplifications of EGFR and PDGFRA have been reported in up to 5% of gliobl

129 In the prespecified analysis of EGFR FISH-positive subpopulation with squamous cell hist

130 r desmosome components shifts the balance of EGFR modifications from ubiquitination to neddylation, i

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

132 f EGFR-expressing GBM using a combination of EGFR and TNF inhibition.

133 Furthermore, tamoxifen-induced deletion of EGFR from epithelial cells of established intestinal tum

134 Deletion of EGFR from intestinal epithelial cells did not affect tum

135 , than control mice or mice with deletion of EGFR from intestinal epithelial cells.

136 Mice with deletion of EGFR from myeloid cells developed more severe colitis af

137 , results in transcriptional derepression of EGFR, and increased EGFR pathway output.

138 lysine 721 in the tyrosine kinase domain of EGFR, and that this methylation leads to enhanced activa

139 ptional repressor, suppresses the effects of EGFR inhibition by partially restoring the EGFR-promoted

140 ergistically enhanced anti-tumour effects of EGFR-directed therapies including erlotinib.

141 rder to interrogate the antitumor effects of EGFR-targeted drugs in mCRC (n = 40).

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

143 Increased expression of EGFR in myeloid cells from the colorectal tumor stroma a

144 4(+) cells, as pharmacological inhibition of EGFR increases the transcription of lytic IE1/IE2 mRNA w

145 Genetic or pharmacologic inhibition of EGFR tyrosine kinase activity or downstream MEK activity

146 t the hypothesis that combined inhibition of EGFR, HER2, and HER3 signalling with the tyrosine kinase

147 rectal tumor biopsies to determine levels of EGFR in tumor and stroma; we also collected information

148 However, the mechanism of EGFR-induced NF-kappaB activation is not fully defined.

149 WHSC1L1-mediated methylation of EGFR in the nucleus enhanced its interaction with PCNA i

150 entified eight novel interaction partners of EGFR, of which half strongly interacted with oncogenic,

151 protein Grb2, it enabled the photocapture of EGFR in a stimulus-dependent manner.

152 ng may noninvasively predict the presence of EGFR mutations in pulmonary nodules of the adenocarcinom

153 ss of the Thr790Met mutation but presence of EGFR-activating mutations in plasma were associated with

154 Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be

155 ility, but little is known about the role of EGFR in these mechanosensing processes.

156 ed cancer cells, we investigated the role of EGFR signaling in drug-naive cancer cells harboring thes

157 This has broad implications for the roles of EGFR and HER2 in the absence of EGF both for normal and

158 und (Erlotinib) into the ATP binding site of EGFR-TK domain (PDB ID:1M17) to elucidate vital structur

159 Here we show that concomitant targeting of EGFR and the nonreceptor tyrosine kinases PYK2/FAK syner

160 d suggest a new approach to the treatment of EGFR-expressing GBM using a combination of EGFR and TNF

161 inib, are active agents for the treatment of EGFR-mutant lung cancer.

162 els of phosphorylation and ubiquitylation of EGFR in tumors in vivo closely resemble patterns and lev

163 in contexts and broaden our understanding of EGFR regulation.

164 The diversity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms pre

165 bstantial challenge for the effective use of EGFR-directed therapeutics.

166 Overexpression and mutations of EGFRs, or aberrant EGFR signaling are commonly associate

167 y and enhanced antiproliferative activity on EGFR TKI-resistant NSCLC.

168 The same effect of macrophage infiltrate on EGFR activation was also seen in a colorectal cancer xen

169 es of HBEGF-transformed cells; however, only EGFR was able to rescue the phenotype in cells lacking b

170 d by EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followed by SRS or WBRT at intracranial progres

171 ous treatment failure with one or more other EGFR TKIs.

172 ge for developing new treatments to overcome EGFR tyrosine kinase inhibitor resistance.

