Key points - personalized treatment in advanced NSCLC Approximately 50% of advanced NSCLCs have a known oncogenic alteration, many of which can be managed with targeted therapies.
Although NTRK fusions seem to be mutually exclusive with other oncogenic drivers, these fusions were recently reported in EGFR-mutant NSCLC as a mechanism of AR to EGFR-TKIs.
尽管 NTRK 融似乎与其他癌驱动因素相互排斥,但最近在 EGFR 突变 NSCLC 中报道了这些融作为 EGFR-TKI AR 机制。
Targeted treatments for known oncogenic drivers (see Chapter 7) should be given until resistance, before proceeding with chemotherapy with or without immunotherapy.
MET amplification is also a common determinant of AR during treatment with TKIs for other oncogenic drivers such as EGFR, ALK, ROS1, KRAS G12C and NTRK.
在使用 TKI 治其他癌驱动因素(例如 EGFR、ALK、ROS1、KRAS G12C 和 NTRK)期间,MET 扩增也是 AR 常见决定因素。
Likewise, BRAF-mutant tumors have higher RR and longer PFS on ICIs than other oncogenic drivers do, without any clear evidence of differing efficacies between BRAF-mutation subtypes.
This personalized medicine approach has a large effect on patients' survival, as when a patient with an oncogenic target receives the appropriate targeted therapy the duration of response is longer than previously seen with chemotherapy.
MET mutation Both MET exon 14-skipping mutation and MET amplification are primary oncogenic drivers in 3- -5% of patients with NSCLC; MET- dysregulated NSCLCs have a poor prognosis.
MET 突变 MET 外显子 14 跳跃突变和 MET 扩增都是 3- -5% NSCLC 患者主要癌驱动因素; MET 失调 NSCLC 预后较差。
However, it should be noted that a negative liquid biopsy result does not rule out an oncogenic driver, and tissue-based testing should be performed if possible.