RAS signaling: isoform and mutation specific roles in oncogenesis

September 13-16, 2018, Stratton, VT

Organized by: Sharon Cambell, Univ. of North Carolina; Mark Phillips, NYU School of Medicine

Meeting Description 

Approximately one-third of all human cancers contain activating mutations in RAS genes. Hotspot oncogenic RAS mutations at positions 12, 13, and 61 have historically been considered oncogenic equivalents, as they are constitutively activated through a defect in GTP hydrolysis.

However, recent observations suggest that residue- and codon-specific RAS mutants show differences in their biochemical properties, ability to engage effectors and signaling properties. Understanding these differences will have important clinical and biological implications. Given the complexity of RAS regulatory networks, the symposium will encompass a bottom up approach.

Topics that will be covered include: 

  • Molecular analyses of mutant RAS isoforms and its interactands 
  • Spatial/Temporal regulation of RAS signaling 
  • Systems biology approaches to study RAS regulatory networks and therapeutic targeting of RAS 

The meeting will emphasize complexities in RAS signaling and tumorigenesis associated with isoform and mutation-specific differences.  The meeting will also highlight new tools/methodologies that have significantly reshaped understanding of RAS signaling and allowed for the emergence of new therapeutic strategies to target RAS. 

Important Dates

June 21: Oral programming abstract submission deadline
July 10: Discounted symposium registration deadline
July 20: Poster programming abstract submission deadline
August 9: Symposium registration deadline
August 14: Registration cancellation deadline