Non-small cell lung cancer is among the most prevalent cancers worldwide, with its high metastatic potential driving poor prognosis and mortality. Advances in molecular testing and high-throughput sequencing have highlighted the roles of driver genes (EGFR, ALK, KRAS) and key non-driver genes (TP53, STK11, KEAP1) in NSCLC metastasis. These mutations influence tumor invasiveness, drug resistance, and organ-specific metastatic patterns—EGFR and ALK mutations favor brain metastasis, KRAS mutations are linked to bone, liver, and multiple lung metastases, while TP53, STK11, and KEAP1 mutations increase multi-organ metastatic risk. This review summarizes the associations between genetic mutations and metastatic sites, explores underlying molecular mechanisms, and discusses mutation-based risk prediction and personalized therapeutic strategies. With multi-omics integration and further clinical research, genetic profiling may become a key tool for guiding metastasis prevention, early intervention, and treatment optimization in NSCLC.
Xue et al. (Sun,) studied this question.