Purpose: The usefulness of 2-[18F]-fluoro-2-deoxy-D-glucose ([18F]FDG) positron emission tomography/computed tomography (PET/CT) can help predict the presence and the extent of malignant cells. The aims of current study were to investigate the expression patterns of genes or enzymes in glucose metabolism, and to determine whether the FDG PET/CT finding correlates with these proteomic markers in surgical specimens. Patients and Methods: Fifty patients with uterine cervical cancer who underwent [18F]FDG PET/CT before treatment were included in this study. Tumor sections were stained by immunohistochemistry for glucose transporter 1 (GLUT1), glucose transporter 3 (GLUT3), hypoxia-inducible factor-1α (HIF-1α), hexokinase 2 (HK2), glycolysis markers (pyruvate kinase M2 (PKM2), phosphofructokinase (PFK), glycoaldehyde-phosphate dehydrogenase (GAPDH), pyruvate dehydrogenase (PDH)), electron transporter chain marker (β-F1-ATPase), mitochondrial transcription factor A (TFAM), oncogene (c-Myc), and peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α).

Results: In vivo glucose uptake of primary cervical cancer (R = −0.298, P = 0.036) and metastatic lymph nodes (R = −0.298, P = 0.037), as assessed by FDG uptake inversely correlates with the mitochondrial biogenesis determined by immunohistochemical staining of PGC-1α. Cellular GLUT1 expression was also inversely correlated with the expression of PGC-1α (R = −0.413, P = 0.003). Moreover, the level of mitochondrial oxidative phosphorylation expressed by β–F1-ATPase inversely correlates with that of PFK (r = −0.337, P = 0.021). Expression of PGC-1α was lower in squamous cell carcinoma than that of adenocarcinoma (P < 0.001), however, GLUT1 expression was higher in squamous cell carcinoma (P = 0.003). Of interest, HK2 expression in primary tumor was significantly lower in patients with lymph node metastasis (P = 0.003).

Conclusion: The results highlight the relevance of the alteration of the glucose metabolism by aerobic glycolysis in cervical cancer, and affording a mechanistic explanation for FDG PET/CT imaging.

Citation Information: Cancer Prev Res 2011;4(10 Suppl):A46.