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Genetic Alterations in Colorectal Cancer Have Different Patterns on 18F-FDG PET/CT
Shang-Wen Chen1, Chien-Yu Lin, Cheng-Man Ho
1From the *Department of Radiation Oncology, China Medical University Hospital; †College of Medicine, China Medical University, Taichung; ‡College of Medicine, Taipei Medical University, Taipei; §Graduate Institute of Clinical Medical Sciences, China Medical University; ║Department of Laboratory Medicine, China Medical University Hospital; ¶Department of Nursing, Hungkuang University; **Epigenome Research Center and ††Department of Nuclear Medicine and PET Center, China Medical University Hospital; and ‡‡Graduate Institute of Clinical Medical Science and School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan.
Purpose:
The aim of this study was to understand the association between various genetic mutation and (18)F-FDG PET-related parameters in patients with colorectal cancer (CRC).
Methods:
One hundred three CRC patients who had undergone preoperative PET/CTs were included in this study. Several PET/CT-related parameters, including SUV(max), and various thresholds of metabolic tumor volume, total lesion glycolysis, and PET/CT-based tumor width (TW) were measured. Using high-resolution melting methods for genetic mutation analysis, tumor- and PET/CT-related parameters were correlated with various genetic alterations including TP53, KRAS, APC, BRAF, and PIK3CA. Mann-Whitney U test and logistic regression analysis were carried out for this analysis.
Results:
Genetic alterations in TP53, KRAS, and APC were found in 41 (40%), 34 (33%), and 27 (26%) of tumors, respectively. PIK3CA and BRAF were exhibited by 5 and 4 of the patients with CRC. TP53 mutants exhibited higher SUV(max). The odds ratio was 1.28 (P = 0.04; 95% confidence interval, 1.01-1.61). Tumors with a mutated KRAS had an increased accumulation of FDG using a 40% threshold level for maximal uptake of TW (TW(40%)), whereas the odds ratio was 1.15 (P = 0.001; 95% confidence interval, 1.06-1.24). The accuracy of SUV(max) greater than 10 in predicting TP53 mutation was 60%, whereas that for TW(40%) for KRAS was 61%.
Conclusions:
Increased SUV(max) and TW(40%) were associated in CRC tumors with TP53 and KRAS mutations, respectively. Further studies are required because of the low predictive accuracy.
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