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1 cific treatment (chemotherapy, radiation, or panitumumab).
2 cific treatment (chemotherapy, radiation, or panitumumab).
3 tor receptor (EGFR) antibodies cetuximab and panitumumab.
4 fractionation RT plus the anti-EGFR antibody panitumumab.
5 monoclonal antibodies, such as cetuximab or panitumumab.
6 b and fluorescein 5(6)-isothiocyanate (FITC) panitumumab.
7 decane-N,N',N'',N'''-tetraacetic acid (DOTA)-panitumumab.
8 signed to arm B received either cetuximab or panitumumab.
9 fractionation RT plus the anti-EGFR antibody panitumumab.
10 K-Ras alterations based on the responses to panitumumab.
11 analysed for interaction with the effect of panitumumab.
12 clinical approval of the drugs cetuximab and panitumumab.
13 led to its targeting by using Cetuximab and Panitumumab.
17 us, with a permuted block method) to receive panitumumab (6 mg/kg once every 2 weeks) or cetuximab (i
18 ours were randomly assigned (1:1) to receive panitumumab (6 mg/kg; every 2 weeks with the first 6 wee
19 diotherapy plus panitumumab (three cycles of panitumumab 9 mg/kg every 3 weeks administered with radi
22 emoradiotherapy (three cycles of intravenous panitumumab 9.0 mg/kg every 3 weeks plus cisplatin 75 mg
33 in expression showed the highest (64)Cu-DOTA-panitumumab accumulation, whereas SQB20 tumors with the
36 clonal immunoglobulin gamma2 (IgG2) antibody panitumumab against human epidermal growth factor recept
37 vival was 10.4 months (95% CI 9.4-11.6) with panitumumab and 10.0 months (9.3-11.0) with cetuximab (H
41 Median OS was 34.2 and 24.3 months in the panitumumab and bevacizumab arms, respectively (HR, 0.62
44 median PFS was 10.0 and 11.4 months for the panitumumab and control arms, respectively (HR, 1.27; 95
46 etween therapeutic efficacy of cetuximab and panitumumab and EGFR expression level as determined by i
48 as confirmed by ex vivo immunostaining using panitumumab and fluorescein 5(6)-isothiocyanate (FITC) p
50 en used to radiolabel an anti-EGFR antibody, Panitumumab, and injected into mice bearing colon cancer
51 countries), including the mAbs cetuximab and panitumumab, and the small molecule TKIs gefitinib, erlo
52 Photoimmunotherapy was performed by binding panitumumab (anti-HER1)-IR700 to HER1-positive tumor cel
53 onal antibodies (mAbs) such as cetuximab and panitumumab are promising; however, most studies indicat
54 3, and 4 of KRAS and NRAS), PFS favored the panitumumab arm (HR, 0.65; 95% CI, 0.44 to 0.96; P = .02
55 RAS analyses showed adverse outcomes for the panitumumab arm in both wild-type and mutant groups.
58 ractionation RT (70 Gy/35 over 6 weeks) plus panitumumab at 9 mg/kg intravenous for 3 doses (arm B).
59 ractionation RT (70 Gy/35 over 6 weeks) plus panitumumab at 9 mg/kg intravenous for 3 doses (arm B).
69 sion-free survival and overall survival with panitumumab-FOLFOX4 treatment, which was consistent with
70 ogression-free survival was 10.1 months with panitumumab-FOLFOX4 versus 7.9 months with FOLFOX4 alone
75 nstrates the potential of (86)Y-CHX-A''-DTPA-panitumumab for quantitative noninvasive PET of HER1-exp
76 ''-diethylenetriaminepentaacetic acid (DTPA)-panitumumab for quantitative PET of HER1-expressing carc
77 ing the beta-particle emitter (177)Lu and to panitumumab for targeting epidermal growth factor recept
79 42%] of 89 patients in the radiotherapy plus panitumumab group), dysphagia (20 [32%] vs 36 [40%]), an
83 randomized controlled trials of cetuximab or panitumumab have evaluated outcomes for patients with me
84 itinib, erlotinib, cetuximab, lapatinib, and panitumumab have less systemic side-effects than traditi
86 ndicating that the low uptake of (64)Cu-DOTA-panitumumab in SQB20 tumors was not due to the loss of E
87 small-animal PET studies with (64)Cu-labeled panitumumab in xenografts derived from 3 cell lines of h
89 Anti-epidermal growth factor receptor (EGFR) panitumumab-IR700 was used for targeting EGFR-expressing
90 cer cell line (2LMP-Luc) in combination with panitumumab-IRDye 700DX (pan-IR700) was used to validate
91 gand model in a randomized clinical trial of panitumumab, irinotecan, and ciclosporin in colorectal c
96 ided more accurate information about (111)In-panitumumab localization in the tumor, as the tumor was
97 day on days 1-21) or modified-dose EOC plus panitumumab (mEOC+P; epirubicin 50 mg/m(2) and oxaliplat
99 ollected in a phase III mCRC trial comparing panitumumab monotherapy to best supportive care (BSC).
