ライフサイエンスコーパス: erlotinib

1 harmacotherapy with an antineoplastic agent (Erlotinib).

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

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

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

5 ssive disease, bevacizumab was combined with erlotinib.

6 mutation who were treated with gefitinib or erlotinib.

7 e lung cancer cells increased sensitivity to erlotinib.

8 tration of an EGFR tyrosine kinase inhibitor erlotinib.

9 regimens combining a HAP, evofosfamide, with erlotinib.

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

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

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

13 o energetic stress induced by treatment with erlotinib.

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

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

16 y treated with the tyrosine kinase inhibitor erlotinib.

17 ase and then treated with the EGFR inhibitor Erlotinib.

18 when treated with the combination of PF and erlotinib.

19 tion, enhances growth inhibitory activity of Erlotinib.

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

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

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

23 nt lung cancer patients treated with the TKI erlotinib.

24 administration of the EGFR inhibitor drug of Erlotinib.

25 e to recurrence was 25 months after stopping erlotinib.

26 effects of EGFR-directed therapies including erlotinib.

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

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

29 00 mg/m(2) days 1, 8, 15, every 4 weeks plus erlotinib 100 mg once per day (GemErlo) or gemcitabine (

30 They were orally administered erlotinib 150 mg once per day, celecoxib 200 mg twice pe

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

32 system) EGFR-mutant NSCLC were treated with erlotinib 150 mg per day for 2 years after standard adju

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

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

35 ible patients in a 1:1 ratio to receive oral erlotinib (150 mg/day) plus either intravenous ramucirum

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

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

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

39 ter oral intake of single ascending doses of erlotinib (300 mg, n = 7; 650 mg, n = 8; or 1,000 mg, n

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

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

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

43 ntified molecular ions of the EGFR inhibitor erlotinib, a phosphatidylcholine lipid, and cholesterol,

44 Erlotinib, a selective EGFR inhibitor, enhanced AQP2 api

45 f AhR activity sensitizes human BC models to Erlotinib, a selective EGFR tyrosine kinase inhibitor, s

46 underwent 2 consecutive PET scans with (11)C-erlotinib: a baseline scan and a second scan either with

47 ~12 and 3.3 fold increase in doxorubicin and erlotinib accumulation in mice brain, respectively compa

48 dverse events (AEs) of EGFR-TKIs (gefitinib, erlotinib, afatinib, osimertinib) by data mining using t

49 nt erlotinib, and patients rechallenged with erlotinib after recurrence experienced durable benefit.

50 th adjuvant IGFBP-3-Fc with erlotinib versus erlotinib after treatment cessation supports that the co

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

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

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

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

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

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

57 PAWI-2 also overcame erlotinib (an EGFR inhibitor) resistance in FGbeta(3) ce

58 RELAY assessed erlotinib, an EGFR tyrosine kinase inhibitor (TKI) stand

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

60 erapeutic testing in mice revealed that both erlotinib and afatinib caused regression of osimertinib-

61 and erlotinib, "hyponatraemia" in gefitinib, erlotinib and afatinib, "alopecia"in erlotinib, "hair gr

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

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

64 (OBD) of methotrexate when given along with erlotinib and celecoxib and to assess the efficacy of th

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

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

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 TWIST1 overexpression resulted in erlotinib and osimertinib resistance in EGFR-mutant NSCL

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 yrosine kinase inhibitors such as gefitinib, erlotinib, and afatinib improve progression-free surviva

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

77 noid to olaparib, an EGFR-mutant organoid to erlotinib, and an EGFR-mutant/MET-amplified organoid to

78 es were rare for patients receiving adjuvant erlotinib, and patients rechallenged with erlotinib afte

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

80 R tyrosine kinase inhibitors (TKIs), such as erlotinib, as the first-line treatment of lung cancers.

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

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

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

84 results in a clinically relevant decrease of erlotinib bioavailability.

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

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

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

88 quidar administration had no effect on (11)C-erlotinib brain distribution, oral erlotinib led, at the

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

90 nisms associated with acquired resistance to erlotinib by carrying out whole exome sequencing, quanti

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

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

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

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

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

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

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

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

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 Ramucirumab plus erlotinib demonstrated superior progression-free surviva

102 Erlotinib depends on stomach pH for its bioavailability.

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

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

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

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

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

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

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

110 Forty percent of patients required erlotinib dose reduction to 100 mg per day and 16% to 50

111 hat prolonged NSCLC cell exposure to the TKI erlotinib drives PFKFB3 expression and that chemical PFK

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

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

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

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

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

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

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

119 [95% CI 15.4-21.6]) than in the placebo plus erlotinib group (12.4 months [11.0-13.5]), with a strati

120 significantly longer in the ramucirumab plus erlotinib group (19.4 months [95% CI 15.4-21.6]) than in

121 29%) of 221 patients in the ramucirumab plus erlotinib group and 47 (21%) of 225 in the placebo plus

122 72%) of 221 patients in the ramucirumab plus erlotinib group versus 121 (54%) of 225 in the placebo p

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

124 cneiform (33 [15%]), and in the placebo plus erlotinib group were dermatitis acneiform (20 [9%]) and

125 rgent adverse events in the ramucirumab plus erlotinib group were hypertension (52 [24%]; grade 3 onl

126 events of any grade in the ramucirumab plus erlotinib group were pneumonia (seven [3%]) and cellulit

127 , each); the most common in the placebo plus erlotinib group were pyrexia (four [2%]) and pneumothora

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

129 r a pleural empyema) in the ramucirumab plus erlotinib group.

