ライフサイエンスコーパス: cetuximab

1 y continuing on weekly cetuximab (continuous cetuximab).

2 ab and two EGFR binding antibodies including Cetuximab.

3 ermal growth factor receptor (EGFR), such as cetuximab.

4 g fragment of a therapeutic antibody such as cetuximab.

5 ng the variable regions of the EGFR antibody cetuximab.

6 54.3% (95% CI, 42.0 to 66.2) for FOLFOX plus cetuximab.

7 ation carboplatin/paclitaxel with or without cetuximab.

8 No responses were seen with single-agent cetuximab.

9 treated with adjuvant FOLFOX with or without cetuximab.

10 e exon 2 KRAS G13D mutation may benefit from cetuximab.

11 , and 110 to high-dose chemoradiotherapy and cetuximab.

12 aluate localization of fluorescently labeled cetuximab.

13 ion of a therapeutic dose of 500 mg.m(-2) of cetuximab.

14 2-PI3K and ERBB-RAS pathways and response to cetuximab.

15 lorectal cancer who received vemurafenib and cetuximab.

16 tion-specific therapeutic antibodies such as cetuximab.

17 h dose), 60 Gy plus cetuximab, or 74 Gy plus cetuximab.

18 lorectal cancer who received vemurafenib and cetuximab.

19 of the therapeutic EGFR monoclonal antibody cetuximab.

20 we performed basophil activation tests with cetuximab.

21 nd cisplatin without (arm A) or with (arm B) cetuximab.

22 iven panitumumab and 48 (10%) patients given cetuximab.

23 cles of FOLFOX4 twice a week with or without cetuximab.

24 e event: a lung infection in a patient given cetuximab.

25 ization by the EGFR inhibitors erlotinib and cetuximab.

26 mittent cetuximab and 91 (54%) to continuous cetuximab.

27 t: 499 received panitumumab and 500 received cetuximab.

28 predicting sensitivity to the EGFR inhibitor cetuximab.

29 ) plus eight once-weekly doses of concurrent cetuximab.

30 olorectal cancer patients that progressed on cetuximab.

31 6 status for PFS in patients treated without cetuximab.

32 us cell carcinoma refractory to platinum and cetuximab.

33 elumetinib (AZD6244/ARRY-142886, MEK1/2i) or cetuximab.

34 Patients were treated by single-agent cetuximab.

35 noms contained lower alpha-gal contents than cetuximab.

36 overall survival (OS), and safety profile of cetuximab.

37 rcinoma previously treated with platinum and cetuximab.

38 cycles of IC with cisplatin, paclitaxel, and cetuximab.

39 fied that together improved the affinity for cetuximab 10-fold to 15 nm Importantly, the increased af

40 surface area), docetaxel (30-40 mg/m(2)), or cetuximab (250 mg/m(2) after a loading dose of 400 mg/m(

41 zumab (15 mg/kg; every 21 days), either with cetuximab (250 mg/m(2) weekly after loading dose; cetuxi

42 irinotecan therapy were randomly assigned to cetuximab 400 mg/m(2) loading dose and then 250 mg/m(2)

43 4 Gy/1.8 Gy fractions with or without weekly cetuximab (400 mg/m2 on day 1 then 250 mg/m2 weekly).

44 For patients assigned to receive cetuximab, 400 mg/m(2) cetuximab was given on day 1 foll

45 as 60.9% (95% CI, 47.9 to 72.8) for ECF plus cetuximab, 45.0% (95% CI, 33.0 to 57.0) for IC plus cetu

46 intravenous bevacizumab-800CW (anti-VEGF-A), cetuximab-800CW (anti-EGFR), control tracer IgG-800CW, o

47 be delineated for both bevacizumab-800CW and cetuximab-800CW tracers.

48 ity of single-targeted ErbB agents including cetuximab (a ligand-blocking anti-EGFR mAb), transtuzuma

49 cal situation occurred after introduction of cetuximab, a chimeric mouse-human antibody, for cancer t

50 l superiority is platinum, fluorouracil, and cetuximab, a monoclonal antibody directed against the ep

51 to investigate the efficacy and tolerance of cetuximab according to these mutations.

