Future Perspectives and Conclusions
The introduction of the EGFR TKIs gefitinib, erlotinib, and afatinib and the ALK inhibitors crizotinib and ceritinib represent the most important innovations in NSCLC treatment over the past ten years. By targeting the main pathways of NSCLC pathophysiology, these new drugs significantly improved survival rates and quality of life in a highly selected subgroup of patients, sparing them from toxic chemotherapy approaches; for the vast majority of patients, however, chemotherapy remains the only potential treatment. Although the target agents were approved only for EGFR and ALK gene alterations, the number of potential biomarkers is rapidly increasing. New driver mutations were identified in both adenocarcinoma, such as K-Ras, Her-2-neu, MET, N-Ras, BRAF, MAP-2-K, PIK3CA, AKT1, ROS, and RET mutations, and squamous cell carcinoma, such as FGFR-1 amplification, EGFR mutation and amplification, PIK3CA mutation and amplification, PTEN loss, and DDR2, but >50% of mutations remain unknown. Several ongoing trials are investigating the activity of new target agents in patients with these mutations (Table 4). The rapidly growing number of targeted treatment options will lead to new insight into personalized treatment in the near future. Nowadays, new techniques such as "next-generation-sequencing" make possible the creation of a molecular–genomic profile of every patient's tumor, based on the analysis of either a single tissue sample, circulating tumor cells, or circulating tumor DNA. Therefore the need for close collaboration between health professionals, including medical oncologists, molecular biologists, pathologists, and family physicians, will increase. The role of family physicians remains critical because of their unique and privileged position of seeing patients on a daily basis; thus they should be updated by other experts on scientific discoveries relevant to their everyday practice and more frequently involved in the global view of care in all the phases.