Defining Pathways for Formation and Suppression of Highly Metastatic Lung Tumors

Cancers arise from the complex interplay of oncogene activation and tumor suppressor inactivation. Loss of the tumor suppressors RB1 and TP53, as well as amplification of the pro-proliferative oncogene MYC, are frequent oncogenic events in small cell lung cancer. There are multiple subtypes of small cell lung cancers, but few targeted therapeutic options for patients. Here, Oliver and colleagues uncovered how Myc cooperates with other oncogene products to promote aggressive, highly metastatic lung tumors. Furthermore, they showed that these tumors are susceptible to Aurora kinase inhibition, indicating a strategy for suppressing tumor progression and increasing survival in patients with this common lung cancer sub-type.