52 Antivenoms, pork kidney, and cetuximab activated basophils from patients with IgE to

53 Importantly, cetuximab-activated NK cells selectively eliminated intr

54 To evaluate the benefit of cetuximab added to concurrent chemoradiation therapy for

55 y, thereby allowing the further tailoring of cetuximab administration to maximize patient benefit.

56 Cetuximab affinity for EGFR-K521 was reduced slightly, b

57 receive 6 months of FOLFOX4 or FOLFOX4 plus cetuximab after surgical resection for stage III colon c

58 with either single-dose irradiation (10 Gy), cetuximab alone, or cetuximab-plus-irradiation combined

59 We observe marked synergy of EAI045 with cetuximab, an antibody therapeutic that blocks EGFR dime

60 hylaxis during first exposure to intravenous cetuximab and (2) delayed-onset anaphylaxis 3 to 6 hours

61 rted here, 78 (46%) assigned to intermittent cetuximab and 91 (54%) to continuous cetuximab.

62 s, and KRAS-WT and KRAS-mutant CRC, combined cetuximab and anti-CD137 mAb administration was synergis

63 significantly different, 59.6% vs 55.2% for cetuximab and bevacizumab, respectively (difference, 4.4

64 espond poorly to the EGFR inhibitors (EGFRI) cetuximab and erlotinib, despite tumor expression of EGF

65 comes were observed between the FOLFIRI plus cetuximab and FOLFIRI plus bevacizumab arms of FIRE-3.

66 eatment modifications compared with ECF plus cetuximab and IC plus cetuximab (P = .013), and fewer pa

67 e responses observed with the combination of cetuximab and irinotecan may reflect true drug synergy o

68 ution data of immuno-PET imaging with (64)Cu-cetuximab and of small-animal SPECT/CT imaging with (177

69 % CI, 0.64-9.65; and HR for KRAS-variant, no cetuximab and p16 negative, 0.61; 95% CI, 0.23-1.59; P =

70 .22; 95% CI, 0.03-1.66; HR for KRAS-variant, cetuximab and p16 negative, 1.43; 95% CI, 0.48-4.26; HR

71 and treatment for OS (HR, for KRAS-variant, cetuximab and p16 positive, 0.22; 95% CI, 0.03-1.66; HR

72 ; 95% CI, 0.48-4.26; HR for KRAS-variant, no cetuximab and p16 positive, 2.48; 95% CI, 0.64-9.65; and

73 eted therapies are the monoclonal antibodies cetuximab and panitumumab, which prevent epidermal growt

74 itopes via immunoblot and in comparison with cetuximab and pork kidney by IgE reactivity assays.

75 therapeutic efficacy with the combination of cetuximab and radioimmunotherapy in CRC, which could pot

76 Using Cetuximab and Trastuzumab, proximity of EGFR and HER2 wa

77 s plus eight once-weekly doses of concurrent cetuximab and two cycles of cisplatin and fluorouracil.

78 , 147 to standard-dose chemoradiotherapy and cetuximab, and 110 to high-dose chemoradiotherapy and ce

79 ab, 45.0% (95% CI, 33.0 to 57.0) for IC plus cetuximab, and 54.3% (95% CI, 42.0 to 66.2) for FOLFOX p

80 f carboplatin and paclitaxel with or without cetuximab, and 60- versus 74-Gy radiation doses.

81 e was associated with allergies to red meat, cetuximab, and gelatin.

82 ribed a regimen of irinotecan hydrochloride, cetuximab, and ramucirumab for metastatic rectal cancer

83 in patients with advanced cSCC treated with cetuximab; and to investigate the efficacy and tolerance

84 i-EGFR monoclonal antibodies panitumumab and cetuximab are effective in patients with chemotherapy-re

85 e therapy, in the FIRE-3 trial (FOLFIRI plus cetuximab [arm A] or bevacizumab [arm B]) for patients w

86 of EREG methylation in patients who received cetuximab as part of a phase II study were associated wi

87 lectra, Herceptin/Trastuzumab B, and Erbitux/Cetuximab B) using a middle-up approach.

