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The RAS family of proteins, which includes the primary members KRAS, NRAS, and HRAS, play a crucial role in the regulation of cell proliferation and survival in normal cells. These proteins function as tightly regulated molecular switches that cycle between the inactive GDP-bound [RAS(OFF)] and active GTP-bound [RAS(ON)] states. This careful regulation maintains a tight balance between RAS in its OFF and ON states.
Oncogenic mutations in the RAS gene can drive cancer initiation and progression, thereby disrupting this balance and resulting in a shift to excessive RAS(ON) signaling in tumor cells. Inhibiting RAS(ON) function can disrupt the activation of signaling pathways and impede tumor growth. However, treatment options for RAS-driven cancers are limited, with currently approved targeted therapies available for a subset of patients with KRAS G12C mutation.
Additional treatment options are needed for patients with G12C mutations, as well as new therapies targeting other oncogenic RAS mutations beyond G12C.
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This activity is sponsored by Revolution Medicines, Inc.
Revolution Medicines provided financial support and content, and has had input into the detailed project scope. This activity is provided by Touch Medical Communications (TMC) for touchONCOLOGY.
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Revolution Medicines provided financial support and content, and has had input into the detailed project scope. This activity is provided by Touch Medical Communications (TMC) for touchONCOLOGY.
Unapproved products or unapproved uses of approved products may be discussed; these situations may reflect the approval status in one or more jurisdictions. TMC has advised the sponsor to ensure that they disclose any such references made to unlabelled or unapproved use. No endorsement by TMC of any unapproved products or unapproved uses is either made or implied by mention of these products or uses in TMC activities. TMC accepts no responsibility for errors or omissions.
The views and opinions expressed are those of the faculty and do not necessarily reflect those of any sponsor.
RVMD-GLO-00073 V1.0 12/2025
Date of preparation: December 2025
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