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RAS Dialogue

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    • Genetic Ablation of KRAS in Pancreas Cancer: When an Essential Oncogene Isn’t
      , by Pan-Yu Chen and Mandar Deepak Muzumdar

      Of all cancers, pancreatic cancers are most dependent on mutant KRAS. However, many pancreatic cancer cell lines survive loss of their mutant KRAS genes. The adaptations these lines make provide opportunities for treating these deadly cancers.

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    • Glutamine, Cystine, and Cancer Susceptibilities
      , by Jim Hartley

      The rapid growth of cancer cells generates increased amounts of toxic reactive oxygen species (ROS). Four recent papers show how understanding how cancers deal with ROS can lead to therapeutic opportunities.

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    • Ras–dependent Paracrine Cascades
      , by Kenneth P. Olive

      Most pancreatic cancers are driven by mutant K-Ras genes, and comprise a minority of cancer cells in a densely fibrotic and highly secretory tumor microenvironment. Interrupting the paracrine cascades in pancreatic cancers may improve treatment.

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    • RAS and MYC: Co-conspirators in Cancer
      , by Brittany L. Allen-Petersen and Rosalie C. Sears

      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
      , by Costas Lyssiotis

      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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