Objective:Our purpose in this study was to evaluate whether Kirsten rat sarcoma viral oncogene (KRAS) exon-2 mutation affected 18F-fluorodeoxyglucose (FDG) accumulation patterns, total lesion glycolysis and metabolic tumor volume in colorectal cancer.Method:This retrospective study included 52 colorectal cancer patients. Dual-time 18F-FDG positron emission tomography/computed tomography (PET/CT) parameters such as the maximum standardized uptake values (SUVmax), tumor-to-liver parenchyma SUVmax ratios (TLR), retention index (RI), metabolic tumor volumes (MTV), total lesion glycolysis (TLG) and glucose corrected-TLGs were measured.Results:There were no statistical differences in PET/CT imaging parameters between mutated and wild-type colon cancer, but RI and RI (TLR) values were statically higher in wild-type than in mutated-type. KRAS exon-2 wild-type rectal cancer patients had low MTV (p=0.044). KRAS mutation status was correlated with MTV (r=-0.277, p=0.048). ROC curves analysis showed that MTV and MTV (%) predicted KRAS exon-2 mutation status accurately.Conclusion:Although we did not find a relationship between KRAS exon-2 mutation status and increased 18F-FDG uptake in both colon and rectal cancer patients in our study, KRAS exon-2 wild-type colon cancer patients showed interestingly increased uptake of 18F-FDG in time. Even if we find a correlation between KRAS exon-2 mutation status and MTV, it was not very strong.
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