ライフサイエンスコーパス: gefitinib

1 confers resistance to EGFR inhibitors (i.e., gefitinib).

2 andomly assigned (160 to afatinib and 159 to gefitinib).

3 nts given afatinib vs 14 [9%] of those given gefitinib).

4 specific siRNA sensitized resistant cells to gefitinib.

5 yrosine kinase inhibitors (TKI) erlotinib or gefitinib.

6 inhibitors (EGFR-TKI), such as erlotinib and gefitinib.

7 active SHP2 reduced cellular sensitivity to gefitinib.

8 3/4 diarrhea was more common with docetaxel/gefitinib.

9 R T790M as a mechanism of drug resistance to gefitinib.

10 tinib, and increased cellular sensitivity to gefitinib.

11 n the placebo arm could receive single-agent gefitinib.

12 or receptor; T790M) following treatment with gefitinib.

13 nse to HS-173 with reversible EGFR inhibitor gefitinib.

14 , DAPT, and ErbB1/2 inhibitors, lapatinib or gefitinib.

15 d synergistic effect of trifluoperazine with gefitinib.

16 east 12 weeks of treatment with erlotinib or gefitinib.

17 significantly lower concentrations than did gefitinib.

18 e of DARPP-32 in gastric tumor resistance to gefitinib.

19 the tyrosine kinase inhibitors erlotinib and gefitinib.

20 mors in mice and increased their response to gefitinib.

21 osis after treatment with an EGFR inhibitor, gefitinib.

22 H secretion, both of which were inhibited by gefitinib.

23 ctivation levels affect cellular response to gefitinib.

24 tant lung cancers becoming more sensitive to gefitinib.

25 h measurements of cellular susceptibility to gefitinib.

26 ly randomly assigned to either vandetanib or gefitinib.

27 ing a significant prolongation of PFS versus gefitinib.

28 ly to gain greatest PFS and ORR benefit from gefitinib.

29 nts who have not received prior erlotinib or gefitinib.

30 here were no unexpected safety findings with gefitinib.

31 of cells with the tyrosine-kinase inhibitor Gefitinib.

32 y were reduced by the addition of 100 muM of gefitinib.

33 way would identify patients benefitting from gefitinib.

34 n dacomitinib and in ten (4%) patients given gefitinib.

35 nib synergistically increased sensitivity to gefitinib.

36 significantly longer with afatinib than with gefitinib.

37 on their correlation toward ethylbenzene and gefitinib.

38 bition can be reversed by the EGFR inhibitor gefitinib.

39 g EGFR mutation but was resistant to the TKI gefitinib.

40 NSCLC with acquired resistance to first-line gefitinib.

41 Oral gefitinib (150 or 112.5 mg/m(2)) was concomitantly given

42 When gefitinib (200 mg/kg) was preadministered to inhibit Bcr

43 (1:1) by central block randomisation to oral gefitinib 250 mg or placebo once daily in tablet form; r

44 Random assignment was 1:1 to gefitinib 250 mg orally per day (Gef) or gefitinib 250 m

45 to gefitinib 250 mg orally per day (Gef) or gefitinib 250 mg orally per day plus pemetrexed 500 mg/m

46 rapy were randomly assigned (1:1) to receive gefitinib 250 mg per day or placebo for 2 years.

47 kly docetaxel plus either placebo (arm A) or gefitinib 250 mg/d, orally (arm B) until disease progres

48 mitinib 45 mg/day (in 28-day cycles) or oral gefitinib 250 mg/day (in 28-day cycles) until disease pr

49 In the gefitinib 250 mg/day, 500 mg/day, and methotrexate group

50 total score) were 13.4%, 18.0%, and 6.0% for gefitinib 250 mg/day, 500 mg/day, and methotrexate, resp

51 responses with gefitinib were seen, neither gefitinib 250 nor 500 mg/day improved overall survival c

52 (1:1) to receive afatinib (40 mg per day) or gefitinib (250 mg per day) until disease progression, or

