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The RAS Initiative

Illustration of a RAS protein

More than 30 percent of all human cancers—including 95 percent of pancreatic cancers and 45 percent of colorectal cancers—are driven by mutations of the RAS family of genes. NCI established the RAS initiative in 2013 to explore innovative approaches for attacking the proteins encoded by mutant forms of RAS genes and to ultimately create effective, new therapies for RAS-related cancers.

  • Dr. Robert D’Ippolito working with the RAS Mass Spec Team

    RAS Research Teams

    Learn about the nine highly collaborative research teams that compose the RAS Initiative. View their progress, projects, tools, collaborators, and team members.

  • Icon of interconnected points

    RAS Tools and Resources

    Find DNA reagents, cell line reagents, and protein production tools developed by researchers with the NCI RAS Initiative.

  • Charts of Cancer and RASopathy

    Publications from the RAS Initiative

    This list of RAS Initiative publications reflects the balance between the public responsibilities of NCI and the requirements of external partners.

  • AT2 cell and Alveolar Macrophage alongside Michelangelo's Creation of Adam

    RAS News & Events

    Through community and technical collaborations, workshops, and symposia, the RAS Initiative seeks to increase the sharing of knowledge and resources that are essential to defeat cancers caused by mutant RAS genes.

  • FNLCR as hub of five elements

    About the RAS Initiative

    The "hub and spoke" model of the RAS Initiative connects researcher collaborators to better understand and target the more than 30% of cancers driven by mutations in RAS genes. Find more on the problem with RAS genes, RAS Initiative origins and oversight, and contact information.

  • Headshot of Alessia Mira and Marie-Julie Nokin

    RAS Dialogue Blog

    Understanding and overcoming resistance to KRAS G12C inhibitors remains a key focus in the fight against RAS-driven cancers. In a new blog post, Drs. Mira and Nokin describe non-genetic methods of resistance to G12C inhibitors that bind to the inactive, GDP-bound form of the protein. They observed an increase in active GTP-loaded KRAS in patient samples, and argue for the dual inhibition of both active and inactive KRAS as a more effective therapeutic strategy.

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