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1 e mechanisms developed in patients receiving osimertinib.
2 om all patients in the first-in-man study of osimertinib.
3 of outcome from a third-generation EGFR-TKI, osimertinib.
4 or assessed as possibly treatment-related to osimertinib.
5 ed tyrosine kinase inhibitors, nilotinib and osimertinib.
6 y or the AKT pathway enhanced the effects of osimertinib.
7 R tyrosine-kinase inhibitor therapy received osimertinib 80 mg orally once daily; treatment could con
8 GFR Thr790Met mutation who were treated with osimertinib, a third-generation EGFR TKI, after previous
9 l patients who received at least one dose of osimertinib and had measurable disease at baseline accor
11 FR tyrosine kinase inhibitors (TKI), such as osimertinib, are active agents for the treatment of EGFR
19 inase inhibitor therapy, and T790M mutation, osimertinib is recommended; if NSCLC lacks the T790M mut
26 itive for T790M in plasma have outcomes with osimertinib that are equivalent to patients positive by
27 patients were screened, of whom 210 started osimertinib treatment between June 13, 2014, and Oct 27,
28 rises in approximately 33% of patients after osimertinib treatment, occurs in <3% after rociletinib.
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