Studying lung cancer progression: insights from genetically engineered mouse models of cancer

摘要

The most intuitive and in many cases successful way of targeting cancer is by inhibiting the driver mutation. This strategy improved treatment options for lung cancer patients with EGFR mutations, EML4-ALK fusion genes [2] and Ros1-rearrangements [3]. However, a variety of mutations are found in adenocarcinomas of the lung and about a third of lung adenocarcinomas lack a known driver mutation. Another 30% of human NSCLC cases carry mutations in KRAS [4] for which no targeted therapies are presently available. Kras is likely to be an initiating and driver mutation [5], but the mutational spectrum at the point of diagnosis is very heterogeneous and therefore very little is known about which subsequent alterations and mutations lead to disease progression.