Does KRAS mutation cause increased 18 FDG uptake in colorectal carcinoma?

Objectives Activating KRAS mutation frequency is approximately % 35-45 in patients with colorectal carcinoma (CRC). It was suggested that the increase in GLUT1 expression and glucose uptake in CRC cell lines was dependent on the presence of KRAS mutation. However, there is very limited and conflicting data on the clinical application. Therefore, this study was done to investigate whether KRAS mutation affect the 18- FDG accumulation in lesions of patients with CRC.

Methods PET/CT study results and medical records of 42 patients (mean age:55±14) with diagnosis of colorectal cancer were reviewed retrospectively. Patients were divided into subgroups according to the presence of KRAS mutation (23 wild-type, 19 mutated). SUVmax and SUVmean values, based on body weight, lean body and body surface area, were calculated for volumetric region of interests drawn on primary tumor or metastatic site. Volume of tumor was measured and glycolytic index (GI=volumeXSUVmean) values were calculated for each lesion and sum of all lesions. In addition, Liver (L) and blood pool (B) SUV values and tumor/liver (T/L), tumor/blood (T/B) ratios were calculated

Results SUVmax (10.7±1.2 vs 7.5±0.8, p=0.03), SUVmean (7±0.8±4.9±0.5, p=0.04), T/L SUVmax (4.8±0.5 vs3.2±0.3, p=0.2), T/L SUVmean (3.8±0.4 vs 2.6±0.3, p=0.017), T/B (6.7±0.6 vs 4.5±0.5, p=0.008), T/B mean (5.7±0.5 vs 3.9±0.4, 0.01) values were significantly higher in mutated group. Glycolytic index and total glycolytic index values were not significantly different between subgroups, due to wide range of tumor volumes.

Conclusions According to the results of this retrospective study, KRAS positive and negative tumors showed different glycolytic phenotype measured by means of SUV values and tumor to liver ratios. Presence of KRAS mutation seems to cause higher 18FDG uptake by tumor compared to wild-type tumors.