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.
MYC drives progression of small cell lung cancer to a variant neuroendocrine subtype with vulnerability to aurora kinase inhibition. Mollaoglu G, Guthrie MR, Böhm S, Brägelmann J, Can I, Ballieu PM, Marx A, George J, Heinen C, Chalishazar MD, Cheng H, Ireland AS, Denning KE, Mukhopadhyay A, Vahrenkamp JM, Berrett KC, Mosbruger TL, Wang J, Kohan JL, Salama ME, Witt BL, Peifer M, Thomas RK, Gertz J, Johnson JE, Gazdar AF, Wechsler-Reya RJ, Sos ML, Oliver TG. Cancer Cell. 2017 Feb;31(2):270.