ライフサイエンスコーパス: erlotinib

1 e randomly assigned (398 to afatinib, 397 to erlotinib).

2 regimens combining a HAP, evofosfamide, with erlotinib.

3 ated by AF-TUSC2-erlotinib compared to TUSC2-erlotinib.

4 t of drug-drug interactions between PPIs and erlotinib.

5 d 1000 mg/m2 of gemcitabine plus 100 mg/d of erlotinib.

6 o energetic stress induced by treatment with erlotinib.

7 non-small cell lung cancer to EGFR inhibitor Erlotinib.

8 ival was prolonged over controls by AF-TUSC2-erlotinib.

9 y treated with the tyrosine kinase inhibitor erlotinib.

10 ase and then treated with the EGFR inhibitor Erlotinib.

11 when treated with the combination of PF and erlotinib.

12 tion, enhances growth inhibitory activity of Erlotinib.

13 tic doses from PET with a microdose of (11)C-erlotinib.

14 effects of EGFR-directed therapies including erlotinib.

15 eks (n = 40) after commencing treatment with erlotinib.

16 R) expression or by using the EGFR inhibitor erlotinib.

17 ay contribute to the exceptional response to erlotinib.

18 nd early clinical studies when combined with erlotinib.

19 delta restoring sensitized H1650-M3 cells to erlotinib.

20 d with a microdose and pharmacologic dose of erlotinib.

21 s switch in cancer cells treated with IR and erlotinib.

22 ncapsulation efficiency of 49.04+/-2.54% for erlotinib.

23 ced increases in brain distribution of (11)C-erlotinib.

24 ssive disease, bevacizumab was combined with erlotinib.

25 mutation who were treated with gefitinib or erlotinib.

26 e lung cancer cells increased sensitivity to erlotinib.

27 tration of an EGFR tyrosine kinase inhibitor erlotinib.

28 t the coinjection of a pharmacologic dose of erlotinib (10 mg/kg) or after pretreatment with the ABCB

29 and during intravenous infusion of high-dose erlotinib (10 mg/kg/h, n = 4) or elacridar (12 mg/kg/h,

30 00 mg/m(2) days 1, 8, 15, every 4 weeks plus erlotinib 100 mg once per day (GemErlo) or gemcitabine (

31 randomly assigned at a 1:1 ratio to receive erlotinib 150 mg daily plus oral tivantinib 360 mg twice

32 Patients received oral erlotinib 150 mg per day and intravenous bevacizumab 15

33 pt the highest-dose cohort (AUY922 70 mg and erlotinib 150 mg), which expanded to six patients becaus

34 (1:1) to receive afatinib (40 mg per day) or erlotinib (150 mg per day) until disease progression.

35 erlotinib (150 mg), cabozantinib (60 mg), or erlotinib (150 mg) and cabozantinib (40 mg).

36 a to receive open-label oral daily dosing of erlotinib (150 mg), cabozantinib (60 mg), or erlotinib (

37 assigned centrally in a 1:1 ratio to receive erlotinib (150 mg/day, orally) or chemotherapy (pemetrex

38 stratified by KRAS status, to four arms: (1) erlotinib, (2) erlotinib plus MK-2206, (3) MK-2206 plus

39 with a rapid adoption of pemetrexed (39.2%), erlotinib (20.3%), and bevacizumab (18.9%) and a decline

40 ] vs none), and of grade 3 rash or acne with erlotinib (23 [6%] vs 41 [10%]).

41 tients received CP; in arm B, seven received erlotinib, 53 were administered CP, and 16 underwent fol

42 domized to sulindac (150 mg) twice daily and erlotinib (75 mg) daily (n = 46) vs placebo (n = 46) for

43 b (an irreversible ErbB family blocker) with erlotinib (a reversible EGFR tyrosine kinase inhibitor),

44 C-827 cells with acquired resistance against Erlotinib, a clinically used inhibitor of the EGF recept

45 Erlotinib, a selective EGFR inhibitor, enhanced AQP2 api

46 -proteomics data acquired in the presence of erlotinib-a tyrosine kinase inhibitor (TKI)-in cancer ce

47 R mutation frequency was 22.1% in NSCLC, and erlotinib achieved a response rate of 60% (95% CI, 32.3%

48 Compared with erlotinib alone (median 1.8 months [95% CI 1.7-2.2]), pr

49 lone or in combination with erlotinib versus erlotinib alone in patients with EGFR wild-type NSCLC.

