RAS Dialogue
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RAS and MYC: Co-conspirators in Cancer
The transcription factor MYC is an important downstream target of mutated RAS genes in human cancers. Inhibiting post-translational modifications of MYC to decrease its transcriptional activity is a new strategy for treating RAS-driven cancers.
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Powering Off Cancer
The uncontrolled growth of cancers is dependent on altered metabolism. For example, many cancers are highly dependent on the altered metabolic reactions that occur in their mitochondria. New therapies that target these reactions are being tested.
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The Mutational Spectra of Cancer Genes in TCGA Data
The Cancer Genome Atlas has catalogued mutations in more than 30 cancer types. The NCI RAS Initiative uses TCGA data to prioritize and inform its research objectives. The bar graphs show data for KRAS, HRAS, NRAS, BRAF, TP53, EGFR, PIK3CA, and PTEN.
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A Panel of Isogenic RAS-Dependent Cell Lines Developed at the Frederick National Laboratory
Mouse embryonic fibroblasts have been engineered to lack all RAS genes on demand. Then individual RAS genes can be introduced. Such cells allow effects of drugs to be tested with more precision.
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RAS Pathway v3.0?
Defining the most important elements of RAS signaling is an important objective of the NCI RAS Initiative. In a new RAS Dialogue post, advisor Frank McCormick invites community input on version 3.0 of the RAS Pathway.

