Initial Experience of 18F-FDG PET/MRI in Thymic Epithelial Tumors: Morphologic, Functional, and Metabolic Biomarkers.

PURPOSE: The aim of this study was to investigate the value of morphologic, functional, and metabolic biomarkers acquired concurrently at PET/MRI in patients with thymic epithelial tumors. PATIENTS AND METHODS: During 1 year, 9 patients with suspected thymic epithelial tumors at contrast-enhanced chest CT were prospectively enrolled and underwent preoperative 18F-FDG PET/MRI. Two chest radiologists prospectively reviewed the CT and MRI scans of PET/MRI in consensus, and 2 nuclear physicians reviewed the PET images. Visual assessment of the tumor morphology, functional biomarkers such as apparent diffusion coefficient from diffusion-weighted images, and metabolic biomarkers (including SUVmax, metabolic tumor volume, total lesion glycolysis, and heterogeneity index) were recorded. All patients underwent operation, and their pathologic reports served as the reference standard. RESULTS: Thymic epithelial tumors were demonstrated in all 9 patients at pathologic examination. Tumor contour (P = 0.012) and shape (P = 0.033) had an association with the World Health Organization subtype, and the presence of septum (P = 0.048) on MRI scans had an association with the Masaoka stage. In terms of functional and metabolic biomarkers, SUVmax (ρ = 0.683, P = 0.042) and SUV/apparent diffusion coefficient (ρ = 0.703, P = 0.035) correlated with the Masaoka stage. Metabolic tumor volume (P = 0.024), heterogeneity index (P = 0.024), and total lesion glycolysis (P = 0.048) were useful for classification between low- and high-risk thymic epithelial tumors. CONCLUSIONS: Although limited by the small number of patients enrolled, morphologic, functional, and metabolic biomarkers derived from PET/MRI scans were useful for the stratification of thymic epithelial tumors.

Cobalt chloride stimulates phosphoinositide 3-kinase/Akt signaling through the epidermal growth factor receptor in oral squamous cell carcinoma

Tumor cells are often found under hypoxic conditions due to the rapid outgrowth of their vascular supply, and, in order to survive hypoxia, these cells induce numerous signaling factors. Akt is an important kinase in cell survival, and its activity is regulated by the upstream phosphoinositide 3-kinase (PI3K) and receptor tyrosine kinases (RTKs). In this study, we examined Akt activation and RTKs/PI3K/Akt signaling using the hypoxia-mimetic cobalt chloride in oral squamous carcinoma cells. Cobalt chloride increases Akt phosphorylation in both a dose- and time-dependent manner. Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that Akt phosphorylation by cobalt chloride is dependent on PI3K. In addition, activation of the PI3K/Akt path way seems to rely on the epidermal growth factor receptor (EGFR), since the inhibition of EGFR attenuated cobalt chloride-induced Akt activation. The results in this study also demonstrate that cobalt chloride increases EGFR protein levels and induces oral squamous cell carcinoma cells to enter S phase.

Cobalt chloride stimulates phosphoinositide 3-kinase/Akt signaling through the epidermal growth factor receptor in oral squamous cell carcinoma

Tumor cells are often found under hypoxic conditions due to the rapid outgrowth of their vascular supply, and, in order to survive hypoxia, these cells induce numerous signaling factors. Akt is an important kinase in cell survival, and its activity is regulated by the upstream phosphoinositide 3-kinase (PI3K) and receptor tyrosine kinases (RTKs). In this study, we examined Akt activation and RTKs/PI3K/Akt signaling using the hypoxia-mimetic cobalt chloride in oral squamous carcinoma cells. Cobalt chloride increases Akt phosphorylation in both a dose- and time-dependent manner. Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that Akt phosphorylation by cobalt chloride is dependent on PI3K. In addition, activation of the PI3K/Akt path way seems to rely on the epidermal growth factor receptor (EGFR), since the inhibition of EGFR attenuated cobalt chloride-induced Akt activation. The results in this study also demonstrate that cobalt chloride increases EGFR protein levels and induces oral squamous cell carcinoma cells to enter S phase.(AU)