53 Following a single oral dose of gefitinib (50 or 150 mg/kg), tumors were processed at se

54 48 UK centres and randomly assigned (1:1) to gefitinib (500 mg) or matching placebo by simple randomi

55 ncer (NSCLC) cells often become resistant to gefitinib (a clinically relevant tyrosine kinase inhibit

56 ndustry, such as the marketed EGFR inhibitor gefitinib, a quinolinecarbonitrile Src tyrosine kinase i

57 Cell treatment with the EGFR inhibitor gefitinib abolished upregulation of the EGFR pathway.

58 nificantly reduced blood flow and subsequent gefitinib accumulation in xenografted EGFR-mutant tumors

59 Our data show that pretreatment with gefitinib (active conformation binder) stabilizes the EG

60 in groups receiving gefitinib, implying that gefitinib administration leads to a greater proportion o

61 ecan exposures, we found that P(tumor) after gefitinib administration was lower.

62 dentification patterns matched to erlotinib, gefitinib, afatinib, and lapatinib.

63 or WT KRAS in cell populations resistant to gefitinib, afatinib, WZ4002, or AZD9291.

64 Of 18 eligible patients who received gefitinib after disease progression in arm A, one patien

65 Continuation of gefitinib after radiological disease progression on firs

66 cohort of lung cancer patients treated with gefitinib alone demonstrated higher response rates and a

67 death response compared with treatment with gefitinib alone.

68 conferring resistance to the EGFR inhibitor gefitinib, also preexists in cancer cells and normal tis

69 States marketing authorization for one drug, gefitinib (an epidermal growth factor receptor [EGFR] in

70 itors (TKIs), PF2341066 and SU11274, or with gefitinib, an EGFR TKI, suggesting kinase activity of bo

71 Blocking EGFR activity with gefitinib, an EGFR tyrosine kinase inhibitor, attenuated

72 These effects were abolished by gefitinib, an EGFR tyrosine kinase inhibitor.

73 Assess efficacy and toxicity of gefitinib, an epidermal growth factor receptor (EGFR) in

74 We hypothesized that the addition of gefitinib, an epidermal growth factor receptor (EGFR) ty

75 Gefitinib, an epidermal growth factor receptor tyrosine

76 fety of vandetanib was compared with that of gefitinib, an inhibitor of EGFR signaling.

77 Gastric tumors can become resistant to gefitinib, an inhibitor of the epidermal growth factor r

78 ted in 109 (49%) of 224 patients assigned to gefitinib and 101 (45%) of 225 on placebo.

79 d patient-reported outcomes (110 patients on gefitinib and 121 on placebo completed both baseline and

80 ent withdrew consent; 224 patients allocated gefitinib and 225 allocated placebo included in analyses

81 nned patients were randomly assigned (251 to gefitinib and 252 to placebo).

82 tion when combined with the EGFR inhibitors, gefitinib and AZD8931.

83 sensitivity of lung cancers to erlotinib and gefitinib and can occur in any patient with this illness

84 d susceptibility to EGFR-targeted inhibitors gefitinib and cetuximab but acquired susceptibility to t

85 ient autoantibodies, and the small-molecules gefitinib and dasatinib.

86 statistically significant difference between gefitinib and docetaxel in biomarker-negative patients.

87 ve factors for differential survival between gefitinib and docetaxel in this setting of previously tr

88 receptor (EGFR) tyrosine kinase inhibitors, gefitinib and erlotinib are effective therapies against

89 Gefitinib and erlotinib are EGFR TK inhibitors (EGFR TKI

90 Most patients who initially respond to gefitinib and erlotinib eventually become resistant and

91 acy of EGF receptor (EGFR) kinase inhibitors gefitinib and erlotinib is limited by the development of

92 vity against the activating mutations, which gefitinib and erlotinib target and inhibition of which g

93 ntestinal obstruction" and "hypokalaemia" in gefitinib and erlotinib, "hyponatraemia" in gefitinib, e

94 ptor tyrosine kinase inhibitors (EGFR TKIs), gefitinib and erlotinib, are reversible competitive inhi

95 yrosine kinase activity and the finding that gefitinib and erlotinib, two agents already used clinica

96 kinase, which is resistant to treatment with gefitinib and erlotinib.

