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EGFR ‐activating mutations have been recognized as the most important predictor of response to EGFR‐tyrosine kinase inhibitors (TKIs); however, 20–30% of patients harboring  EGFR ‐activating mutations show poor responses. The mechanisms of such EGFR‐TKI primary resistance are still poorly understood. In our case, a non‐small cell lung cancer patient developed intrinsic EGFR‐TKI resistance and was then confirmed to simultaneously harbor an L858R mutation and  ROS1  rearrangement. Salvage chemotherapy plus Endostar showed enduring therapeutic effects, achieving a disease‐free survival period of 24 months and overall survival of 30 months. This suggests that co‐activation of different oncogenic signal pathways might be a potential mechanism of EGFR‐TKI primary resistance. Chemotherapy combined with anti‐angiogenesis should be considered an important salvage strategy. Further studies are warranted to verify these findings and explore the underlying mechanisms involved.

thoracic cancer

Chemotherapy combined with Endostar as salvage treatment for EGFR‐tyrosine kinase inhibitor primary resistance in an advanced non‐small cell lung cancer patient with  EGFR  L858R mutation and  ROS1  fusion: A case report