RAS Dialogue Blog

The NCI ART Initiative is making headway in better understanding RASopathies and driving new therapies through cross-institutional collaboration.

Scientists share key takeaways from the Reproducibility in Science Symposium, emphasizing important highlights for RAS researchers.

Phase 3 study provides compelling evidence that direct RAS inhibition can translate into meaningful clinical benefit.

Single-cell analysis reveals PDAC evolution is more complex than “KRAS-driven”—with diverse clones, variable dependence, and alternative pathways shaping tumors.

KRAS pathway inhibition rewires PDAC metabolism, increasing oxidative stress—and revealing a new vulnerability: ferroptosis as a strategy to overcome resistance.

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.

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.

Nature’s own delivery system meets precision oncology: the decade-long journey of engineered exosomes to a first-in-human KRAS trial.

New structures reveal how LZTR1 recognizes inactive RAS proteins for degradation, opening a new path to therapeutically eliminate oncogenic KRAS.

From KRAS G12D to KRAS G12R, new research uncovers how each mutation drives pancreatic cancer differently—and why it matters for patient outcomes.