97 r rate of partial responses to the EGFR TKIs gefitinib and erlotinib.

98 e tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib.

99 R tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib.

100 s that truly overcome acquired resistance to gefitinib and erlotinib.

101 armacokinetic/pharmacodynamic variability of gefitinib and immunohistochemical indices followed by th

102 M2 modulates the sensitivity of CRC cells to gefitinib and indicate that small molecule pharmacologic

103 but contrary to this, we uncovered here that gefitinib and osimertinib increased STAT3 phosphorylatio

104 ed lung adenocarcinoma patients treated with gefitinib and osimertinib show a therapeutic benefit lim

105 ith previous disease control with first-line gefitinib and recent disease progression (Response Evalu

106 , MEK inhibition enhanced the sensitivity to gefitinib and slowed cell migration.

107 s given afatinib vs five [3%] of those given gefitinib) and liver enzyme elevations (no patients give

108 ents given afatinib vs two [1%] of 159 given gefitinib) and rash or acne (15 [9%] patients given afat

109 rize binding of three inhibitors (erlotinib, gefitinib, and AEE788) with wildtype EGFR and three muta

110 ment with EGFR inhibitors such as erlotinib, gefitinib, and afatinib, but outcomes are limited by the

111 and have a similar structure (i.e., iressa, gefitinib, and erlotinib).

112 phosphorylation, basally and in response to gefitinib, and increased cellular sensitivity to gefitin

113 dministration of the ABCG2 inhibitors Ko143, gefitinib, and nilotinib, but not an ABCB1 inhibitor.

114 he reversible EGFR tyrosine kinase inhibitor gefitinib are approved for first-line treatment of EGFR

115 ically significant difference between either gefitinib arm and methotrexate.

116 The use of gefitinib as a second-line treatment in oesophageal canc

117 with esophageal cancer who may benefit from gefitinib as a second-line treatment.

118 ve tyrosine kinase inhibitors, erlotinib and gefitinib, blocked not only EGFRvIII signaling to ERK bu

119 variations in intratumoral concentrations of gefitinib, but only up to half this variability in pERK

120 cancer cell line (HCC827), made resistant to gefitinib by exogenous heregulin, was resensitized by MM

121 omotes resistance of gastric cancer cells to gefitinib by promoting interaction between EGFR and ERBB

122 Gefitinib can be administered with FHX and as maintenanc

123 This suggests gefitinib can provide similar overall survival to doceta

124 tatements regarding the efficacy of adjuvant gefitinib cannot be made, these results indicate that it

125 assess the efficacy and safety of continuing gefitinib combined with chemotherapy versus chemotherapy

126 (20.2%), overall survival was improved with gefitinib compared with placebo (hazard ratio [HR] for d

127 e was no difference in overall survival with gefitinib compared with placebo (HR for death, 0.90; 95%

128 col that generated serial samples to measure gefitinib concentrations, phosphorylated extracellular s

129 The ErbB inhibitors gefitinib, CP-724714, erbstatin and tyrphostin AG825 sig

130 n1 deficiency and EGFR inhibition (AG1478 or gefitinib) decreased their activation.

131 ERBB target selectivity between afatinib and gefitinib; despite effectively disrupting ERBB2 phosphor

132 Inhibition of EGF signalling by gefitinib destabilizes PD-L1, enhances antitumour T-cell

133 o EGFR-targeting drugs such as Erlotinib and Gefitinib develops quickly.

134 en dacomitinib vs none of 224 patients given gefitinib), diarrhoea (19 [8%] vs two [1%]), and raised

135 diological disease progression on first-line gefitinib did not prolong progression-free survival in p

136 nhibition of tyrosine autophosphorylation by gefitinib: distinct for WT and oncogenic L834R mutant fo

137 24714 failed to enhance the effect of HS-173 gefitinib dual therapy.

