ライフサイエンスコーパス: cetuximab

1 characterization of the monoclonal antibody Cetuximab.

2 ents benefit from the EGFR-blocking antibody cetuximab.

3 predicting sensitivity to the EGFR inhibitor cetuximab.

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

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

6 ab and two EGFR binding antibodies including Cetuximab.

7 olorectal cancer patients that progressed on cetuximab.

8 The experimental arm received adjuvant cetuximab.

9 6 status for PFS in patients treated without cetuximab.

10 us cell carcinoma refractory to platinum and cetuximab.

11 Patients were treated by single-agent cetuximab.

12 noms contained lower alpha-gal contents than cetuximab.

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

14 rcinoma previously treated with platinum and cetuximab.

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

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

17 g fragment of a therapeutic antibody such as cetuximab.

18 ng the variable regions of the EGFR antibody cetuximab.

19 whose signaling activities can be impeded by cetuximab.

20 54.3% (95% CI, 42.0 to 66.2) for FOLFOX plus cetuximab.

21 ation carboplatin/paclitaxel with or without cetuximab.

22 No responses were seen with single-agent cetuximab.

23 treated with adjuvant FOLFOX with or without cetuximab.

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

25 rsions of B7-H6 and the Fab arm derived from cetuximab.

26 , the same regimen was used with addition of cetuximab.

27 aRIIIa, including the clinically approved Ab cetuximab.

28 with chemotherapy plus either bevacizumab or cetuximab.

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

30 tients, 13 displayed intrinsic resistance to cetuximab; 12 were intrinsically sensitive.

31 before radiotherapy initiation, followed by cetuximab 250 mg/m(2) weekly for seven doses (total 2150

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

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

34 y assigned 1:1 to receive either intravenous cetuximab 400 mg/m(2) 1 week before start of RT followed

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

36 , 22, and 43 of radiotherapy) or intravenous cetuximab (400 mg/m(2) loading dose followed by seven we

37 y (125 mg/day, on days 1-21) and intravenous cetuximab (400 mg/m(2) on cycle one, day 1, then 250 mg/

38 4 Gy/1.8 Gy fractions with or without weekly cetuximab (400 mg/m2 on day 1 then 250 mg/m2 weekly).

39 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

40 to receive afatinib 40 mg orally daily plus cetuximab 500 mg/m(2) intravenously every 2 weeks or afa

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

42 ts: Seven formulations were investigated for cetuximab-800CW and 10 for trastuzumab-800CW.

43 Methods: The production process for cetuximab-800CW and trastuzumab-800CW was optimized with

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

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

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

47 Cetuximab, a monoclonal neutralizing antibody against EG

48 After SC administration cetuximab absolute bioavailability increased from 67 % t

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

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

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

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

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

54 or response observed in some HNSCC patients, cetuximab alone or combined with radio- or chemotherapy

55 ib (a selective CDK4/6 inhibitor) given with cetuximab (an EGFR inhibitor) was safe.

56 umour samples from 25 CRC patients receiving cetuximab (an EGFR inhibitor).

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

58 Cetuximab, an epidermal growth factor receptor inhibitor

59 Whether replacement of cisplatin with cetuximab-an antibody against the epidermal growth facto

60 plied to produce batches of (89)Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab suitable for cl

61 ts: Radiochemical yields of (89)Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab were all more t

62 2.0% and 62.6% +/- 3.0% for (89)Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab, respectively,

63 0.6% and 87.1% +/- 2.2% for (89)Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab, respectively.

64 399 patients assigned to receive cetuximab and 406 patients assigned to receive cisplatin

65 randomly assigned, and 168 (83 on afatinib + cetuximab and 85 on afatinib) were eligible.

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

67 6.4-24.8; p=0.1904) were similar between the cetuximab and cisplatin groups.

68 interaction, the interaction surface between Cetuximab and EGFR was mapped.

