RAS Oncoproteins Therapeutic Vulnerabilities

With RAS proteins being members of small GTPases and RAS genes the most frequently mutated oncogenes, they are part of an intense interest for cancer treatments. Discussing the vulnerabilities of RAS that have been exploited for the development of pharmacologic inhibitors of RAS function.
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The three human RAS genes (HRAS, KRAS and NRAS) encode four highly related RAS small GTPases (HRAS, KRAS4A, KRAS4B and NRAS). RAS proteins function as GDP-GTP regulated binary on-off switches that regulate diverse cytoplasmic signaling networks.

In cancer and developmental disorders (RASopathies), mutationally activated RAS proteins drive aberrant signal transduction. RAS proteins are also the founding members of a large superfamily of small GTPases comprised of 150+ members.

Since their initial identification decades ago as drivers of human cancers, there has been intense interest and effort in targeting RAS for cancer treatment. RAS genes are the most frequently mutated oncogenes in the top three causes of cancer deaths in the US in 2016 (lung, colorectal and pancreatic cancers).