130 roup and 47 (21%) of 225 in the placebo plus erlotinib group.

131 versus 121 (54%) of 225 in the placebo plus erlotinib group.

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

133 with EGFR-mutant NSCLC treated with adjuvant erlotinib had an improved 2-year DFS compared with histo

134 itinib, erlotinib and afatinib, "alopecia"in erlotinib, "hair growth abnormal" in afatinib, but not i

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

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

137 ruction" and "hypokalaemia" in gefitinib and erlotinib, "hyponatraemia" in gefitinib, erlotinib and a

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

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

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

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

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

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

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

145 t chemical PFKFB3 inhibition synergizes with erlotinib in increasing erlotinib's anti-proliferative a

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

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

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

149 cell lung cancer (NSCLC), we tested adjuvant erlotinib in patients with EGFR-mutant early-stage NSCLC

150 ion-free survival compared with placebo plus erlotinib in patients with untreated EGFR-mutated metast

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

152 mediates insensitivity to the EGFR inhibitor erlotinib in TNBC cells by promoting the synthesis of th

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

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

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

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

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

158 Similar to VP, erlotinib increased exocytosis and decreased endocytosis

159 Erlotinib increased phosphorylation of AQP2 at Ser-256 a

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

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

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

163 d in erlotinib resistance and suppression of erlotinib-induced apoptosis.

164 increases the sensitivity of mutant EGFR to erlotinib-induced degradation.

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

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

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

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

169 Erlotinib-induced skin rash was associated with improved

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

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

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

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

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

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

176 We loaded doxorubicin and erlotinib into liposomes to enhance their translocation

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

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

179 Erlotinib is an EGFR tyrosine kinase inhibitor that has

180 Erlotinib is an epidermal growth factor receptor inhibit

181 Erlotinib is approved for the treatment of all patients

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

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

184 When erlotinib is taken concurrently with a proton pump inhib

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

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

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

188 Saturable transport of erlotinib leads to nonlinear pharmacokinetics, possibly

189 on (11)C-erlotinib brain distribution, oral erlotinib led, at the 650-mg dose, to significant increa

190 Co-delivery of doxorubicin and erlotinib loaded Tf-Pen liposomes revealed significantly

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

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

193 Conclusion: Supratherapeutic-dose erlotinib may be used to enhance brain delivery of ABCB1

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

195 AZD4547 (FGFR alteration), rilotumumab plus erlotinib (MET), talazoparib (homologous recombination r

196 Triple oral metronomic chemotherapy with erlotinib, methotrexate, and celecoxib is efficacious in

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

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

199 patients with recurrence were retreated with erlotinib (n = 26; 65%) for a median duration of 13 mont

200 assigned to treatment with ramucirumab plus erlotinib (n=224) or placebo plus erlotinib (n=225).

201 rumab plus erlotinib (n=224) or placebo plus erlotinib (n=225).

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

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

204 The EGFR inhibitor, erlotinib, neutralized ST6Gal-I-dependent differences in

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

206 ve breast cancer cells and of treatment with erlotinib of PC-9 non-small cell lung cancer cells.

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

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

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

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

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

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

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

214 oncentration of erlotinib, without affecting erlotinib plasma concentration.

215 0.05), with a concomitant increase in (11)C-erlotinib plasma exposure.

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

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

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

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

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

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

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

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

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

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

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

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

228 ith acquired resistance to EGFR-TKIs such as erlotinib remains an unmet need and a therapeutic challe

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

230 ng cancer, Twist1 overexpression resulted in erlotinib resistance and suppression of erlotinib-induce

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

232 1alpha knockdown can also attenuate acquired erlotinib resistance, supporting a role for activated NF

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

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

235 phosphoproteomic alterations associated with erlotinib resistant SCC-R cells.

236 stitutively active mutant MAP2K1 (p.K57E) in erlotinib resistant SCC-R cells.

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

238 We demonstrate that erlotinib-resistant cells are sensitive to MAPK pathway

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

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

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

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

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

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

245 athway is an effective strategy for treating erlotinib-resistant HNSCC tumors.

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

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

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

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

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

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

252 tion synergizes with erlotinib in increasing erlotinib's anti-proliferative activity in NSCLC cells.

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

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

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

256 Furthermore, erlotinib selectively blocked mammalian target of rapamy

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

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

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

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

261 Toxicities were typical of erlotinib; there were no grade 4 or 5 adverse events.

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

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

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

265 the potential of supratherapeutic-dose oral erlotinib to inhibit ABCB1/ABCG2 activity at the human B

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

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

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

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

270 Erlotinib treatment also induced AMPK activation despite

271 58R) and resistant (T790M) EGFR mutants upon erlotinib treatment correlates with drug sensitivity.

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

273 Combination first-line osimertinib plus erlotinib treatment prevented the emergence of secondary

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

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

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

277 patients, with only four recurrences during erlotinib treatment.

278 t lung cancer and disease progression during erlotinib treatment.

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

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

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

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

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

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

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

286 growth in vivo with adjuvant IGFBP-3-Fc with erlotinib versus erlotinib after treatment cessation sup

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

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

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

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

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

292 Also, using the inhibitor erlotinib, we could not confirm a role for the epidermal

293 e sustained when substoichiometric levels of erlotinib were added to reduce duration of EGFR kinase a

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

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

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

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

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

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

300 DSC confirmed encapsulation of erlotinib within CYnLIP.

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