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

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

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

72 ic binding dynamics between a model antibody cetuximab and its target, the epidermal growth factor re

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

74 % CI, 0.64-9.65; and HR for KRAS-variant, no cetuximab and p16 negative, 0.61; 95% CI, 0.23-1.59; P =

75 .22; 95% CI, 0.03-1.66; HR for KRAS-variant, cetuximab and p16 negative, 1.43; 95% CI, 0.48-4.26; HR

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

77 ; 95% CI, 0.48-4.26; HR for KRAS-variant, no cetuximab and p16 positive, 2.48; 95% CI, 0.64-9.65; and

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

79 e lymphatic transport and bioavailability of cetuximab and trastuzumab after SC and ID coadministrati

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

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

82 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

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

84 rs benefited more from bevacizumab than from cetuximab, and studies to confirm this effect of MSI-H a

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

86 wth factor receptor (EGFR) therapies such as cetuximab are in part caused by genetic alterations in p

87 observed in the bevacizumab arm than in the cetuximab arm (HR, 0.13 [95% CI, 0.06 to 0.30]; interact

88 At interim analysis, the FOLFOX-cetuximab arm was stopped (lack of efficacy).

89 terations with either the bevacizumab or the cetuximab arms was tested.

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

91 l design with radiation dose as 1 factor and cetuximab as the other, with a primary end point of over

92 were assigned to receive either intravenous cetuximab at a loading dose of 400 mg/m(2) 5-7 days befo

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

94 We generated Cetuximab-based IL-10 fusion protein (CmAb-(IL10)(2)) to

95 1:1) to receive chemotherapy with or without cetuximab before and after liver resection.

96 Compared to the binding in vitro, cetuximab bound to EGFR to a "slower-but-tighter" degree

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

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

99 e found to be powerful for the separation of Cetuximab charge variants with eight major peaks being b

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

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

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

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

104 d in 72% of patients receiving afatinib plus cetuximab compared with 40% of those receiving afatinib

105 t in PFS in patients receiving afatinib plus cetuximab compared with afatinib alone (hazard ratio [HR

106 ied whether the combination of afatinib plus cetuximab compared with afatinib alone would improve pro

107 The use of cetuximab conferred no survival benefit at the expense o

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 There is a need to formulate oral cetuximab (CTX) for targeting colorectal cancer, which i

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

112 -up duration of 4.5 years, radiotherapy plus cetuximab did not meet the non-inferiority criteria for

113 and 30% of patients in this arm discontinued cetuximab due to toxicity.

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

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

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

117 ce of the culture environment on response to Cetuximab (EGFR monoclonal antibody) and AZD8055 (mTOR i

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

119 Because cetuximab enhances the effect of radiation therapy in hu

120 Because cetuximab enhances the effect of radiation therapy in hu

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

122 equency of somatic variants, suggesting that cetuximab exposure dramatically selected for rare resist

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

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

125 chemotherapy and determined the efficacy of cetuximab for stage III non-small-cell lung cancer (NSCL

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

127 months (13.8-19.0) in the chemotherapy plus cetuximab group (hazard ratio [HR] 1.17, 95% CI 0.87-1.5

128 months (43.5-71.5) in the chemotherapy plus cetuximab group (HR 1.45, 1.02-2.05; p=0.036).

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

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

131 194 progression-free survival events in the cetuximab group and 198 in the control group in the EGFR

132 59 (9%) patients in the cetuximab group and 31 (5%) patients in the control grou

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

134 free survival was significantly lower in the cetuximab group compared with the cisplatin group (HR 1.

135 onal failure was significantly higher in the cetuximab group compared with the cisplatin group (HR 2.

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

137 survival was 77.9% (95% CI 73.4-82.5) in the cetuximab group versus 84.6% (80.6-88.6) in the cisplati

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

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

140 vs 21 [15%] of 137 in the chemotherapy plus cetuximab group), diarrhoea (13 [10%] vs 14 [10%]), skin

141 d (166 in the cisplatin group and 168 in the cetuximab group).

142 lone group and four in the chemotherapy plus cetuximab group).

143 ab-naive (group 1) or disease progression on cetuximab (group 2).