173 es and mutation status (e.g., EGFR-positive [EGFR+] vs. EGFR-negative) was assessed using the Wilcoxo

174 RA study, had shown resistance to a previous EGFR TKI, and had EGFR-activating mutations and acquired

175 Exclusion criteria included prior EGFR-TKI use, EGFR-TKI resistance mutation, failure to r

176 -TKI resistance mutation, failure to receive EGFR-TKI after WBRT/SRS, or insufficient follow-up.

177 The tyrosine kinase receptor EGFR is expressed in Schwann cell precursors (SCP), whic

178 inase inhibitors (TKIs) of the EGF receptor (EGFR) have provided a significant improvement in the dis

179 etalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface during invadopodium formation.

180 or (HBEGF) is a ligand for the EGF receptor (EGFR), one of the most commonly amplified receptor tyros

181 ion of the epidermal growth factor receptor (EGFR) and of its ligand, amphiregulin, for the formation

182 K-Ras and epidermal growth factor receptor (EGFR) are mutually exclusive, but it is not known how K-

183 phorylated epidermal growth factor receptor (EGFR) as a model system.

184 ether with epidermal growth factor receptor (EGFR) forms a signaling complex regulating epidermal hom

185 he role of epidermal growth factor receptor (EGFR) inhibition in chemoradiation strategies in the non

186 Epidermal growth factor receptor (EGFR) interacts with integrins during cell spreading and

187 nic mutant epidermal growth factor receptor (EGFR) is a breakthrough in targeted cancer therapy and m

188 The epidermal growth factor receptor (EGFR) is a clinically validated target in head and neck

189 on of anti-epidermal growth factor receptor (EGFR) monoclonal antibodies with radiotherapy (RT) to st

190 l specific epidermal growth factor receptor (EGFR) null mouse, we show that exendin-4 induced an incr

191 to harbor epidermal growth factor receptor (EGFR) or Kristen rat sarcoma viral (KRAS) mutations, res

192 nd mutated epidermal growth factor receptor (EGFR) presents a substantial challenge for the effective

193 GFR)-2 and epidermal growth factor receptor (EGFR) signaling by enhancing their stability and recycli

194 Epidermal growth factor receptor (EGFR) signaling is a known mediator of colorectal carcin

195 addition, epidermal growth factor receptor (EGFR) signaling is regulated by its accumulation within

196 Aberrant epidermal growth factor receptor (EGFR) signaling is widespread in cancer, making the EGFR

197 ing on the epidermal growth factor receptor (EGFR) signaling network in HEK293T cells, we analyze 20

198 rch in the epidermal growth factor receptor (EGFR) signalling field, and many targeted anti-cancer dr

199 uch as the epidermal growth factor receptor (EGFR) that effectively induces complement activation and

200 rrent anti-epidermal growth factor receptor (EGFR) therapy for oral cancer does not provide satisfact

201 led by the epidermal growth factor receptor (EGFR), is critical to recovery from SARS-CoV-induced tis

202 unction of epidermal growth factor receptor (EGFR), the effect of protein methylation on its function

203 y enhanced epidermal growth factor receptor (EGFR)-mediated mitogenic signaling, promoting tumor cell

204 tases-from epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) are asso

205 aradigm of epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has identified dynamic features

206 WBRT), and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are treatment op

207 ted to the epidermal growth factor receptor (EGFR).

208 d with the epidermal growth factor receptor (EGFR).

209 rmation of epidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) an

210 ctive anti-epidermal-growth-factor-receptor (EGFR) therapy.

211 rected to Epidermal Growth Factor Receptors (EGFR) or to human EGF receptors 2 (HER2), which are over

212 ses four distinct tyrosine kinase receptors, EGFR/ErbB1/HER1, ErbB2/HER2, ErbB3/HER3, and ErbB4/HER4,

213 ments using TM domains from other receptors, EGFR and FGFR1, failed to stimulate TrkB phosphorylation

214 y efficacy due to drug resistance or reduced EGFR level.