50 progression-free survival in patients given erlotinib alone versus cabozantinib alone, and in patien

51 us cabozantinib alone, and in patients given erlotinib alone versus the combination of erlotinib plus

52 therapy schedule with either evofosfamide or erlotinib alone, (ii) sequentially alternating single do

53 lly meaningful, superior efficacy to that of erlotinib alone, with additional toxicity that was gener

54 overall survival with afatinib compared with erlotinib, along with a manageable safety profile and th

55 Erlotinib also led to AMPK-dependent phosphorylation of

56 dy, we examined the effect of treatment with erlotinib, an inhibitor of EGFR tyrosine kinase activity

57 tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib and afatinib are approved treatments for non-s

58 evidence of benefit for the combined use of erlotinib and bevacizumab in patients with NSCLC harbour

59 t NSCLC were treated with the combination of erlotinib and bevacizumab, stratified by the presence of

60 ficantly increased the antitumor activity of erlotinib and cetuximab in vivo.

61 tive power of this test in the comparison of erlotinib and chemotherapy in patients with non-small-ce

62 al, progression-free survival of gemcitabine-erlotinib and erlotinib maintenance with gemcitabine alo

63 In patients treated with erlotinib and esomeprazole with cola, the mean AUC0-12h

64 ge IVA HNSCC received 13 days of neoadjuvant erlotinib and experienced a near-complete histologic res

65 , resistance to EGFR-targeting drugs such as Erlotinib and Gefitinib develops quickly.

66 rosine kinase inhibitors (EGFR-TKI), such as erlotinib and gefitinib.

67 s tissue distribution and excretion of (11)C-erlotinib and has an influence on the ability of (11)C-e

68 time the concurrent transdermal delivery of erlotinib and IL36alpha siRNA as a potential dual therap

69 The enhanced co-transdermal delivery of erlotinib and IL36alpha siRNA by CYnLIP efficaciously tr

70 was rapid, dose-dependent, and inhibited by erlotinib and lapatinib, although to differing extents.

71 nsible for the reduced antitumor efficacy of erlotinib and other EGFRIs, and blockade of IL1 signalin

72 observed when treated with a combination of erlotinib and PF compared to either agent alone.

73 Secondary outcomes were the effect of erlotinib and quality assurance of radiotherapy on overa

74 1% of the patients who will not benefit from erlotinib and stop the treatment at this time.

75 rters influence in vivo disposition of (11)C-erlotinib and thereby affect its distribution to normal

76 st-line treatment with EGFR TKIs (gefitinib, erlotinib, and afatinib) has been approved for patients

77 sine kinase inhibitors, including gefitinib, erlotinib, and afatinib.

78 cultured cells, treatment with sunitinib and erlotinib, approved anticancer drugs that inhibit AAK1 o

79 ally possible, there are no prior reports of erlotinib-associated retinal toxicity despite over a dec

80 Thus, pretreatment with erlotinib augments multiple mechanisms of PDT effect tha

81 strate that short-duration administration of erlotinib before PDT can greatly improve the responsiven

82 The effects of cola on erlotinib bioavailability in patients not treated with a

83 results in a clinically relevant decrease of erlotinib bioavailability.

84 rmal growth factor receptor (EGFR) inhibitor erlotinib blocked ERK1/2 phosphorylation and increased P

85 In mice, erlotinib blocks the LPS-induced expression of tumor nec

86 During high-dose erlotinib infusion, (11)C-erlotinib brain distribution was also significantly (1.7

87 (11)C-erlotinib brain uptake was quantified by pharmacokinetic

88 s showed enhanced (p<0.01) skin retention of erlotinib by CYnLIP (40.76-fold) than solution and more

89 Although it is efficacious, erlotinib can cause skin toxicity.

90 Inhibition of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this sign

91 els of dengue and Ebola infection, sunitinib/erlotinib combination protected against morbidity and mo

92 After erlotinib commencement, SBRT with equipotent fractionati

93 atures significantly upregulated by AF-TUSC2-erlotinib compared to TUSC2-erlotinib.