144 8% (95% CI, 71% to 85%) in the cisplatin and cetuximab groups, respectively (adjusted hazard ratio, 1

145 In the CMS2 cohort, patients treated with cetuximab had a significantly longer OS than patients tr

146 Cetuximab had no effect on OS.

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

148 Cetuximab harbors four glycans per molecule, two on each

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

150 significant difference between cisplatin and cetuximab in 2-year overall survival (97.5% vs 89.4%, ha

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

152 ith concomitant cisplatin versus concomitant cetuximab in patients with locoregionally advanced head

153 to evaluate the activity of palbociclib and cetuximab in platinum-resistant (group 1) and cetuximab-

154 g an objective response with palbociclib and cetuximab in recurrent or metastatic HNSCC.

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

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

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

158 e receptor expression changes in response to cetuximab, indicating a potential for assessment of adeq

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

160 Cetuximab-induced apoptosis was assessed in vitro and in

161 tandard doses of methotrexate, docetaxel, or cetuximab intravenously (standard-of-care group).

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

163 The model suggested that cetuximab is bound differently to EGFR in the stroma-ric

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

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

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

167 The EGFR monoclonal antibody cetuximab is generally used in combination with radiatio

168 Cetuximab is inferior to cisplatin regarding locoregiona

169 arker stratification, the anti-EGFR antibody cetuximab is only effective against a subgroup of colore

170 So far, cetuximab is the only approved anti-EGFR monoclonal anti

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

172 rmal growth factor receptor (EGFR) antibody, cetuximab, is an approved therapy for head and neck squa

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

174 ), although the proportional contribution of cetuximab lymphatic transport reduced slightly (6.2-fold

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

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

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

178 r burden and allow for dynamic monitoring of cetuximab-mediated changes in receptor expression.

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

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

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

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

183 emotherapy with cetuximab (n=129) or without cetuximab (n=128).

184 were randomly assigned to chemotherapy with cetuximab (n=129) or without cetuximab (n=128).

185 ndomly assigned to receive radiotherapy plus cetuximab (n=425) or radiotherapy plus cisplatin (n=424)

186 atients: (89)Zr-obinutuzumab [n = 9], (89)Zr-cetuximab [n = 7], (89)Zr-huJ591 [n = 10], and (89)Zr-tr

187 der, and disease progression on platinum but cetuximab-naive (group 1) or disease progression on cetu

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

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

190 All treatment programs included cetuximab once per week.

191 ts (1:1) to receive either radiotherapy plus cetuximab or radiotherapy plus cisplatin.

192 ith agents to which the model was resistant (cetuximab) or sensitive (INC280 and trametinib).

193 nificantly longer OS than those treated with cetuximab (P < .001).

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

195 1.0] with cisplatin vs 30.1 [28.3-31.9] with cetuximab; p=0.49).

196 .2-5.4] with cisplatin vs 4.8 [4.2-5.4] with cetuximab; p=0.98).

197 increased 10-fold in the presence of rHuPH20 cetuximab plasma exposure increased approximately linear

198 uracil (pembrolizumab with chemotherapy), or cetuximab plus a platinum and 5-fluorouracil (cetuximab

199 ssion-free survival in patients allocated to cetuximab plus chemotherapy compared with those given ch

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

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

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

203 months with either cetuximab monotherapy or cetuximab plus irinotecan.

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

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

206 Cetuximab recovery in the lymphatics also increased afte

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 Fibroblast-supernatant conferred cetuximab resistance in vitro, confirming a major role f

210 s genomic and transcriptomic analysis of the cetuximab resistance landscape in 35 RAS wild-type CRCs

211 expression plays a critical role in acquired cetuximab resistance of OSCC and that combination therap

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

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

214 a clinically actionable, epigenetic cause of cetuximab resistance.

215 howed that PI3K/mTOR inhibition could rescue cetuximab resistance.

216 on to explore alternative mechanisms driving cetuximab-resistance in OSCC cells.

217 K1/2 phosphorylation and this pathway drives cetuximab-resistance in the absence of EGFR overexpressi

218 etuximab in platinum-resistant (group 1) and cetuximab-resistant (group 2) HPV-unrelated HNSCC.

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

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

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

222 potentially providing opportunities to treat cetuximab-resistant CRCs with immunotherapy.

223 In patients with platinum-resistant or cetuximab-resistant HPV-unrelated HNSCC, palbociclib and

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

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

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

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

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

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

230 bition in cetuximab-resistant cells restored cetuximab responsiveness.

