A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors. A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors

A missense change in RRAS2 (Gln72-to-Leu), analogous to the Gln61-to-Leu mutation of RAS oncoproteins, has been identified as a hotspot mutation in cancer and Noonan syndrome. However, the relevance of this mutation for in vivo tumorigenesis remains unknown. Here, we show that R-RAS2(Q72L) is required for optimal tumorigenic activity of human cancer cells. Overall design: Genome-wide gene expression analyses of control and Rras2(Q72L) knockdown (sh#89) fibrosarcoma cells.