94 C trial demonstrated the greater efficacy of erlotinib compared with chemotherapy for the first-line

95 rticipants with FAP, the use of sulindac and erlotinib compared with placebo resulted in a lower duod

96 f time after an evofosfamide dose and before erlotinib confer further benefits in reduction of tumor

97 the approved anticancer drugs sunitinib and erlotinib, could block HCV assembly.

98 on, being a mixture of four drugs (axitinib, erlotinib, dasatinib and AZD4547) at low doses, inhibiti

99 (11)C-erlotinib data were analyzed using single-tissue and 2-t

100 how that a single dose of the EGFR inhibitor erlotinib delivered prior to DEN-induced injury was suff

101 Erlotinib depends on stomach pH for its bioavailability.

102 to the EGFR inhibitors (EGFRI) cetuximab and erlotinib, despite tumor expression of EGFR.

103 In patients, the VT of (11)C-erlotinib did not increase after intake of elacridar (0.

104 This phase II study of AUY922 and erlotinib did not meet its primary end point.

105 Erlotinib did not, however, improve CFS in high-risk pat

106 Under baseline conditions, (11)C-erlotinib distribution to the brain (total volume of dis

107 lted in a 3.5 +/- 0.9-fold increase in (11)C-erlotinib distribution to the brain (VT, 0.81 +/- 0.21 m

108 (11)C-erlotinib distribution to the brain was restricted by Ab

109 When combined with the EGFR-targeted drug erlotinib, DLL-1 significantly improved progression-free

110 We find that low-dose (1 muM erlotinib) drugging actually increases cellular energy p

111 gnificant increase in the bioavailability of erlotinib during esomeprazole treatment.

112 EGFR gene copy number was not predictive of erlotinib efficacy.

113 anti-HER2 mAb), H3.105.5 (anti-HER3 mAb) and erlotinib (EGFR small-molecule tyrosine kinase inhibitor

114 ing five biomarker-matched treatment groups: erlotinib for EGFR mutations; selumetinib for KRAS, NRAS

115 ree survival on therapy that did not contain erlotinib for KRAS mut+ patients and improved prognosis

116 ed a phase I/II trial to evaluate AUY922 and erlotinib for patients with EGFR-mutant lung cancer and

117 from treatment with EGFR inhibitors such as erlotinib, gefitinib, and afatinib, but outcomes are lim

118 setting, recommendations include docetaxel, erlotinib, gefitinib, or pemetrexed for patients with no

119 fatinib group versus 227 (57%) of 395 in the erlotinib group had grade 3 or higher adverse events.

120 ents were diarrhoea (three [8%] cases in the erlotinib group vs three [8%] in the cabozantinib group

121 erse events were more common in the sulindac-erlotinib group, with an acne-like rash observed in 87%

122 were randomized, 75 each to the placebo and erlotinib groups.

123 e NSCLC, cabozantinib alone or combined with erlotinib has clinically meaningful, superior efficacy t

124 the 219 patients receiving gemcitabine plus erlotinib (HR, 1.19; 95% CI, 0.97-1.45; P = .09; 188 dea

125 TAT3, TNFalpha, NFkappaB, IL23 and IL17) for erlotinib/IL36alpha siRNA-CYnLIP (p<0.05) comparable to

126 ition, brain uptake was measured using (11)C-erlotinib imaging and ex vivo scintillation counting in

127 binds to the EGFR upon LPS stimulation, and erlotinib impairs this association.