88 atio to receive chemotherapy with or without cetuximab before and after liver resection.

89 allowed the analysis of the specific PEI-PEG-cetuximab binding to EGFR and the determination of bindi

90 -glycan analysis of the therapeutic antibody cetuximab by LC-MS/MS analyses tightly integrated with (

91 ve parental cells were rendered resistant to cetuximab by stable overexpression of AXL or stimulation

92 affinity of a recently reported meditope for cetuximab can be substantially enhanced using a combinat

93 ts indicate that the combination of NTP with cetuximab can decrease invasiveness in cetuximab-resista

94 activation of T cells bearing high-affinity cetuximab-CAR was not affected by the density of EGFR.

95 Either cetuximab (cet) or trastuzumab (tra) conjugated with IR7

96 trategy was validated with the separation of Cetuximab charge variant by the middle-up approach.

97 ression-free survival was 10.5 months in the cetuximab-chemotherapy group and 10.6 months in the beva

98 dian overall survival was 30.0 months in the cetuximab-chemotherapy group and 29.0 months in the beva

99 First-line FOLFIRI plus cetuximab clearly benefitted patients with left-sided tu

100 nrolled in a novel neoadjuvant, single-agent cetuximab clinical trial.

101 Furthermore, monocyte-mediated ADCC against cetuximab-coated tumor targets was enhanced by TLR8 agon

102 d irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Combined With Irinotecan in First-line Therapy

103 d irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Combined With Irinotecan in First-line Therapy

104 Median follow-up for the cetuximab comparison was 21.3 months (IQR 23.5-29.8).

105 therapy comparison: eight vs three patients; cetuximab comparison: ten vs five patients).

106 planned maintenance by continuing on weekly cetuximab (continuous cetuximab).

107 d with EGFR expression in cells resistant to cetuximab (Ctx(R) cells).

108 IgE-reactive monoclonal therapeutic antibody cetuximab (CTX) and is associated with delayed anaphylax

109 comitant cisplatin (CDDP) versus concomitant cetuximab (CTX) as first-line treatment of locally advan

110 onstrated that, irrespective of KRAS status, cetuximab did not induce an antitumor response in a majo

111 , erlotinib) or monoclonal antibodies (i.e., cetuximab) does not provide long-term therapeutic benefi

112 In combination with cetuximab, ECF and FOLFOX had similar efficacy, but FOLF

113 RAS, BRAF, and EGFR genes and association of cetuximab efficacy with these mutations was investigated

114 y, suggesting a structural basis for reduced cetuximab efficacy.

115 ting EGFRt with the IgG1 monoclonal antibody cetuximab eliminates CD19 CAR T cells both early and lat

116 Because cetuximab enhances the effect of radiation therapy in hu

117 Because cetuximab enhances the effect of radiation therapy in hu

118 ll carcinoma (HNSCC) cell lines resistant to cetuximab (Erbitux).

119 The ICECREAM (Irinotecan Cetuximab Evaluation and Cetuximab Response Evaluation A

120 Cetuximab expanded CTLA-4(+)FOXP3(+) Treg in vitro, in p

121 Intratumoral distribution of (111)In-cetuximab-F(ab')(2) as determined by autoradiography cor

122 a significant increase in uptake of (111)In-cetuximab-F(ab')(2) in the SCCNij202 tumors after irradi

123 accessibility can be visualized with (111)In-cetuximab-F(ab')(2).

124 185, were imaged with SPECT/CT using (111)In-cetuximab-F(ab')2 (5 mug, 28 +/- 6.1 MBq, 24 h after inj

125 (111)In-cetuximab-F(ab')2 predicted and monitored the effects of

126 Thus, the additional value of the (111)In-cetuximab-F(ab')2 tracer is emphasized and the tracer ca

127 terized by a significantly increased (111)In-cetuximab-F(ab')2 tumor uptake; tumor-to-liver ratio was

128 (111)In-cetuximab-F(ab')2 uptake (tumor-to-liver ratio, scan 2 -

129 ng systemically accessible EGFR with (111)In-cetuximab-F(ab')2 while simultaneously evaluating tumor

130 In several EGFR-mediated cancer models, cetuximab failed to inhibit downstream signaling or to k

131 ts in both groups received FOLFOX and weekly cetuximab for 12 weeks, then either had a planned interr

132 uvant FOLFOX4 alone or FOLFOX4 combined with cetuximab for 6 months.