138 ib therapy, whereas PKM2 knockdown increased gefitinib efficacy.

139 )-directed tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib and afatinib are approved treatment

140 gefitinib and erlotinib, "hyponatraemia" in gefitinib, erlotinib and afatinib, "alopecia"in erlotini

141 o clinically achievable doses of reversible (gefitinib, erlotinib) and irreversible (neratinib, afati

142 is of the adverse events (AEs) of EGFR-TKIs (gefitinib, erlotinib, afatinib, osimertinib) by data min

143 Tyrosine kinase inhibitors such as gefitinib, erlotinib, and afatinib improve progression-f

144 resent, first-line treatment with EGFR TKIs (gefitinib, erlotinib, and afatinib) has been approved fo

145 ceptor tyrosine kinase inhibitors, including gefitinib, erlotinib, and afatinib.

146 Although agents such as gefitinib, erlotinib, cetuximab, lapatinib, and panitumu

147 R, 1.24; 95% CI, 0.90 to 1.71; P = .18) from gefitinib for 344 patients with epidermal growth factor

148 , 3.16; 95% CI, 0.61 to 16.45; P = .15) from gefitinib for the 15 patients with EGFR mutation-positiv

149 for those with PS 2; afatinib, erlotinib, or gefitinib for those with sensitizing EGFR mutations; cri

150 ous cell carcinoma; docetaxel, erlotinib, or gefitinib for those with squamous cell carcinoma; and ch

151 Furthermore, withdrawal of gefitinib from previously resistant clones correlated wi

152 inate a KI with little or no cardiotoxicity (gefitinib) from one with demonstrated cardiotoxicity (su

153 carboxyaminoimidazole, docetaxel, erlotinib, gefitinib, gemcitabine, and pemetrexed have evaluated ou

154 odynophagia was significantly better in the gefitinib group (adjusted mean difference -8.61, 95% CI

155 tinib group and 9.2 months (9.1-11.0) in the gefitinib group (hazard ratio 0.59, 95% CI 0.47-0.74; p<

156 cholelithases/liver disease) and one in the gefitinib group (related to sigmoid colon diverticulitis

157 54 (24%) of patients in the gefitinib group achieved disease control at 8 weeks, as

158 patients were randomly assigned: 133 to the gefitinib group and 132 to the placebo group.

159 37 (28%) of 132 patients in the gefitinib group and 28 (21%) of 132 patients in the plac

160 months in both groups [95% CI 4.5-5.7 in the gefitinib group and 4.6-5.5 in the placebo group]).

161 were nausea (85 [64%] of 132 patients in the gefitinib group and 81 [61%] of 132 patients in the plac

162 were anaemia (11 [8%] of 132 patients in the gefitinib group and five [4%] of 132 patients in the pla

163 74%) patients had disease progression in the gefitinib group compared with 107 (81%) in the placebo g

164 d unrelated to treatment; one patient in the gefitinib group died from drug-related hepatic and renal

165 lacebo (1.57 months, 95% CI 1.23-1.90 in the gefitinib group vs 1.17 months, 95% CI 1.07-1.37 in the

166 in the afatinib group and seven (4%) in the gefitinib group.

167 ed in the afatinib group and ten (6%) in the gefitinib group.

168 rt A, vandetanib prolonged PFS compared with gefitinib (hazard ratio = 0.69; 95% CI, 0.50 to 0.96; on

169 with afatinib vs 10.9 months [9.1-11.5] with gefitinib; hazard ratio [HR] 0.73 [95% CI 0.57-0.95], p=

170 fication (7.2%) gained greatest benefit from gefitinib (HR for death, 0.21; 95% CI, 0.07 to 0.64; P =

171 ith afatinib vs 11.5 months [10.1-13.1] with gefitinib; HR 0.73 [95% CI 0.58-0.92], p=0.0073) were si

172 Of particular note is gefitinib, identified as among the candidate therapeutic

173 was significantly higher in groups receiving gefitinib, implying that gefitinib administration leads

174 An unplanned subset analysis showed that gefitinib improved survival in patients younger than 65

175 the antitumor activities of chemotherapy or gefitinib in combination treatment regimens.

