Abstract
Treatment decisions for patients with lung cancer have historically been based upon tumor histology. Among the numerous molecular alterations observed in cancer cells, some specific mutations have been identified as being necessary and sufficient to drive tumor formation and maintenance. These “driver” mutations occur in genes that encode signaling proteins critical for cellular proliferation and survival. With the development of agents specifically designed to target these key proteins, the paradigm is changing to “personalized medicine,” which consists of the individual genotyping of each patient tumor to identify driver mutations that are predictive biomarkers of the efficacy of these agents. This paper reviews the clinical and biologic evidence for the major driver mutations occurring in lung cancer.
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