Abstract

Objective: Our purpose in this study was to evaluate whether KRAS exon-2 mutation affects 18F-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 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 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 relation in our study between KRAS exon-2 mutation status and increased 18F-FDG uptake in both colon and rectal cancer patients, 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.

Key words: KRAS protein, human; Positron-Emission Tomography; Fluorodeoxyglucose F18; Colorectal Neoplasms