The use of tyrosine kinase inhibitors (TKIs) to treat the 10–20% of lung adenocarcinomas with mutations in the EGFR gene is a recent success story in cancer medicine, but many tumors develop drug resistance after an initial response. Developing effective second-line therapy requires knowledge of the molecular basis of resistance, which is still unknown in many cases. Here, Katerina Politi and colleagues describe a mouse model of EGFR-induced lung tumors that, when treated with the TKI inhibitor erlotinib, become drug-resistant. This model will allow the mutations that cause resistance to be quickly identified and can also be used as a preclinical system to evaluate new therapeutic strategies. This research report is freely accessible online.
