GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6194/primaryOK2000000GenomicsMus musculusExpression profiling by arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6194GEOGSE0falseOncogenic potential of RAS isoforms in melanocytesWe compared the transformation efficiencies of mutant NRAS and KRAS in immortal, non-transformed Ink4a/Arf-deficient melanocytes. NRAS mutation leads to increased cellular proliferation and is potently tumorigenic. In contrast, KRAS mutation does not enhance melanocyte proliferation and is only weakly tumorigenic on its own. While both NRAS and KRAS activate MAPK signaling, only NRAS enhances MYC activity in these cells. Our data suggests that the activity of specific RAS isoforms is context dependent and provides a possible explanation for the prevalence of NRAS mutations in melanoma.In addition, understanding this mechanism will have important implications for cancer therapies targeting RAS pathways. Keywords: RAS isoforms2006/10/30GSE6194GSM143151GSM143140GSM143141GSM143150GSM143148GSM143149GSM143146GSM143147GSM143144GSM143145GSM143142GSM14314344876194Mus musculus[17297468]