176 ntly improved progression-free survival over gefitinib in first-line treatment of patients with EGFR-

177 owth and enhanced the inhibitory activity of gefitinib in lung cancer metastatic and orthotopic CSC a

178 ynamic characteristics of the EGFR inhibitor gefitinib in mice with intracerebral tumors and develope

179 sponses to the EGFR inhibitors erlotinib and gefitinib in nonsmall cell lung cancer patients.

180 he reversible EGFR tyrosine kinase inhibitor gefitinib in the first-line treatment of patients with a

181 pare the efficacy and safety of afatinib and gefitinib in this setting.

182 Gefitinib increased the bioavailability of oral irinotec

183 ed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal t

184 ch do not normally express DARPP-32, blocked gefitinib-induced apoptosis and increased the drug's IC(

185 UMA or BH3 mimetics sensitize HNSCC cells to gefitinib-induced apoptosis.

186 ression by small hairpin RNA (shRNA) impairs gefitinib-induced apoptosis.

187 tability of the EGFR, and suppressed EGF- or gefitinib-induced degradation of the EGFR.

188 Combining neutralizing IL6 antibodies and gefitinib inhibited malignant cell growth in 2D and 3D c

189 AG1478 and gefitinib, inhibitors of EGFR tyrosine kinase, reduced f

190 ur laboratory has previously shown that some gefitinib-insensitive head and neck squamous cell carcin

191 ed apoptosis of both gefitinib-sensitive and gefitinib-insensitive NSCLC cells.

192 factor receptor) tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva) were found to

193 y tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited

194 r in breast cancer and confers resistance to gefitinib (Iressa) and tamoxifen.

195 The EGFR inhibitor gefitinib (Iressa) and the phosphatidylinositol 3-kinase

196 growth factor receptor (Egfr) inhibition by gefitinib (Iressa) in males markedly increases hepcidin

197 d-type (WT) and L834R EGFR and the effect of gefitinib (Iressa) on the phosphorylation of individual

198 Gefitinib (Iressa, ZD-1839), a small molecule tyrosine k

199 re is evidence from independent studies that gefitinib is highly effective in treating women, non-smo

200 mutant, L834R EGFR, the binding affinity of gefitinib is substantially enhanced and likely contribut

201 ow that for WT EGFR the binding affinity for gefitinib is weaker for the phosphorylated protein while

202 IV irinotecan given with 12 days of oral gefitinib is well tolerated in children.

203 Moreover, inhibition of MAPK signaling by gefitinib led to decreased ETS1 and miR-29b expression w

204 The first-line use of gefitinib may be recommended for patients with known epi

205 Gefitinib-mediated ROS correlated with epithelial-mesenc

206 or acquired resistance to the EGFR inhibitor gefitinib, MEK inhibition enhanced the sensitivity to ge

207 y assigned to receive dacomitinib (n=227) or gefitinib (n=225).

208 inhibitory effect of EGF receptor inhibitor gefitinib on invasive motility by activating HER2 signal

209 of a combination of anti-IL6 antibodies and gefitinib on malignant cell growth.

210 ssessed the impact of postoperative adjuvant gefitinib on overall survival (OS).

211 ation approach to characterize the effect of gefitinib on topotecan P(tumor).

212 mor ECF (tECF) penetration and the effect of gefitinib on topotecan tECF penetration and intratumor t

213 novo sensitivity to the EGFR-targeted agents gefitinib or cetuximab in two of three cell lines accomp

214 e combination of trifluoperazine with either gefitinib or cisplatin overcame drug resistance in lung

215 er (NSCLC) were randomly assigned to receive gefitinib or docetaxel.

216 vening systemic therapy between cessation of gefitinib or erlotinib and initiation of new therapy.