128 The tyrosine kinase inhibitor erlotinib improves the outcomes of patients with advance

129 th factor receptor tyrosine kinase inhibitor erlotinib in combination with gemcitabine has shown effi

130 findings show that PF enhances the effect of erlotinib in ErbB3-expressing pancreatic cancer cells by

131 activation was maintained in the presence of erlotinib in heregulin-overexpressing, EGFR-mutant NSCLC

132 itors to enhance brain distribution of (11)C-erlotinib in nonhuman primates as a model of the human B

133 f miR-214 may reverse acquired resistance to erlotinib in NSCLC through mediating its direct target g

134 ole of miR-214 in the acquired resistance to erlotinib in NSCLC, and elucidate the underlying mechani

135 event and/or overcome acquired resistance to erlotinib in several EGFR-mutant non-small cell lung can

136 Patients receiving erlotinib in the second- or third-line setting for advan

137 nd EPHA2 kinases in conferring resistance to erlotinib in TKI sensitive strains.

138 ient cells exhibited enhanced sensitivity to erlotinib in vitro and in vivo that was associated with

139 itro and increased the antitumor activity of erlotinib in vivo.

140 rlying the antiviral effect of sunitinib and erlotinib (in addition to EGFR), respectively.

141 mal growth factor receptor (EGFR) inhibitor, erlotinib, in Non-Small Cell Lung Cancer cell lines.

142 ere disrupted in mice, brain uptake of (11)C-erlotinib increased both at a tracer dose and at a pharm

143 Similar to VP, erlotinib increased exocytosis and decreased endocytosis

144 Erlotinib increased phosphorylation of AQP2 at Ser-256 a

145 combination of TUSC2 forced expression with erlotinib increased tumor cell apoptosis and inhibited c

146 ompanied by increased vascular shutdown, and erlotinib increases the in vitro cytotoxicity of PDT to

147 GA) abrogated cell death induced by AF-TUSC2-erlotinib, indicating a regulatory role for ROS in the e

148 overexpression rescued tumors from AF-TUSC2-erlotinib induced apoptosis.

149 A pan-caspase inhibitor reduced erlotinib-induced IL1alpha secretion, suggesting that IL

150 sion of IL1R signaling significantly reduced erlotinib-induced IL6 production.

151 Suppression of MyD88 expression blocked erlotinib-induced IL6 secretion in vitro and increased t

152 ike receptor or IL18 receptor involvement in erlotinib-induced IL6 secretion.

153 table options for the necessary treatment of erlotinib-induced rash in the second- or third-line sett

154 Erlotinib-induced skin rash was associated with improved

155 ined the effect of prophylactic treatment of erlotinib-induced skin rash.

156 findings show that the combination of TUSC2-erlotinib induces additional novel vulnerabilities that

157 During high-dose erlotinib infusion, (11)C-erlotinib brain distribution w

158 ddition to affecting assembly, sunitinib and erlotinib inhibited HCV entry at a postbinding step, the

159 ), and treatment with the EGFR-specific SMKI erlotinib inhibited non-CSCs.

160 her (9%; range, -10% to +30%; P = .03) after erlotinib intake with cola.

161 d out on the analogs and reference compound (Erlotinib) into the ATP binding site of EGFR-TK domain (

162 (11)C-erlotinib is a PET tracer to distinguish responders from

163 Similar benefit is found when erlotinib is added to PDT of A549 NCSLC xenografts.

164 lete response rates of 63% are achieved when erlotinib is administered in three doses before PDT of H

165 Erlotinib is an EGFR tyrosine kinase inhibitor that has

166 Erlotinib is an epidermal growth factor receptor inhibit

167 Erlotinib is approved for the treatment of all patients

168 Response to erlotinib is associated with reduced heterogeneity at (1

169 ErbB3 activation, and PF in combination with erlotinib is much more effective as an antitumor agent c

170 eived erlotinib or gefitinib, treatment with erlotinib is recommended.

171 When erlotinib is taken concurrently with a proton pump inhib

172 Although synergy with erlotinib is theoretically possible, there are no prior

173 therapy is controversial and the efficacy of erlotinib is unknown.

174 sion of EMT genes or to confer resistance to erlotinib, it caused downregulation of PKCdelta expressi

175 lls to tyrosine kinase inhibitors, including erlotinib, lapatinib and sunitinib.

