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RAS Dialogue Blog

Posts written by RAS experts on the latest research, updates, and scientific RAS news curated by the RAS Initiative.

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Phase 3 study reported that daraxonrasib significantly improved survival in previously treated metastatic pancreatic ductal adenocarcinoma, providing compelling evidence that direct RAS inhibition can translate into meaningful clinical benefit.
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Single-cell analysis reveals PDAC evolution is more complex than “KRAS-driven”—with diverse clones, variable dependence, and alternative pathways shaping tumors.
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KRAS pathway inhibition rewires PDAC metabolism, increasing oxidative stress—and revealing a new vulnerability: ferroptosis as a strategy to overcome resistance.
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New research reveals that activating KRAS mutations can quietly expand in normal colon tissue and prime cells for cancer, overturning the long‑held idea that APC loss must always be the first step in colorectal tumorigenesis.
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Resistance to RAS/MAPK inhibitors isn’t just about runaway kinases—it’s about silenced phosphatases. In this JCI study, Dr. Goutham Narla shows that KRAS-mutant tumors evade therapy by disabling PP2A, and that pharmacologically restoring phosphatase activity rewires signaling, blocks resistance, and delivers durable responses.
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Nature’s own delivery system meets precision oncology: the decade-long journey of engineered exosomes to a first-in-human KRAS trial.
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New structures reveal how LZTR1 recognizes inactive RAS proteins for degradation, opening a new path to therapeutically eliminate oncogenic KRAS.
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From KRAS G12D to KRAS G12R, new research uncovers how each mutation drives pancreatic cancer differently—and why it matters for patient outcomes.
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KRAS mutants don’t just anchor to membranes—they choose their lipid partners. Discover how this specificity could unlock new cancer therapies.
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Understanding and overcoming resistance to KRAS G12C inhibitors remains a key focus in the fight against RAS-driven cancers. Experts describe non-genetic methods of resistance to G12C inhibitors that bind to the inactive, GDP-bound form of the protein, and propose the best therapeutic strategy.