217 ] or WHO) while on continuous treatment with gefitinib or erlotinib within the last 30 days; and no i

218 d after the first therapeutic dose of a TKI (gefitinib or erlotinib).

219 treatment with a single-agent EGFR TKI (eg, gefitinib or erlotinib); either or both of the following

220 ee previous lines of chemotherapy and either gefitinib or erlotinib, and had assessable disease (RECI

221 activity in patients previously treated with gefitinib or erlotinib.

222 ted with the EGFR tyrosine-kinase inhibitors gefitinib or erlotinib.

223 h the EGFR tyrosine kinase inhibitors (TKIs) gefitinib or erlotinib.

224 ctor receptor mutation who were treated with gefitinib or erlotinib.

225 se effects were abolished in the presence of gefitinib or HB-EGF-neutralizing antibody.

226 of ZAP-70 using tyrosine kinase inhibitors, gefitinib or ibrutinib, diminishes HA formation and trog

227 found that concomitant Notch inhibition with gefitinib or osimertinib treatment induced a p-STAT3-dep

228 combined treatment of Notch inhibitors with gefitinib or osimertinib, respectively.

229 When given the anticancer drug gefitinib or the retroviral drug atazanavir, the Por-del

230 latin were treated with trifluoperazine plus gefitinib or trifluoperazine plus cisplatin.

231 ecommendations include docetaxel, erlotinib, gefitinib, or pemetrexed for patients with nonsquamous c

232 Docetaxel, erlotinib, gefitinib, or pemetrexed is recommended as second-line t

233 Treatment with anti-IL6, gefitinib, or their combination all led to partial resto

234 d points of PFS and ORR, some advantages for gefitinib over docetaxel were seen in EGFR mutation-posi

235 in SNU-16 cells increased the sensitivity to gefitinib (P < .01).

236 er genetically or by treating the cells with Gefitinib, paradoxically, the cells demonstrated increas

237 rgeted agents (PBTC-007: phase I/II study of gefitinib; PBTC-014: phase I/II study of tipifarnib).

238 cycles, followed by maintenance pemetrexed (gefitinib plus chemotherapy [Gef+C]).

239 at a single-molecule level) increased after gefitinib pretreatment or DEP-1 phosphatase overexpressi

240 umate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disru

241 as reduced further by DAPT/lapatinib or DAPT/gefitinib regardless of ErbB2 receptor status.

242 GFR tyrosine kinase inhibitors erlotinib and gefitinib, relapse inevitably occurs, suggesting the dev

243 or receptor (EGFR) tyrosine kinase inhibitor gefitinib relative to placebo in patients with advanced

244 PKM2) levels were positively correlated with gefitinib resistance in CRC cells.

245 llular perturbations that accompany acquired gefitinib resistance in lung cancer cells.

246 of STAT3 by nuclear PKM2 was associated with gefitinib resistance.

247 with covalently binding inhibitors against a gefitinib resistant T790M mutant cell line.

248 elevated the intracellular calcium level in gefitinib-resistant (G-R) non-small-cell lung cancer (NS

249 quantification of membrane proteins between Gefitinib-resistant and -sensitive lung cancer cell line

250 to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic cu

251 minopropanamides suppressed proliferation of gefitinib-resistant H1975 cells, harboring the T790M mut

252 zine inhibited Wnt/beta-catenin signaling in gefitinib-resistant lung cancer spheroids.

253 tends a potentially broader ability to treat gefitinib-resistant NSCLC.

254 le to predict mutation status and associated gefitinib response non-invasively, demonstrating the pot

255 we investigated if radiomics can identify a gefitinib response-phenotype, studying high-resolution c

256 DARPP-32-mediated resistance to gefitinib resulted from increased phosphorylation of and

257 50 clone by long-term, chronic culture under gefitinib selection of parental cell line.

