¹⁸F-FDG and 3′-deoxy-3′-¹⁸F-fluorothymidine (¹⁸F-FLT) have been proven useful in diagnosing and staging many types of cancer but with emphasis on different aspects of tumor biology. The aim of the current study was to evaluate whether ¹⁸F-FDG and ¹⁸F-FLT can be used complementarily in monitoring the biologic characteristics of colorectal cancer (CRC). Methods: Human CRC cell lines SW480 and SW620 of the same genetic origin but different metastatic potential were cultured and implanted into nude mice to create CRC models. Uptake of ¹⁸F-FDG and ¹⁸F-FLT in SW480 and SW620 cells in vitro was assessed after incubation with radiotracers for 0, 30, 60, 90, and 120 min. In vivo imaging of SW480 and SW620 tumor-bearing mice was performed using small-animal PET/CT at 60 min after injection of each tracer. A region of interest was drawn over tumor and background to calculate the tumor-to-nontumor ratio (T/NT) using software on reconstructed images. Tumor growth rate, metastatic status, and survival time were assessed in tumor-bearing mice. The relationship between uptake of the tracers, metastatic capability, and tumor marker expression was evaluated using linear regression. Results: SW480 tumors grew more quickly than SW620 tumors (t = 3.332, P = 0.004). A higher incidence of lung and liver metastases was noted for SW480 than for SW620 (P = 0.023). Uptake in SW480 and SW620 cells was significantly different between ¹⁸F-FDG and ¹⁸F-FLT (t = 2.507, P = 0.021, vs. t = 3.497, P = 0.002). In the small-animal PET study, the T/NT of ¹⁸F-FDG did not differ between SW480 and SW620 tumors (2.69 ± 0.98 vs. 3.09 ± 1.26, P = 0.524), but the T/NT of ¹⁸F-FLT differed significantly between SW480 and SW620 tumors (3.65 ± 0.51 vs. 2.22 ± 0.42, P < 0.001). Heat shock protein 27 (HSP27) expression and integrin β₃ expression were higher, whereas vascular endothelial growth factor receptor 2 (VEGFR2) expression and Ki67 expression were lower, in SW480 cells than in SW620 cells. For SW480, metastases in lung and liver correlated significantly with ¹⁸F-FLT uptake in tumors (r = 0.763, P = 0.005) and with expression of HSP27 (r = 0.894, P = 0.008) and integrin β₃ (r = 0.635, P = 0.088). A correlation was also found between ¹⁸F-FLT uptake and expression of HSP27 (r = 0.924, P = 0.004) and integrin β₃ (r = 0.813, P = 0.025). No correlation was found between ¹⁸F-FDG uptake in tumors and metastasis in lung and liver (r = −0.111, P = 0.388). However, there was a significantly negative correlation between ¹⁸F-FDG uptake and the survival time of tumor-bearing mice (r = −0.500, P = 0.017), to which ¹⁸F-FLT did not relate (r = 0.262, P = 0.182). Conclusion: High uptake of ¹⁸F-FDG and ¹⁸F-FLT may reflect poorer survival and a higher metastatic potential for CRC in mice. Combining ¹⁸F-FDG with ¹⁸F-FLT PET would be helpful in better predicting the biologic behavior of CRC.

18F-FDG PET/MRI has been applied to the diagnosis and preoperative staging in various tumor types; however, reports using PET/MRI in gastric cancer are rare because of motion artifacts. We investigated the value of PET/MRI for preoperative staging compared with PET/CT in gastric cancer (GC). Thirty patients with confirmed GC underwent PET/CT and PET/MRI. TNM staging for each patient was determined from the PET/MRI and PET/CT images. The diagnostic performance of PET/MRI and PET/CT was calculated compared with the pathologic TNM stage. The two methods were compared using statistical analyses. The accuracy for T staging between PET/MRI and PET/CT was 76.9% vs. 57.7%, respectively. In T₁ and T_4a staging, the sensitivity and specificity for PET/MRI vs. PET/CT was 1.0 vs. 0.6 and 1.0 vs. 0.8, respectively. The area under the curve (AUC) for PET/MRI vs. PET/CT was 1.00 vs. 0.78 in the T₁ stage, 0.73 vs. 0.66 in the T₂ stage, 0.72 vs. 0.57 in the T₃ stage, and 0.86 vs. 0.83 in the T₄ stage. The accuracy for N staging of PET/MRI vs. PET/CT was 53.9% vs. 34.0%, and that for N₀ vs. N₊ was 85.0% vs. 77.0%. The sensitivity for PET/MRI in N3 staging was 0.67 and 0 for PET/CT. There was a statistically significant difference in the AUC for N₁ staging (PET/MRI vs. PET/CT, 0.63 vs. 0.53, p=0.03). SUVmax/ADC positively correlated with tumor volume and Ki-67. PET/MRI performs more accurately in TNM staging compared with PET/CT and is optimal for accurate N staging. SUVmax/ADC has positive correlations with tumor volume and Ki-67.

