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The **Ras family proteins** are a group of small GTPases that act as binary molecular switches controlling intracellular signaling networks. They regulate key cellular processes such as cell proliferation, differentiation, apoptosis, cytoskeletal organization, adhesion, and migration. The most clinically significant members—HRas, KRas, and NRas—are frequently mutated in human cancers. These mutations lead to constitutive activation of downstream pathways like MAP kinase and PI3K/AKT/mTOR cascades that drive uncontrolled cell growth and survival. Because activating mutations in these genes are found in more than two-thirds of all human cancers—including many metastatic diseases—the Ras family is a major focus for targeted cancer therapy development. While once considered "undruggable," recent advances have led to the development of direct inhibitors against certain mutant forms as well as oncolytic viral therapies that exploit aberrant Ras activity for selective tumor killing[1][2][4].
– Oncolytic viruses selectively replicate in and kill cells with activated/mutant Ras pathway[2] – siRNA therapies silence mutated RAS gene expression[2] – Small molecules inhibit specific mutant forms of RAS by binding to unique pockets or interfering with its activation cycle[4]
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