258 resulted in BimEL-mediated apoptosis of both gefitinib-sensitive and gefitinib-insensitive NSCLC cell

259 RC-3 expression is inversely correlated with gefitinib sensitivity and that SRC-3 knockdown results i

260 CLC cells with EGFR mutation display reduced gefitinib sensitivity when ERK activation is augmented b

261 A rational combination of bosutinib and gefitinib showed additive and synergistic effects in can

262 Gefitinib significantly enhances the bioavailability of

263 g pemetrexed and carboplatin chemotherapy to gefitinib significantly prolonged PFS and OS but increas

264 Inhibitors of H(2)O(2) (catalase) and EGFR (gefitinib) significantly blocked E. faecalis-induced EGF

265 tion of EGFR signaling, utilizing AG1478 and gefitinib, significantly reduced the ability of TGF-beta

266 tivozanib with EGFR small molecule inhibitor gefitinib synergistically increased sensitivity to gefit

267 ion-free survival was marginally longer with gefitinib than it was with placebo (1.57 months, 95% CI

268 ception of tumor hemorrhage-type events with gefitinib, the adverse event profiles were generally con

269 hat daily treatment with the EGF-R inhibitor gefitinib, the FGF-R inhibitor dovitinib, and the PDGF-R

270 Gefitinib, the first small molecule inhibitor of EGFR ki

271 Gefitinib, the tyrosine kinase inhibitor, suppressed her

272 r PKM2 in HT29 cells decreased the effect of gefitinib therapy, whereas PKM2 knockdown increased gefi

273 The addition of gefitinib to docetaxel was well tolerated but did not im

274 dual inhibitors showed a higher potency than gefitinib to inhibit cell growth of EGFR-overexpressing

275 reclinical rationale to combine anti-IL6 and gefitinib to treat patients with advanced stage ovarian

276 a NSCLC cell line expressing wild-type EGFR, gefitinib treatment along with or following MEK inhibiti

277 established isogenic cell lines by prolonged gefitinib treatment at concentrations that are in excess

278 Gefitinib treatment decreased both tumor size and cortic

279 ed the applicability of the model using EGFR-gefitinib treatment for Lung Adenocarcinoma (LUAD) and L

280 However, gefitinib treatment in the presence of ROS scavenger pro

281 Gefitinib treatment of primary GBM cells resulted in a r

282 These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfu

283 We observed that although chronic gefitinib treatment provided effective action against it

284 patients who have not received erlotinib or gefitinib, treatment with erlotinib is recommended.

285 Purpose The Cancer Esophagus Gefitinib trial demonstrated improved progression-free s

286 inded molecular analysis of Cancer Esophagus Gefitinib trial tumors was conducted to compare efficacy

287 le porous gelatin nanocore encapsulated with gefitinib (tyrosine kinase inhibitor (TKI)) and surface

288 breast cancer cell growth and resistance to gefitinib, U0126, and genotoxicity.

289 had higher ORR (13.0% v 7.4%; P = .04) with gefitinib versus docetaxel.

290 re was no difference in overall survival for gefitinib versus placebo for patients with EGFR, KRAS, B

291 s (median 3.73 months, 95% CI 3.23-4.50, for gefitinib vs 3.67 months, 95% CI 2.97-4.37, for placebo;

292 were diarrhoea (36 [16%] of 224 patients on gefitinib vs six [3%] of 225 on placebo) and skin toxici

293 corresponding resistant lung cancer cells to gefitinib was reduced by desialylation and was enhanced

294 markers and the FDA-approved RIPK2 inhibitor Gefitinib, we show that pharmacologic RIPK2 inhibition d

295 nt or metastatic SCCHN, while responses with gefitinib were seen, neither gefitinib 250 nor 500 mg/da

296 f the network governing cellular response to gefitinib, which we term "oncogene imbalance," portends

297 The 21-day regimen of oral gefitinib with irinotecan was not tolerated.

298 We aimed to compare gefitinib with placebo in previously treated advanced oe

299 tumors was conducted to compare efficacy of gefitinib with that of placebo according to EGFR copy nu

300 tients with EGFR-mutated NSCLC compared with gefitinib, with a manageable tolerability profile.

301 ould have a role in the striking response to gefitinib witnessed with EGFR mutation.