Cancer arises when a cell gains the ability to inappropriately proliferate.  The EGFR/Ras/MAPK signaling pathway transmits growth signals that regulate cell proliferation, and mutations that inappropriately activate this pathway are among the most commonly found in human cancers.  The EGFR/RasMAPK pathway is evolutionarily conserved between humans and the nematode worm, Caenorhabditis elegans.  Our lab uses C. elegans as a genetic model organism to study the genes and cellular mechanisms that regulate EGFR/Ras/MAPK signaling.  Pioneering studies in C. elegans have identified new fundamental mechanisms of EGFR/Ras/MAPK regulation that are conserved in humans.  We identified two novel mutations that enhance EGFR/Ras/MAPK signaling in C. elegans.  Funding from the Cancer Research Society will make it possible for us to identify the genes and mechanisms by which these mutations regulate signaling, leading to the identification of new tumor suppressive targets for the development of anti-cancer therapeutics.