| Resumen: | Lung cancer remains as one of the most aggressive cancer types with nearly 1.6 million new cases worldwide each year. There are an estimated 222,520 new cases and 157,300 deaths from lung cancer in the United States in 2010 [1]. Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, comprising three major histological subtypes: adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. Chronic exposure to carcinogens drives genetic and epigenetic damage that can result in lung epithelial cells progressively acquiring growth and/or survival advantages, giving as a result the generation of tumor cells. Studies have shown that some specific molecules contribute to sporadic tumors of lung cancer; even now, they are useful as predictive biomarkers. Mutations in at least one of the established lung cancer driver genes including egfr, kras, braf, her2, akt1, nras, pik3ca, mek1, eml4-alk and met amplification are found in approximately 60% of tumor specimens, and greater than 90% were “exclusive”: only one mutation was found in a particular tumor [2]. Epidermal growth factor receptor (EGFR) exhibits overexpression or aberrant activation by mutations in 50 to 90% of NSCLC. Much effort has been focused on the development of targeted molecular inhibitors for this molecule, but it has become clear that molecular-targeted cancer therapies can only reach their full potential through appropriate patient selection |
