Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer

Abstract

Pancreatic cancer is an aggressive and lethal disease with an overall 5-year survival rate of only 5%. Studies have demonstrated the ability of (18)F-fludrodeoxyglucose ((18)F-FDG) positron emission tomography/computed tomography (PET/CT) to measure the metabolic tumor burden in patients with various tumors, including pancreatic cancer. In a previous study, we investigated the predictive significance of the metabolic tumor burden in terms of the metabolic tumor volume (MTV) and total lesion glycolysis (TLG). In this study, we analyzed the correlation between metabolic tumor burden and the status of the KRAS, TP53, CDKN2A/p16, and SMAD4/DPC4 genes. Our results showed that the metabolic tumor burden was associated with oncogenomic alterations that reflected the abnormal expression of carbohydrate metabolic enzymes (GLUT1, ALDOA and FBP1). We also identified a linear correlation between serum tumor markers and the metabolic tumor burden. To estimate the metabolic tumor burden when (18)F-FDG PET/CT is not available, we used the linear regression models to establish equations for MTV and TLG using CA19-9 and CA125 as independent variables. Our results suggest that the metabolic tumor burden, as evaluated by (18)F-FDG PET/CT or estimated by serum tumor markers, may be suitable for monitoring treatment response and disease progression of pancreatic cancer. Further research is needed to better understand why pancreatic cancer patients with abnormal expressions of TP53, CDKN2A/p16, and SMAD4/DPC4 get high metabolic tumor burden.

Keywords: Gene mutation; Metabolic tumor burden; Pancreatic cancer; Serum tumor markers.