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1 20 insertion mutants restored sensitivity to dacomitinib.
2 inantly grade 1 to 2, and more frequent with dacomitinib.
3 ed 878 patients and randomly assigned 439 to dacomitinib (256 KRAS wild type) and 439 (263 KRAS wild
4 and were then randomly allocated 2:1 to oral dacomitinib 45 mg once-daily or matched placebo centrall
5  assigned participants (1:1) to receive oral dacomitinib 45 mg/day (in 28-day cycles) or oral gefitin
6 randomly assigned patients in a 1:1 ratio to dacomitinib (45 mg/day) or erlotinib (150 mg/day) with m
7 progression-free survival was 2.6 months for dacomitinib (95% CI 1.9-2.9) and erlotinib (95% CI 1.9-3
8                 In this report, we show that dacomitinib, a pan-ErbB receptor inhibitor, diminished g
9                                              Dacomitinib, an irreversible pan-HER inhibitor, had show
10 FS was 2.21 months for patients treated with dacomitinib and 1.84 months for patients treated with er
11 t) was 2.86 months for patients treated with dacomitinib and 1.91 months for patients treated with er
12 FS was 3.71 months for patients treated with dacomitinib and 1.91 months for patients treated with er
13 , 2013, we randomly assigned 480 patients to dacomitinib and 240 patients to placebo.
14 were reported in 52 (12%) patients receiving dacomitinib and 40 (9%) patients receiving erlotinib.
15 al was 9.53 months for patients treated with dacomitinib and 7.44 months for patients treated with er
16       185 (39%) of 477 patients who received dacomitinib and 86 (36%) of 239 patients who received pl
17 tations seldom achieve clinical responses to dacomitinib and afatinib, two covalent quinazoline-based
18 ents were reported in 21 (9%) patients given dacomitinib and in ten (4%) patients given gefitinib.
19 99804) has been assigned the nomenclature of dacomitinib and is currently under clinical evaluation.
20                            We did a trial of dacomitinib as initial systemic therapy in clinically an
21                                    Moreover, dacomitinib attenuated migration and invasion of the EOC
22 y enhanced the sensitivity of SCCHN cells to dacomitinib by the loss of both translesion synthesis an
23 l lung cancer showed favourable efficacy for dacomitinib compared with erlotinib.
24                                              Dacomitinib demonstrated significantly improved PFS vers
25                                              Dacomitinib did not improve overall survival compared wi
26                                              Dacomitinib did not increase overall survival and cannot
27 Two treatment-related deaths occurred in the dacomitinib group (one related to untreated diarrhoea an
28 4 months (IQR 15.6-29.6) for patients in the dacomitinib group and 24.4 months (11.5-38.9) for those
29 ew was 14.7 months (95% CI 11.1-16.6) in the dacomitinib group and 9.2 months (9.1-11.0) in the gefit
30  was 2.6 months (95% CI 1.9-2.8) in both the dacomitinib group and the erlotinib group (stratified ha
31                     However, patients in the dacomitinib group had longer progression-free survival t
32 nts were diarrhoea (47 [11%] patients in the dacomitinib group vs ten [2%] patients in the erlotinib
33                                              Dacomitinib had encouraging clinical activity as initial
34    Compared with placebo, patients allocated dacomitinib had significantly longer time to deteriorati
35          We designed BR.26 to assess whether dacomitinib improved overall survival in heavily pretrea
36 (version 1.0) to investigate the activity of dacomitinib in all patients with a baseline scan and at
37 nvestigation on the therapeutic potential of dacomitinib in treatment of the chemoresistant EOC.
38                                              Dacomitinib is a covalent pan-HER inhibitor that has sho
39                                              Dacomitinib is a second-generation, irreversible EGFR ty
40                                              Dacomitinib is an irreversible pan-EGFR family tyrosine
41                                              Dacomitinib is an irreversible pan-HER tyrosine-kinase i
42 e patients were randomly assigned to receive dacomitinib (n=227) or gefitinib (n=225).
43 ted qualitative differences in the effect of dacomitinib on overall survival for patients with KRAS-m
44         Compared with placebo, the effect of dacomitinib on overall survival seemed similar in patien
45                                      We gave dacomitinib orally once daily (45 mg or 30 mg) until pro
46 nts who derived extended clinical benefit to dacomitinib (P = 0.04).
47   This randomized, open-label trial compared dacomitinib (PF-00299804), an irreversible inhibitor of
48              Introduction of Gly770 into two dacomitinib-resistant EGFR exon 20 insertion mutants res
49 identify potential predictive biomarkers for dacomitinib sensitivity, we performed whole exome sequen
50                              INTERPRETATION: Dacomitinib significantly improved progression-free surv
51 clinically achieved a partial response after dacomitinib treatment.
52 o (median 6.83 months [95% CI 6.08-7.49] for dacomitinib vs 6.31 months [5.32-7.52] for placebo; haza
53  events were diarrhoea (59 [12%] patients on dacomitinib vs no controls), acneiform rash (48 [10%] vs
54 is acneiform (31 [14%] of 227 patients given dacomitinib vs none of 224 patients given gefitinib), di
55            Irreversible EGFR inhibition with dacomitinib was not superior to erlotinib in an unselect
56                          We aimed to compare dacomitinib with erlotinib in a phase 3 study.

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