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KRAS gene mutations occur in approximately 40% of colorectal cancers (CRCs) and are associated with resistance to anti-epidermal growth factor receptor antibody therapy. We previously demonstrated that (18)F-FDG accumulation in PET was significantly higher in CRCs with mutated KRAS than in those with wild-type KRAS in a clinical setting. Here, we investigated the mechanisms by which mutated KRAS increased (18)F-FDG accumulation.

Regulation of 18F-FDG Accumulation in Colorectal Cancer Cells with Mutated KRAS

Regulation of ¹⁸F-FDG Accumulation in Colorectal Cancer Cells with Mutated KRAS