133 NT-mAb (3)] or without [SmCl3@SWCNT-NH2 (2)] Cetuximab functionalization were tested.

134 in the intention-to-treat population) or the cetuximab group (n=656; 283 with bevacizumab and 373 wit

135 e were three deaths in the chemotherapy plus cetuximab group (one interstitial lung disease and pulmo

136 reatment occurred in 32 (6%) patients in the cetuximab group and 13 (2%) patients in the control grou

137 194 progression-free survival events in the cetuximab group and 198 in the control group in the EGFR

138 59 (9%) patients in the cetuximab group and 31 (5%) patients in the control grou

139 After 570 deaths in the cetuximab group and 593 in the control group, overall su

140 gnificantly shorter in the chemotherapy plus cetuximab group than in the chemotherapy alone group (14

141 all survival was significantly longer in the cetuximab group than in the control group (HR 0.58, 95%

142 decreased neutrophil count (210 [37%] in the cetuximab group vs 158 [25%] in the control group), decr

143 imab (250 mg/m(2) weekly after loading dose; cetuximab group) or without (control group), stratified

144 months (12.2-28.7) in the chemotherapy plus cetuximab group.

145 eaths in the high-dose chemoradiotherapy and cetuximab groups (radiotherapy comparison: eight vs thre

146 tients with the KRAS-variant treated without cetuximab had worse PFS than patients without the KRAS-v

147 Recently, the addition of cetuximab has shown promise as a way to improve outcomes

148 Overall, for patients with the KRAS-variant, cetuximab improved both progression-free survival (PFS)

149 yonic antigen antibody ((131)I-huA5B7), with cetuximab in colorectal cancer (CRC).

150 xicity (eg, trastuzumab in breast cancer and cetuximab in colorectal cancer).

151 d biomarkers of response to radiotherapy and cetuximab in locally advanced head and neck squamous cel

152 sufficient to mediate acquired resistance to cetuximab in models of non-small cell lung cancer (NSCLC

153 potential of treatment that combines NTP and cetuximab in OSCC.

154 er investigation of the role of FOLFOX4 plus cetuximab in specific patient subgroups is warranted.

155 l, leucovorin, and irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Combined With Irinotecan in F

156 l, leucovorin, and irinotecan (FOLFIRI) plus cetuximab in the Cetuximab Combined With Irinotecan in F

157 This trial cannot conclude on the benefit of cetuximab in the studied population, but the heterogenei

158 efficacy and toxicity of panitumumab versus cetuximab in these patients.

159 raction are needed but at present the use of cetuximab in this setting cannot be recommended.

160 tuximab-sensitive colorectal cancer cells to cetuximab in three-dimensional culture.

161 ased the antitumor activity of erlotinib and cetuximab in vivo.

162 f small-animal SPECT/CT imaging with (177)Lu-cetuximab, including blood and TE-8 tumor.

163 actor receptor (EGFR) inhibitor therapy with cetuximab, indicating the need for patient selection.

164 Both antivenoms and cetuximab induced positive skin prick test results in pa

165 panitumumab (6 mg/kg once every 2 weeks) or cetuximab (initial dose 400 mg/m(2); 250 mg/m(2) once a

166 ial evaluating the safety and specificity of cetuximab-IRDye800.