176 Saturable transport of erlotinib leads to nonlinear pharmacokinetics, possibly

177 n-free survival of gemcitabine-erlotinib and erlotinib maintenance with gemcitabine alone at the seco

178 er regimens; the addition of capecitabine or erlotinib may be offered.

179 significantly longer with afatinib than with erlotinib (median 2.4 months [95% CI 1.9-2.9] vs 1.9 mon

180 Suppression of SOX2 sensitizes cells to erlotinib-mediated apoptosis, ultimately decreasing the

181 We validated sunitinib- and erlotinib-mediated inhibition of AAK1 and GAK activity a

182 A brief course of erlotinib monotherapy followed by surgical resection.

183 ent with locally advanced HNSCC who received erlotinib monotherapy in a window-of-opportunity clinica

184 tumors, were adaptively randomly assigned to erlotinib (n = 22), erlotinib plus MK-2206 (n = 42), MK-

185 pants included in the safety analysis of the erlotinib (n=40), cabozantinib (n=40), and erlotinib plu

186 total were included in the primary analysis (erlotinib [n=38], cabozantinib [n=38], erlotinib plus ca

187 s increased by the in vivo administration of erlotinib; nevertheless, this elevation of BPD levels on

188 with AUY922 intravenously once per week and erlotinib once per day in 28-day cycles using a 3 + 3 do

189 for metastatic disease and were treated with erlotinib or chemotherapy.

190 setting, for patients who have not received erlotinib or gefitinib, treatment with erlotinib is reco

191 to the EGFR tyrosine kinase inhibitors (TKI) erlotinib or gefitinib.

192 oroquine plus the tyrosine kinase inhibitors erlotinib or sunitinib, suggesting that the antiprolifer

193 ceptor with small-molecule inhibitors (i.e., erlotinib) or monoclonal antibodies (i.e., cetuximab) do

194 ve care alone for those with PS 2; afatinib, erlotinib, or gefitinib for those with sensitizing EGFR

195 with nonsquamous cell carcinoma; docetaxel, erlotinib, or gefitinib for those with squamous cell car

196 Patients who received bevacizumab, erlotinib, or pemetrexed had the longest treatment durat

197 s with advanced solid tumors underwent (11)C-erlotinib PET scans before and after a 1,000-mg dose of

198 and has an influence on the ability of (11)C-erlotinib PET to predict erlotinib tissue distribution a

199 ibitor elacridar on brain uptake using (11)C-erlotinib PET.

200 b1a/b or Abcg2 knockout mice underwent (11)C-erlotinib PET/MR scans, with or without the coinjection

201 oncentration of erlotinib, without affecting erlotinib plasma concentration.

202 0.05), with a concomitant increase in (11)C-erlotinib plasma exposure.

203 ose in muscle tissue, without changing (11)C-erlotinib plasma pharmacokinetics.

204 e erlotinib (n=40), cabozantinib (n=40), and erlotinib plus cabozantinib (n=39) groups, the most comm

205 ysis (erlotinib [n=38], cabozantinib [n=38], erlotinib plus cabozantinib [n=35]).

206 CI 0.27-0.55; one-sided p=0.0003) and in the erlotinib plus cabozantinib group (4.7 months [2.4-7.4];

207 in the cabozantinib group vs 11 [28%] in the erlotinib plus cabozantinib group), hypertension (none v

208 one death due to pneumonitis occurred in the erlotinib plus cabozantinib group, deemed related to eit

209 o cabozantinib treatment, and 43 patients to erlotinib plus cabozantinib treatment, of whom 111 (89%)

210 en erlotinib alone versus the combination of erlotinib plus cabozantinib.

