Abstract
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Objectives: Hypoxia in liver metastasis from colorectal carcinoma (mCRC) may be a cause of treatment resistance, but it is not currently known whether these tumors are hypoxic. We aim to assess FMISO uptake in liver metastases and compare it with FDG uptake, and assess the influence of hypoxia on angiogenesis.
Methods: Fourteen patients with mCRC in the liver had 18F-FDG and 18F-FMISO PET/CT scans performed. Maximum standardised uptake value (SUVmax) was measured for the metabolically active liver lesions identified on concurrent low dose CT for both PET scans, as well as the calculation of tumor to normal liver ratio (TNR). Tissue and plasma samples was obtained to assess hypoxia and angiogenesis.
Results: For the FMISO scan, mean tumor SUVmax was 2.5 (range 1.3-3.8) and mean normal liver SUVmax was 2.2 (range 1.3-2.7). There was a statistically significant difference in SUVmax between the tumor and normal liver (p-value <0.05; 95%CI 0.07-0.54). For the FDG scan, mean tumor SUVmax was 6.8 (range 4.3-10.6) and mean normal liver SUVmax was 2.6 (range 1.7-3.6), which also showed a statistically significant difference (p-value <0.05; 95% CI 3.0-5.4). The TNR was 1.13 for FMISO and 2.72 for FDG, with a statistically significant difference between the two radiotracers (p-value <0.05; 95% CI 1.0-2.18).
Conclusions: The study shows that hypoxia is present in liver metastases in colorectal carcinoma, as assessed by 18F-FMISO. Further analysis of tissue and plasma markers of hypoxia and angiogenesis are ongoing.
Research Support: Cancer Council of Victoria & University of Melbourne Faculty Research Scholarship
- Society of Nuclear Medicine, Inc.