167 fluorescently labeled therapeutic antibody, cetuximab-IRDye800CW (2.5 mg/m(2), 25 mg/m(2), and 62.5

168 Cetuximab is a murine-human chimeric IgG1 mAb directed a

169 This suggests that cetuximab is certainly warranted in the treatment of adv

170 t, we demonstrate that primary resistance to cetuximab is dependent upon both KRAS mutational status

171 The EGFR-targeted antibody cetuximab is effective against head and neck cancer (HNS

172 EAI045 in combination with cetuximab is effective in mouse models of lung cancer dr

173 esponders, reduced-dose IMRT with concurrent cetuximab is worthy of further study in favorable-risk p

174 Here we show that the EGFR blocking with cetuximab leads to varied autophagic responses, which mo

175 first time that combining NTP treatment with cetuximab led to inhibition of migration and invasion in

176 patients with the KRAS-variant suggests that cetuximab may help these patients by overcoming TGF-beta

177 Although addition of cetuximab may result in less LRF, the 20% recurrence and

178 These Treg suppressed cetuximab-mediated antibody-dependent cellular cytotoxic

179 ed susceptibility of cells undergoing EMT to cetuximab-mediated CDC.

180 patients, and the variability and extent of cetuximab-mediated cellular immunity is not fully unders

181 increased affinity translated into enhanced cetuximab-mediated recruitment to EGF receptor-overexpre

182 We aimed to assess cetuximab monotherapy and cetuximab plus irinotecan in p

183 t in disease control at 6 months with either cetuximab monotherapy or cetuximab plus irinotecan.

184 herapy and were randomized to receive either cetuximab (n = 578) or bevacizumab (n = 559).

185 nd oxaliplatin) chemotherapy with or without cetuximab (North Central Cancer Treatment Group N0147 tr

186 cisplatin plus radiotherapy with or without cetuximab (NRG Oncology RTOG 0522) were included in this

187 etained 105.7% (81.9-129.5) of the effect of cetuximab on overall survival seen in this study.

188 All treatment programs included cetuximab once per week.

189 actions was lower with panitumumab than with cetuximab (one [<0.5%] patient vs nine [2%] patients), a

190 On RECIST progression, FOLFOX plus cetuximab or FOLFOX was recommenced for 12 weeks followe

191 originally assigned to arm B received either cetuximab or panitumumab.

192 PF-00299804 but not with anti-EGFR antibody (Cetuximab) or etoposide, triggers a burst in emission of

193 nned interruption (those taking intermittent cetuximab) or planned maintenance by continuing on weekl

194 tandard dose), 74 Gy (high dose), 60 Gy plus cetuximab, or 74 Gy plus cetuximab.

195 compared with ECF plus cetuximab and IC plus cetuximab (P = .013), and fewer patients were removed fr

196 free survival upon palliative treatment with cetuximab plus chemotherapy or radiation.

197 Cetuximab plus cisplatin-radiation, versus cisplatin-rad

198 We aimed to assess cetuximab monotherapy and cetuximab plus irinotecan in patients with molecularly s

199 cetuximab versus 23% (95% CI, 9% to 40%) for cetuximab plus irinotecan with a hazard ratio of 0.74 (9

200 months with either cetuximab monotherapy or cetuximab plus irinotecan.

201 Cetuximab plus platinum regimens also increase OS in met

202 ose irradiation (10 Gy), cetuximab alone, or cetuximab-plus-irradiation combined or on untreated cont

203 biting resistance to the EGFR-targeting drug cetuximab poses a challenge to their effective clinical

204 h 1 receptor antibody, in this platinum- and cetuximab-pretreated population with poor prognosis.

205 Responses of PDXs to cetuximab recapitulate also clinical data in patients, w

206 samples, and inhibiting CSN6 stability with cetuximab reduced colon cancer growth.

207 FOLFOX plus cetuximab required fewer treatment modifications compare

208 this 3D system, we have identified a mode of cetuximab resistance and a potential prognostic marker i

209 ce enhances growth factor ligand binding and cetuximab resistance through induction and stabilization

210 t EGFR-K521 expression as a key mechanism of cetuximab resistance to evaluate prospectively as a pred

211 a clinically actionable, epigenetic cause of cetuximab resistance.

212 he absence of known genetic events linked to cetuximab resistance.

