Prognostic correlation of the expression of glucose transporter with positron emission tomography in gallbladder cancer

Abstract

The aim of the present study was to investigate whether the uptake level of 18-fluorodeoxyglucose (FDG) in PET/CT would correlate to the expression level of glucose transporter (GLUT1, GLUT4) and hexokinase (HK 1 and HK3) in GB cancers and its clinicopathological implication in tumor cell differentiation and prognosis for GB cancer. This study included a total of 90 patients with GB pathology (44 benign lesions and 46 GB cancer) who underwent 18-FDG PET-CT. The maximum standardized uptake value of the tumor (SUVmax) was calculated in the targeted lesion. The correlation was analysed between clinicalpathological characteristics and SUVmax. Immunochemistry of GLUT1, GLUT4, HK 1 and HK3 was performed and analyzed in benign (n=10) and cancer (n=11) specimens, and the relation of their expression levels to SUV max in 18-FDG PET-CT was determined.

The clinical charateristics showed that the mean age was higher in GB cance than in benign GB lesions (66.1 vs. 57.3, p=0.036).

GLUT1 in cytoplasm and membrane were strongly expressed in cancer than in benign lesions. A GLUT1 score correlated positively to the SUVmax but the GLUT4, HK 1 and HK3 score did not. SUVmax was more elevated in poorly-differentiated or undifferentiated cell types than in well-differentiated or moderately-differentiated cells (9.62 ± 4.3 vs. 5.74 ± 3.1, p = 0.038) and was also more elevated in patients with advanced stages than in those with early stages (4.0 ± 2.3 in stage I and II vs. 7.2 ± 3.0 in stage III and IV, p = 0.016). When using a cut-off value of 4, we found that the progression-free survival rate was better in the low SUVmax (≤4) group than in the high SUVmax (>4) group (p = 0.0216; unadjusted Hazard ratio 3.13; 95% CI 1.18-8.29). In conclusion, the increased uptake of FDG in GB cancer was associated with elevated GLUT-1 expression, dedifferentiation, advanced stages, and a poor progression-free survival rate.