215 We show that LOX regulates EGFR by suppressing TGFbeta1 signalling through the secr

216 ER2/HER3 heterodimers and by down-regulating EGFR via a mechanism involving its degradation.

217 recognized function of the CSN in regulating EGFR neddylation has broad-reaching implications for und

218 VGF silencing resensitized EGFR-mutated lung adenocarcinoma cells to TKI.

219 le, target gatekeeper mutated drug-resistant EGFR-L858R/T790M, and covalently alkylate Cys797.

220 YES1 was amplified in osimertinib-resistant EGFR-mutant tumor cells, the effects of which were overc

221 n the tumor, which was NSCLC with responsive EGFR exon 19 deleted.

222 icacy and safety with that of the reversible EGFR tyrosine kinase inhibitor gefitinib in the first-li

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

224 Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertin

225 For sensing EGFR activity in cells, we used a genetically encoded Cr

226 In patients with a sensitizing EGFR mutation, disease progression after first-line epid

227 In several EGFR-mediated cancer models, cetuximab failed to inhibit

228 alterations in patients with advanced-stage EGFR-mutant lung cancer.

229 RT versus EGFR-TKI, age, performance status, EGFR exon 19 mutation, and absence of extracranial metas

230 weakened dimerization elicits more sustained EGFR signaling than seen with EGF, provoking responses i

231 Here, we demonstrate that EGFR-targeting small-molecule inhibitors have efficacy i

232 Here, we document that EGFR and PDGFRA protein co-expression occurs in 37% of G

233 We hypothesised that EGFR copy number by fluorescence in-situ hybridisation (

234 Our results indicate that EGFR mutations may drive different metabolic tumor pheno

235 Overall, our results indicate that EGFR promotes survival of prostate TIC and CTC that meta

236 We show that EGFR Abs directed against clinically relevant epitopes c

237 r previous work with monocytes, suggest that EGFR likely serves as an important determinant of HCMV t

238 The EGFR belongs to the well-studied ErbB family of receptor

239 Additionally, the EGFR T790M mutation was found in 46.7% (7/15) of the pat

240 r 45a with an IC50 value of 1 nM against the EGFR L858R/T790M double mutant.

241 ents with non-small-cell lung cancer and the EGFR Thr790Met mutation who were treated with osimertini

242 t synergy in neuroblastoma cells between the EGFR kinase inhibitor lapatinib and the anticancer compo

243 Both the EGFR and EREG genes displayed a genetic association with

244 of concept for a strategy of cotargeting the EGFR and PYK2/FAK kinases to improve TNBC therapy.

245 graphy and other approaches, we show how the EGFR ligands epiregulin (EREG) and epigen (EPGN) stabili

246 supports mutational testing for genes in the EGFR signaling pathway, since they provide clinically ac

247 ignaling is widespread in cancer, making the EGFR an important target for therapy.

248 ilize different dimeric conformations of the EGFR extracellular region.

249 ngements fusing the 3' coding portion of the EGFR gene to the 5'-UTR of the SEC61G, yielding products

250 hrough direct non-histone methylation of the EGFR protein with effects both in its cytoplasmic and nu

251 hiometry and the association constant of the EGFR-Grb2 binding interaction in the plasma membrane, in

252 f EGFR inhibition by partially restoring the EGFR-promoted gene expression program, including the sus

253 We argue that the EGFR allows HCMV to regulate the cellular functions of t

254 y and kinetics of acquired resistance to the EGFR inhibition than gliomasphere cultures.

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

256 tion 3 (STAT3), reduces STAT3 binding to the EGFR promoter, results in transcriptional derepression o

257 cinomas (HNSCC) exhibiting resistance to the EGFR-targeting drug cetuximab poses a challenge to their

258 Third, EGFR enabled bypass signaling to critical downstream pat

259 in proliferation and beta-cell mass through EGFR.

