Proposed mechanism of combined KRAS inhibition and CTLA-4 blockade in KRAS-mutant gastric adenocarcinoma (IMAGE)
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KRAS mutation drives a TGF-beta-dependent, Treg-dominant immunosuppressive microenvironment. Combination of the KRASG12D inhibitor with CTLA-4 blockade suppresses TGF-beta signaling, impairs regulatory T cell function and restores effective antitumor immunity.
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