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

232 sistant HPV-unrelated HNSCC, palbociclib and cetuximab results in promising activity outcomes.

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

234 tosis was assessed in vitro and in vivo with cetuximab-sensitive (DiFi) and insensitive (HCT-116) hum

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

236 In cetuximab-sensitive patients, we found KRAS K117N and A1

237 Most of these had switched from a cetuximab-sensitive transcriptomic subtype at baseline t

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

239 fts provide remarkable resolution to measure Cetuximab sensitivity.

240 revealing additive effects on promoting OSCC cetuximab-sensitivity in vitro and in vivo.

241 Cetuximab should not be used in this setting.

242 e oropharyngeal carcinoma, radiotherapy plus cetuximab showed inferior overall survival and progressi

243 ompared with the standard cisplatin regimen, cetuximab showed no benefit in terms of reduced toxicity

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

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

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

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

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

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

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

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

252 The addition of cetuximab to afatinib did not improve outcomes in previo

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

254 Although the addition of cetuximab to chemotherapy improves the overall survival

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

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

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

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

259 that compared the addition of bevacizumab or cetuximab to infusional fluorouracil, leucovorin, and ox

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

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

262 tometry detected apoptotic cell shrinkage in cetuximab-treated DiFi cells, and significant apoptosis

263 redictive biomarker to stratify patients for cetuximab treatment have been unsuccessful.

264 Cetuximab treatment increased cytotoxic immune infiltrat

265 Results: Cetuximab treatment resulted in continued tumor growth,

266 All patients could continue cetuximab treatment without dose reduction.

267 progression within 6 months of platinum and cetuximab treatment.

268 oups that still may benefit from concomitant cetuximab treatment.

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

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

271 compared with 9% (95% CI, 4% to 14%) in the cetuximab versus the cisplatin group (Gray's test P = .0

272 Cetuximab vs bevacizumab combined with either mFOLFOX6 o

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

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

275 Cetuximab was added to each treatment arm based on promi

276 In the second trial, cetuximab was added to the same neoadjuvant treatment co

277 ts, a third arm testing perioperative FOLFOX-cetuximab was added.

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

279 Cetuximab was given intravenously, 500 mg/m(2) every 2 w

280 downregulate the EGFR level, treatment with cetuximab was performed, and (18)F-aluminium fluoride-NO

281 ) afatinib plus the EGFR monoclonal antibody cetuximab was previously shown to overcome resistance to

282 Cetuximab was recently proposed for advanced cutaneous s

283 A deep insight into the heterogeneity of Cetuximab was unveiled, the high level of sensitivity ac

284 -1,3-galactose, located on the Fab region of cetuximab, was identified as the target responsible for

285 thods: (89)Zr-DFO-trastuzumab and (89)Zr-DFO-cetuximab were prepared using (89)ZrCl(4) The stability

286 Cl(4), (89)Zr-DFO-trastuzumab and (89)Zr-DFO-cetuximab were prepared with increased specific activity

287 interstitial bioavailability was higher for cetuximab where intrinsic interstitial bioavailability w

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

289 pembrolizumab with chemotherapy (n=281), or cetuximab with chemotherapy (n=300); of these, 754 (85%)

290 nd of pembrolizumab with chemotherapy versus cetuximab with chemotherapy for overall survival and pro

291 e and pembrolizumab with chemotherapy versus cetuximab with chemotherapy for overall survival in the

292 with chemotherapy group, and 28 (10%) in the cetuximab with chemotherapy group.

293 motherapy group, and 239 (83%) of 287 in the cetuximab with chemotherapy group.

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

295 zumab alone improved overall survival versus cetuximab with chemotherapy in the CPS of 20 or more pop

296 hemotherapy improved overall survival versus cetuximab with chemotherapy in the total population (13.

297 etuximab plus a platinum and 5-fluorouracil (cetuximab with chemotherapy).

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

299 ens were randomly assigned to irinotecan and cetuximab with or without vemurafenib (960 mg PO twice d

300 We investigated whether cetuximab would maintain a high proportion of patient su