101 rmal growth factor receptor (EGFR) inhibitor panitumumab on cell lines expressing wild-type Kirsten-R
103 ed patients who received one or more dose of panitumumab or cetuximab, analysed per allocated treatme
106 a median follow-up of 46 months, the PFS of panitumumab plus accelerated-fractionation RT was not su
107 a median follow-up of 46 months, the PFS of panitumumab plus accelerated-fractionation RT was not su
108 y (three cycles of cisplatin 100 mg/m(2)) or panitumumab plus chemoradiotherapy (three cycles of intr
109 oradiotherapy group vs 35 [40%] of 87 in the panitumumab plus chemoradiotherapy group), mucosal infla
113 e randomly assigned at a one-to-one ratio to panitumumab plus mFOLFOX6 or bevacizumab plus mFOLFOX6.
114 ysis, we assessed the efficacy and safety of panitumumab plus oxaliplatin, fluorouracil, and leucovor
115 prospectively stratified design, restricting panitumumab randomisation to patients with KRAS wild-typ
116 atients in the irinotecan-vs-irinotecan with panitumumab randomization, 331 had sufficient tumor tiss
117 PFS was similar and OS was improved with panitumumab relative to bevacizumab when combined with m
122 grade 3-4 infusion reactions was lower with panitumumab than with cetuximab (one [<0.5%] patient vs
123 ression of either AREG or EREG would predict panitumumab therapy benefit in RAS-wt patients; and low
124 ligand expression is a predictive marker for panitumumab therapy benefit on PFS in RAS wt patients; c
127 during radiotherapy) or to radiotherapy plus panitumumab (three cycles of panitumumab 9 mg/kg every 3
128 The utility of PET and MRI using (89)Zr-panitumumab to assess the status of HER1 in distant meta
131 to assess addition of the anti-EGFR antibody panitumumab to epirubicin, oxaliplatin, and capecitabine
134 PICCOLO trial, which tested the addition of panitumumab to irinotecan therapy in patients with KRAS
135 cinoma of the head and neck, the addition of panitumumab to standard fractionation radiotherapy and c
136 epidermal growth factor receptor antagonist panitumumab to treat advanced colorectal cancer--was dev
139 At 2 days after injection, the mean (111)In-panitumumab uptake of 29.6% injected dose (ID) per gram
140 uptake of 13.6% ID/g +/- 1.0 and the (125)I-panitumumab uptake of 7.4% ID/g +/- 1.2 (P = .0006 and P
141 /4 adverse events in the oxaliplatin cohort (panitumumab v control) included skin toxicity (36% v 1%)
142 as awaited the recent regulatory approval of panitumumab (Vectibix), a fully human antibody directed
145 FS was 3.2 [2.7-8.1] months (irinotecan with panitumumab) vs 4.0 [2.7-7.5] months (irinotecan); HR, 0
146 S was 8.3 [4.0-11.0] months (irinotecan with panitumumab) vs 4.4 [2.8-6.7] months (irinotecan alone);
147 mor uptake in mice coinjected with 0.1 mg of panitumumab was 9.3 +/- 1.5, 8.8 +/- 0.9, and 10.0 +/- 1
151 ponent with the largest spectral response to panitumumab was lipid droplets, but this effect was not
152 or the primary analysis of overall survival, panitumumab was non-inferior to cetuximab (Z score -3.19
155 pproved monoclonal antibodies, cetuximab and panitumumab, which displaced each other and displayed no
156 are the monoclonal antibodies cetuximab and panitumumab, which prevent epidermal growth factor recep
157 We aimed to compare chemoradiotherapy plus panitumumab with chemoradiotherapy alone in patients wit
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