Published in:
01-02-2012 | Original Article
Molecular Mechanism Underlying the Detection of Colorectal Cancer by 18F-2-Fluoro-2-Deoxy-d-Glucose Positron Emission Tomography
Published in: Journal of Gastrointestinal Surgery | Issue 2/2012
Login to get accessAbstract
Background
Biological imaging by positron emission tomography (PET) using 18F-2-fluoro-2-deoxy-d-glucose (FDG) has been widely used clinically for the detection of primary tumors and for early prediction of response to chemotherapy. In this study, we examined the molecular mechanism underlying the detection of colorectal cancers by FDG-PET.
Material and Methods
In all, 37 patients with colorectal cancer were examined with FDG-PET, and the maximal standardized uptake value (SUV) was calculated. Using surgical tissue samples, we examined the expression levels of hypoxia-inducible factor alpha (HIF1α), a marker of tissue hypoxia; proliferative cellular nuclear antigen (PCNA), a marker of proliferation; and glucose transporter (GLUT)1 and hexokinase (HK)2, protein of glucose uptake by using reverse transcriptase-polymerase chain reaction.
Results
All except two colorectal cancer lesions showed increased uptake of FDG. The mean SUV of FDG-PET was 12.0 ± 1.2 (±SEM). The mean mRNA expression levels of GLUT1 and HK2 were significantly higher in cancer tissues than in the surrounding normal mucosa. Moreover, to promote the upregulation of glucose uptake, the expressions of HIF1α and PCNA were induced to 2.6 and 3.3 times higher than that in the normal mucosa. However, the quantitative correlation analysis showed SUV was correlated with HIF1α expression but not with PCNA expression.
Conclusion
Our molecular-based analysis suggested that FDG accumulation due to induction of glucose uptake proteins might be associated with the hypoxic environment in tumors rather than the tumor growth. Therefore, for assessing the efficacy of chemotherapy using FDG-PET, we must keep in mind that SUV does not indicate the tumor growth directly.