TY - T1的靶向疗法:混乱关系不利atment for nonsmall cell lung cancer without driver mutations JF - European Respiratory Journal JO - Eur Respir J SP - 19 LP - 21 DO - 10.1183/09031936.00021315 VL - 46 IS - 1 AU - Berghmans, Thierry AU - Meert, Anne-Pascale AU - Quoix, Elisabeth Y1 - 2015/07/01 UR - //www.qdcxjkg.com/content/46/1/19.abstract N2 - The search for oncogenic driver mutations is currently a standard in the management of advanced nonsquamous nonsmall cell lung cancer (NSCLC) [1], at least for epidermal growth factor receptor (EGFR) activating mutations and anaplastic lymphoma kinase (ALK) rearrangement. At the beginning of the 21st century, two small orally available molecules with EGFR tyrosine kinase inhibitor (TKI) activity, erlotinib and gefitinib, have been developed and tested mainly in unselected Caucasian populations, concomitantly or sequentially with chemotherapy. Five randomised phase III trials did not demonstrate any supplemental activity by adding the TKI to a conventional platinum-based chemotherapy [2–6]. After these disappointing data, additional research showed that these small molecules had a major activity in the presence of EGFR-activating mutations [7, 8]. Multiple randomised trials have now confirmed that first-generation (erlotinib, gefitinib) or second-generation (afatinib) TKIs are more active than platinum-based chemotherapy in terms of response rate and progression-free survival, while their impact on overall survival remains debatable, probably because of the large crossover noted in those trials [9–14].Targeted therapies are detrimental in patients with wild-type tumours fit for conventional chemotherapy http://ow.ly/MTgy8 ER -