Nearly 40% of all childhood cancers contain abnormal gene fusions, yet targeted therapies exist for only a subset of these alterations. Fusions, formed when two separate genes are joined together, promote tumor growth and often drive disease, making them attractive therapeutic targets. However, the complicated structure of fusion proteins often impedes small molecule inhibitor development, and when drugs are available, resistance to therapy inevitably develops. Furthermore, the diversity of rare fusion partners hinders traditional drug development mechanisms.