211 ely randomly assigned to erlotinib (n = 22), erlotinib plus MK-2206 (n = 42), MK-2206 plus AZD6244 (n

212 RAS status, to four arms: (1) erlotinib, (2) erlotinib plus MK-2206, (3) MK-2206 plus AZD6244, or (4)

213 ral tivantinib 360 mg twice daily (E + T) or erlotinib plus placebo (E + P) until disease progression

214 The tyrosine kinase inhibitor erlotinib poorly penetrates the blood-brain barrier (BBB

215 The Erlotinib Prevention of Oral Cancer (EPOC) study was a r

216 Erlotinib reduced EGFR phosphorylation in hepatic stella

217 We show that erlotinib relieves EGFR-dependent suppression of FOXO6,

218 important roles for specific PKC isozymes in erlotinib resistance and EMT in lung cancer cells, and h

219 can be induced in NSCLC cells with acquired Erlotinib resistance by direct inhibition of STAT3.

220 Importantly, CK1alpha suppression prevented erlotinib resistance in an HCC827 xenograft model in viv

221 ion 0.13), which predicts ERK activation and erlotinib resistance in EGFR-mutant lung cancer.

222 1alpha knockdown can also attenuate acquired erlotinib resistance, supporting a role for activated NF

223 C) tumor biopsy from a patient with acquired erlotinib resistance.

224 xpression of PIK3Cbeta(D1067V) also promoted erlotinib resistance.

225 g via Smad2/3/4 occurred differently between erlotinib-resistant A549 and erlotinib- sensitive PC9 ce

226 Targeting EPHA2 in erlotinib-resistant cells decreased S6K1-mediated phosph

227 reening and whole-exome sequencing, that our erlotinib-resistant colonies acquired diverse resistance

228 Here we compare persister-derived, erlotinib-resistant colonies that arose from a single, E

229 d the isogenic NSCLC H1650 cell line and its erlotinib-resistant derivative H1650-M3, a cell line tha

230 or to EGFR-TKI therapy, and in the generated erlotinib-resistant HCC827 (HCC827/ER) cells than in HCC

231 wn reversed the reduction in the invasion of erlotinib-resistant HCC827 cells caused by miR-214 down-

232 ression was detected to be down-regulated in erlotinib-resistant HCC827 cells.

233 Z-TMS also inhibited proliferation of erlotinib-resistant lung adenocarcinoma cells (H1975) be

234 can improve treatment response in typically erlotinib-resistant NSCLC tumor xenografts.

235 decreased both survival and proliferation of erlotinib-resistant tumor cells and inhibited tumor grow

236 Loss of EPHA2 reduced the viability of erlotinib-resistant tumor cells harboring EGFR(T790M) mu

237 n greatly improve the responsiveness of even erlotinib-resistant tumors to treatment.

238 knocked down in the mutant cell line H1975 (erlotinib-resistant), it became sensitive to MET inhibit

239 ypotheses were formulated regarding enhanced erlotinib response in preclinical models harboring the p

240 expression of the miRNA genes comprising an erlotinib response signature in NSCLC.

241 as experimentally investigated for mediating erlotinib response.

242 Treatment of EGFR-mutant lung cancer with erlotinib results in dramatic tumor regression but it is

243 F receptor (EGFR), an HCV entry cofactor and erlotinib's cancer target.

244 l blood flow were acquired before each (11)C-erlotinib scan.

245 measure for quantitative assessment of (11)C-erlotinib scans acquired 40-60 min after injection.

246 Dynamic (15)O-H2O and (11)C-erlotinib scans were obtained in 17 NSCLC patients, 8 wi

247 Furthermore, erlotinib selectively blocked mammalian target of rapamy

248 erently between erlotinib-resistant A549 and erlotinib- sensitive PC9 cells.

249 exhibited enhanced EGFR phosphorylation and erlotinib sensitivity compared with wild-type MAPK1 cell

250 PRISM recapitulated the expected pattern of erlotinib sensitivity in vivo.

251 Erlotinib significantly upregulated IL6 secretion in HNS

252 itors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development

253 Thus, combining the antioxidant CAT-SKL with erlotinib targeted both CSCs and bulk cancer cells in cu

254 -small cell lung cancer (NSCLC) patients for erlotinib therapy.

255 ics, possibly compromising the prediction of erlotinib tissue distribution at therapeutic doses from

256 he ability of (11)C-erlotinib PET to predict erlotinib tissue distribution at therapeutic doses.