We compared PET/MRI with PET/CT in terms of lesion detection and quantitative measurement to verify the feasibility of the novel integrated imaging modality for oncological applications. In total, 285 patients referred to our PET/CT center for oncological indications voluntarily participated in this same-day PET/CT and PET/MRI comparative study. PET/CT images were acquired and reconstructed following routine protocols, and then PET/MRI was performed at a mean time interval of 28±11 min (range 15–45 min). PET/MRI covered the body trunk with a sequence combination of transverse T1WI 3D-volumetric interpolated breath-hold, T2WI turbo spin echo with fat saturation, diffusion-weighted imaging with double b values (50 and 800 s/mm²), and simultaneous PET acquisition over 45 min/5 bed positions. The maximum standardized uptake value (SUVmax) was assessed by manually drawn regions of interest over fluorodeoxyglucose-positive lesions. Among 285 cases, 57 showed no abnormalities, and 368 lesions (278 malignant, 68 benign and 22 undetermined) were detected in 228 patients. When stand-alone modalities were evaluated, PET revealed 31 and 12 lesions missed by CT and MRI, respectively, and CT and MRI revealed 38 and 61 more lesions, respectively, than PET. Compared to CT, MRI detected 40 more lesions and missed 8. In the integrated mode, PET/CT correctly detected 6 lesions misdiagnosed by PET/MRI, but was false-negative in 30 cases that were detected by PET/MRI. The overall diagnosis did not differ between integrated PET/MRI and PET/CT. SUVmax for lesions were slightly higher from PET/MRI than PET/CT but correlated well (ρ = 0.85–0.91). The novel integrated PET/MRI performed comparatively to PET/CT in lesion detection and quantitative measurements. PET from either scanner modality offered almost the same information despite differences in hardware. Further study is needed to explore features of integrated PET/MRI not addressed in this study.

Introduction: Ferroptosis has recently been recognized as a new cause of ischemia reperfusion injury due to blood–brain barrier (BBB) disruption followed by secondary iron‐loaded transferrin (TF) influx. As a novel and independent cell death pathway, ferroptosis was characterized by iron‐dependent lipid peroxidation, decline of GSH, GPX4, and shrinking mitochondria. Cottonseed oil (CSO), a liposoluble solvent, can alleviate ischemia stroke injuries and oxidative stress. However, the effect of CSO on ischemic stroke–induced ferroptosis has not been explored. In this study, we investigated the effect of CSO on ferroptosis caused by cerebral ischemic injury in rats.Methods: We conducted the subcutaneous injection of 1.3 mL/kg CSO every other day for 3 weeks on rats with middle cerebral artery occlusion–reperfusion (MCAO‐R) injury. We used Garcia Test, TTC staining, HE, Nissl and NeuN staining, Evans blue test, ⁶⁸Ga‐citrate PET, Western blot, immunofluorescence staining, Elisa kits, and transmission electron microscopy to detect the infarct volume, neural injuries, and ferroptosis‐related indexes.Results: CSO treatment could significantly ameliorate MCAO‐R‐induced neurological dysfunction in a male rat model. Furthermore, it reduced infarct volume and neuronal injuries; protected BBB integrity; reduced the influx of iron ion, TF, and TF receptors; up‐regulated anti‐ferroptosis proteins (GPX4, xCT, HO1, FTH1), while down‐regulating ferroptosis‐related protein ACSL4; increased the activity of GSH and SOD; and decreased MDA and LPO levels. Mitochondrial destruction induced by ischemic stroke was also alleviated by CSO treatment.Conclusion: CSO treatment can alleviate ischemic stroke injury via ferroptosis inhibition, which provides a new potential therapeutic mechanism for CSO neuroprotection against ischemic stroke.