260 Thus, EGFR or HER2 can catalyse rigidity sensing after associa

261 gefitinib with that of placebo according to EGFR copy number gain (CNG) and EGFR, KRAS, BRAF, and PI

262 ell as many TSGs not previously connected to EGFR and whose biological functions in tumorigenesis are

263 ks EGFR signalling via the binding of ENb to EGFR which in turn induces DR5 clustering at the plasma

264 h acquired EGFR-TKI resistance than prior to EGFR-TKI therapy, and in the generated erlotinib-resista

265 ON) administering AZD9291 and selumetinib to EGFR-mutant lung cancer patients.

266 a cells with primary resistance sensitive to EGFR inhibition.

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

268 o and in vivo models restores sensitivity to EGFR TKIs.

269 s exhibited strong inhibitory effects toward EGFR kinase activity and excellent inhibition of cell gr

270 positively/negatively correlated with TP53, EGFR, and MMP members mediated OS development, including

271 170 deaths) were used for TP53/KRAS and TP53/EGFR analyses.

272 c and predictive roles of TP53/KRAS and TP53/EGFR comutations in randomized trials of adjuvant chemot

273 adenocarcinoma subgroup as well as the TP53/EGFR comutation in adenocarcinoma only through a multiva

274 dition to regulating HCMV entry/trafficking, EGFR signaling may also shape the early steps required f

275 GF-like domain-containing protein that traps EGFR at the cell surface to facilitate its activation by

276 rane-bound, constitutively active, truncated EGFR.

277 tion of low ligand concentrations in tumors, EGFR endocytosis was kinase-dependent and blocked by inh

278 Two EGFR mutants (DeltaN566 and DeltaN599) were identified a

279 ntibodies Trastuzumab and Pertuzumab and two EGFR binding antibodies including Cetuximab.

280 gnaling pathway, RelA/p65 is regulated under EGFR activation remains to be further clarified.

281 nalysis demonstrated that the use of upfront EGFR-TKI, and deferral of radiotherapy, is associated wi

282 lusion criteria included prior EGFR-TKI use, EGFR-TKI resistance mutation, failure to receive EGFR-TK

283 On multivariable analysis, SRS versus EGFR-TKI, WBRT versus EGFR-TKI, age, performance status,

284 zed trial of SRS followed by EGFR-TKI versus EGFR-TKI followed by SRS at intracranial progression is

285 e analysis, SRS versus EGFR-TKI, WBRT versus EGFR-TKI, age, performance status, EGFR exon 19 mutation

286 tion status (e.g., EGFR-positive [EGFR+] vs. EGFR-negative) was assessed using the Wilcoxon rank-sum

287 neck squamous cell carcinoma (HNSCC), where EGFR-blocking antibodies are approved for first-line tre

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

289 features were significantly associated with EGFR mutation status (FDRWilcoxon = 0.01-0.10).

290 Proteins associated with EGFR signaling, including downstream AKT-mTOR pathways,

291 21.3, BTNL2) which is specific to cases with EGFR mutations.

292 e progression-free survival in patients with EGFR FISH-positive cancer and overall survival in the en

293 specified subgroup analyses of patients with EGFR FISH-positive squamous-cell carcinoma cancers are e

294 ptions for brain metastases in patients with EGFR-mutant non-small-cell lung cancer (NSCLC).

295 associated with inferior OS in patients with EGFR-mutant NSCLC who develop brain metastases.

296 cs, and efficacy of AZD3759 in patients with EGFR-mutant NSCLC with brain and leptomeningeal metastas

297 Clinical Application: Patients with EGFR-mutant or ALK-positive non-small-cell lung cancer w

298 s found in 46.7% (7/15) of the patients with EGFR-TKI-resistant NSCLC, suggesting that the NGS-based

299 nder tumor cells sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI).

300 accumulation of oncogenic mutations in Wnt, EGFR, P53, and TGF-beta signaling pathways facilitates e