213 creased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiven

214 To generate cetuximab-resistant cells, we exposed cetuximab-sensitiv

215 miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck

216 d to inhibition of migration and invasion in cetuximab-resistant OSCC cells, which could be a promisi

217 with cetuximab can decrease invasiveness in cetuximab-resistant OSCCs through a novel mechanism invo

218 ulted in antitumor efficacy in a majority of cetuximab-resistant tumors.

219 lowed by further interruption or maintenance cetuximab, respectively.

220 ns showed a partial and complete response to cetuximab, respectively.

221 ivity of 3.70/12.95 MBq, for (64)Cu-/(177)Lu-cetuximab, respectively.

222 g site in KRAS, is a predictive biomarker of cetuximab response and altered immunity in the setting o

223 The correlation of KRAS-variant status with cetuximab response and outcome, p16 status, and plasma T

224 CECREAM (Irinotecan Cetuximab Evaluation and Cetuximab Response Evaluation Among Patients with a G13D

225 bition in cetuximab-resistant cells restored cetuximab responsiveness.

226 glycosylation targeting the same epitope as cetuximab, restored HNSCC sensitivity in a manner associ

227 Both the radiation-dose and cetuximab results crossed protocol-specified futility bo

228 ugh differences were nonsignificant, IC plus cetuximab seemed to be the least effective and most toxi

229 nerate cetuximab-resistant cells, we exposed cetuximab-sensitive colorectal cancer cells to cetuximab

230 Cetuximab-sensitive parental cells were rendered resista

231 osine kinase inhibitor, crizotinib, restored cetuximab sensitivity in SC.

232 fts provide remarkable resolution to measure Cetuximab sensitivity.

233 eutic anti-epidermal growth factor antibody (cetuximab) showed significant signal in the skin after t

234 rmal growth factor receptor (EGFR) inhibitor cetuximab shows an improved response in a subgroup of pa

235 with RAS wt left-sided tumors, FOLFIRI plus cetuximab significantly improved OS relative to the resp

236 bitor (TKI)) and surface functionalized with cetuximab-siRNA conjugate has been synthesized.

237 , the EGFR-neutralizing monoclonal antibody, cetuximab, strongly inhibited growth of CC, whereas SC w

238 e variants detected in the CZE separation of Cetuximab subunits.

239 nation regimen suggests that the addition of cetuximab suppressed DNA repair.

240 equent in patients treated with FOLFOX4 plus cetuximab than in those patients who received FOLFOX4 al

241 r enhancing the secondary immune response to cetuximab that involves sequential targeting with an ago

242 anion diagnostic/therapeutic (64)Cu-/(177)Lu-cetuximab that may be considered as a step for determini

243 u-/(177)Lu-labeled antibody ((64)Cu-/(177)Lu-cetuximab), that acts as anti-epidermal growth factor re

244 In patients receiving cetuximab, the level of CD137 on circulating and intratu

245 TM1/p62, is associated with poor response to cetuximab therapy.

246 d radiation therapy (IMRT) 54 Gy with weekly cetuximab; those with less than cCR to IC at the primary

247 Conclusion Although the addition of cetuximab to chemoradiation for SCCAC was associated wit

248 Addition of cetuximab to concurrent chemoradiation and consolidation

249 The addition of cetuximab to concurrent chemoradiation did not improve O

250 concurrent chemotherapy and the addition of cetuximab to concurrent chemoradiation for patients with

251 opharyngeal SCC, we hypothesized that adding cetuximab to CRT would reduce LRF in SCCAC.

252 cell carcinoma, we hypothesized that adding cetuximab to CRT would reduce LRF in SCCAC.

253 CRYSTAL study demonstrated that addition of cetuximab to fluorouracil, leucovorin, and irinotecan (F

254 benefits were observed upon the addition of cetuximab to FOLFIRI in CRYSTAL, and comparable outcomes

255 d points was associated with the addition of cetuximab to FOLFIRI.

256 d a significant benefit from the addition of cetuximab to FOLFIRI; patients with RAS tumor mutations

257 ivery of postoperative chemoradiotherapy and cetuximab to patients with SCCHN is feasible and tolerat

258 Adding cetuximab to radiation-cisplatin did not improve outcome

259 C significantly benefit from the addition of cetuximab to radiotherapy and cisplatin, and there is a

260 The addition of cetuximab to these chemotherapy regimens results in an o

261 e primary site or nodes received 69.3 Gy and cetuximab to those regions.

