Lung cancer is the leading cause of cancer-related death worldwide. Most patients have advanced disease at the time of diagnosis. Cytotoxic chemotherapy results in a modest increase in survival (several months) but at the cost of significant toxicity to the patient.
The concept of personalized cancer therapy has attracted much attention because oncogenic molecules have been researched and specific molecular target treatment strategies are developed. Recently, a strong association of somatic mutations in the tyrosine kinase domain of EGFR with clinical efficacy to EGFR tyrosine kinase inhibitors (TKIs) has been demonstrated. Another example is that crizotinib (PF-02341066), a dual MET/ALK tyrosine kinase inhibitor, has a favorable treatment response in EML4-ALK positive patients with advanced lung cancer.
These mutations occur in genes that encode signaling proteins critical for cellular proliferation and survival. Mutant oncogenes drive tumor formation and maintenance. This concept is called driver mutation and oncogene addiction. In addition to EGFR and EML4-ALK, there are other driver mutations found in lung adenocarcinoma, such as: K-Ras, HER2, B-Raf, PIK3CA, ROS1 translocation, RET translocation, MEK1..etc. Those driver mutations have important roles in lung cancer carcinogenesis of lung adenocarcinoma and may have different distribution among different ethnicities.
In addition, squamous cell lung cancer also has some driver mutations with potential target therapy, such as: amplification of SOX2, PDGFRA and FGFR1, DDR2 mutation, PIK3CA mutation,..etc. Those are potential therapeutic targets in squamous cell lung cancer.

Comprehensive and concurrent analysis of recurrent driver mutations in a large cohort of advanced lung cancer is necessary. Combinations of the gene testing for those mutations and clinical trials with specific target therapy, will pave the way for personalized therapy for lung cancer.