257 urvival (DFS) from 14 to 18 months by adding erlotinib to gemcitabine.

258 ng approach to enhance brain distribution of erlotinib to increase its efficacy in the treatment of b

259 s only partially accounts for the benefit of erlotinib to PDT.

260 nterestingly, we have found that addition of erlotinib to photodynamic therapy (PDT) can improve trea

261 nounced differences in distribution of (11)C-erlotinib to the brain, liver, kidney, and lung and hepa

262 so be of interest to predict distribution of erlotinib to tissues targeted for treatment.

263 Gene expression analysis of erlotinib-treated HNSCC cells revealed an upregulation o

264 prediction of response on a later CT scan in erlotinib-treated non-small cell lung cancer patients.

265 The 3-year CFS rates in placebo- and erlotinib-treated patients were 74% and 70%, respectivel

266 Oral erlotinib treatment (150 mg/d) or placebo for 12 months.

267 Erlotinib treatment also induced AMPK activation despite

268 ans were obtained before and after 7-10 d of erlotinib treatment in 50 non-small cell lung cancer pat

269 In addition, we demonstrate that erlotinib treatment increases the clonogenicity of lung

270 patients with EGFR mutations in cfDNA, only erlotinib treatment remained an independent predictor of

271 ies from a CT scan obtained after 9-11 wk of erlotinib treatment using receiver-operating-characteris

272 nrolled and randomly assigned 42 patients to erlotinib treatment, 40 patients to cabozantinib treatme

273 but not IL1beta was observed in response to erlotinib treatment, and IL1alpha blockade significantly

274 expression altered the cellular response to erlotinib treatment, resulting in impaired ATP homeostas

275 t lung cancer and disease progression during erlotinib treatment.

276 SC2 inducible lung cancer cells treated with erlotinib uncovered defects in the response to oxidative

277 e brain after intravenous injection of (11)C-erlotinib under baseline conditions (n = 4) and during i

278 lified methods for routine analysis of (11)C-erlotinib uptake in NSCLC patients.

279 l model for quantitative assessment of (11)C-erlotinib uptake in NSCLC was the 2T4k-WB model.

280 Quantitative assessment of (11)C-erlotinib uptake may be useful in selecting non-small ce

281 Selective erlotinib use in HNSCC may be informed by precision onco

282 routine clinical practice but do not support erlotinib use in this setting.

283 h gemcitabine compared with gemcitabine plus erlotinib used as maintenance therapy.

284 of cabozantinib alone or in combination with erlotinib versus erlotinib alone in patients with EGFR w

285 Brain uptake of (11)C-erlotinib was 2.6-fold higher in Abcb1a/b;Abcg2 knockout

286 Response to erlotinib was assessed by using the Response Evaluation

287 Response to erlotinib was associated with reduced heterogeneity (fir

288 However, unlike VP, the effect of erlotinib was independent of cAMP, cGMP, and protein kin

289 ut the duration of treatment with AUY922 and erlotinib was limited by toxicities, especially night bl

290 In patients, brain uptake of (11)C-erlotinib was not higher after administration of elacrid

291 -fluorouracil) or tyrosine kinase inhibitor (erlotinib), we show that these models can effectively as

292 Elacridar and cold erlotinib were administered orally to wild-type (WT) and

293 re, these viruses were resistant to the drug erlotinib, which targets epidermal growth factor recepto

294 of EGFR-mutated lung cancer cell lines with erlotinib, while showing robust cell death, enriches the

295 HER3-AKT activation was blocked by combining erlotinib with either anti-HER2 or anti-HER3 antibody.

296 Treatment with a pan-ErbB kinase inhibitor erlotinib with nanomolar activity against ErbB4 signific

297 drug-drug interaction is reversed by taking erlotinib with the acidic beverage cola.

298 s to investigate if the known interaction of erlotinib with the multidrug efflux transporters breast

299 DSC confirmed encapsulation of erlotinib within CYnLIP.

300 ulted in an increased brain concentration of erlotinib, without affecting erlotinib plasma concentrat