262 ding targeted agents, namely bevacizumab and cetuximab, to standard chemotherapies in stage III disea

263 and clinical impact on antitumor immunity in cetuximab-treated individuals.

264 he circulation and tumor microenvironment of cetuximab-treated patients with HNSCC enrolled in a nove

265 d 1.4 +/- 0.4 to 2.0 +/- 0.3, P < 0.05, for (cetuximab-treated) SCCNij185, respectively.

266 sponded to combined treatment (P < 0.01) and cetuximab treatment alone (P < 0.05) but not to irradiat

267 0.05) and irradiation (P < 0.05) but not to cetuximab treatment alone (P = 0.34).

268 rrelated with a higher recurrence rate after cetuximab treatment and reduced overall survival.

269 Moreover, these tumors were resistant to cetuximab treatment despite augmented EGFR signaling, at

270 Notably, cetuximab treatment increased the frequency of CD4(+)FOX

271 of NFkappaB/RelA acetylation by IFRD1 shRNA, cetuximab treatment or the HDAC1/3 inhibitor entinostat

272 All patients could continue cetuximab treatment without dose reduction.

273 ssion contribute to the clinical response to cetuximab treatment, suggesting its improvement by addin

274 ulating EGFR functionality and resistance to cetuximab treatment.

275 progression within 6 months of platinum and cetuximab treatment.

276 urvival rate was 10% (95% CI, 2% to 26%) for cetuximab versus 23% (95% CI, 9% to 40%) for cetuximab p

277 ctal Cancer (CRYSTAL) trial and FOLFIRI Plus Cetuximab Versus FOLFIRI Plus Bevacizumab as First-Line

278 ctal Cancer (CRYSTAL) trial and FOLFIRI Plus Cetuximab Versus FOLFIRI Plus Bevacizumab as First-Line

279 Cetuximab vs bevacizumab combined with either mFOLFOX6 o

280 in overall survival between the addition of cetuximab vs bevacizumab to chemotherapy as initial biol

281 To determine if the addition of cetuximab vs bevacizumab to the combination of leucovori

282 an overall survival in patients who received cetuximab was 25.0 months (95% CI 20.2-30.5) compared wi

283 Cetuximab was added to each treatment arm based on promi

284 By contrast, the use of cetuximab was associated with a higher rate of grade 3 o

285 esistance following prolonged treatment with cetuximab was associated with AXL hyperactivation and EG

286 Even in elderly patients with advanced cSCC, cetuximab was efficacious and well-tolerated.

287 Cetuximab was given as an intravenous dose of 500 mg/m(2

288 s assigned to receive cetuximab, 400 mg/m(2) cetuximab was given on day 1 followed by weekly doses of

289 Cetuximab was recently proposed for advanced cutaneous s

290 Cetuximab was safely incorporated in two first-line inte

291 -1,3-galactose, located on the Fab region of cetuximab, was identified as the target responsible for

292 possibility to perform skin prick tests with cetuximab, which carries the alpha-gal epitope.

293 be transcytosed better than the G1m3,-1 mAb cetuximab, which explains why infliximab is a better com

294 rapy and we aimed to explore the activity of cetuximab with chemotherapy in patients with advanced NS

295 -site cCR to IC and 51 patients continued to cetuximab with IMRT 54 Gy.

296 Compared with monotherapy, combining cetuximab with radioimmunotherapy significantly and syne

297 PET/CT-based radiation dosimetry for (89)Zr-cetuximab, with special emphasis on determining RM-absor

298 l cancer received 36.9 +/- 0.8 MBq of (89)Zr-cetuximab within 2 h after administration of a therapeut

299 h (131)I-huA5B7 alone or in combination with cetuximab without observable toxicity.

300 ll survival, panitumumab was non-inferior to cetuximab (Z score -3.19; p=0.0007).