Dataset Information


Oncogenic potential of RAS isoforms in melanocytes

ABSTRACT: We 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 isoforms Common Reference

ORGANISM(S): Mus musculus  

SUBMITTER: Sheri Holmen   Karl Dykema 

PROVIDER: E-GEOD-6194 | ArrayExpress | 2010-06-10



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Differential oncogenic potential of activated RAS isoforms in melanocytes.

Whitwam T   Vanbrocklin MW   Russo ME   Haak PT   Bilgili D   Resau JH   Koo HM   Holmen SL  

Oncogene 20070205 31

RAS genes are mutated in approximately 30% of all human cancers. Interestingly, there exists a strong bias in favor of mutation of only one of the three major RAS genes in tumors of different cellular origins. NRAS mutations occur in approximately 20% of human melanomas, whereas HRAS and KRAS mutations are rare in this disease. To define the mechanism(s) responsible for this preference in melanocytes, we compared the transformation efficiencies of mutant NRAS and KRAS in immortal, non-transforme  ...[more]

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