PET/MRI would have a number of advantages over PET/CT, such as improved soft-tissue contrast, the possibility of performing truly simultaneous instead of sequential acquisitions, and the availability of sophisticated MRI sequences, such as diffusion and perfusion imaging, functional MRI, and MR spectroscopy, which can add important information

PET/MRI would have a number of advantages over PET/CT, such as improved soft-tissue contrast, the possibility of performing truly simultaneous instead of sequential acquisitions, and the availability of sophisticated MRI sequences, such as diffusion and perfusion imaging, functional MRI, and MR spectroscopy, which can add important information. that a higher maximum standardized uptake value (SUVmax) on 18F-FDG PET was associated with elevated tumor levels of phosphorylated-Akt, phosphorylated-S6 protein, aggressive behavior and metastatic potential, early relapse, and shorter OS after radical nephrectomy. Their KaplanCMeier survival analysis indicated that patients with a high SUVmax (4.35) had a significantly lower OS rate than those with a low SUV-max ( 4.35) irrespective of the presence of distant metastasis before surgery, and among 52 patients without distant Flumatinib mesylate metastasis before surgery, those with a high SUVmax (3.50) had a significantly lower recurrence-free survival rate than those with a low SUVmax ( 3.50) [12]. In another study by Kayani et al., multivariate analysis demonstrated that a high SUVmax (7.1) and an increased number of PET-positive lesions (8 or more) demonstrated by 18F-FDG PET/CT before treatment were significantly correlated with shorter OS [hazard ratio (HR): 3.30 and 3.67, respectively] in 44 patients with metastatic clear cell RCC who were treated with sunitinib [14]. Two major groups of targeted drugs currently approved for use against metastatic RCC are multikinase inhibitors and mammalian target of Dock4 rapamycin (mTOR) inhibitors. Sorafenib and sunitinib are two representatives of the former, inhibiting tyrosine kinase vascular endothelial growth factor (VEGF) receptor 2 and platelet-derived growth factor receptor in endothelial cells and pericytes, respectively [21]. Because expression of Glut is a downstream result of HIF transcriptional activity, it is conceivable that the intensity of 18F-FDG uptake on PET may reflect the Flumatinib mesylate activity of the entire pathway. This means that the variable intensity of 18F-FDG uptake on PET by clear cell RCC may reflect Flumatinib mesylate the variable strength of the HIF signaling pathway and expression of its downstream products, thus being predictive of the effects of inhibitors of this pathway. A recent study by Ueno et al. involving 35 patients with advanced RCC evaluated the response to tyrosine kinase inhibitors (TKI) (sunitinib 19 cases, sorafenib 16 cases) in terms of tumor size and 18F-FDG uptake using 18F-FDG PET/CT before and 1 month after treatment [16]. They showed that PET was able to predict not only the duration of response to TKIs, but also survival duration (OS and progression-free survival [PFS]), and that early assessment by 18F-FDG PET/CT provided useful information for determining individual patient management strategies [16]. In another study, Faenebo et al. [20] determined whether early changes in the glucose metabolism of metastatic RCC assessed by 18F-FDG PET according to the PERCIST 1.0 criteria [22] after 14 and 28 days of treatment with TKIs (sunitinib 18 cases, sorafenib 19 cases, or pazopanib 2 Flumatinib mesylate cases) were able to predict OS and PFS in 39 patients. They found that early changes in SUVpeak (peak standardized uptake normalized to lean body mass) and total lesion glycolysis after only 14 days of TKI treatment were significantly correlated with both PFS and OS [20]. Several new PET Flumatinib mesylate tracers are currently under investigation for potential use in the staging and monitoring of response to therapy in patients with RCC. These new tracers exploit various cellular process that are altered in malignant cells, including cellular proliferation [18F-fluoro-thymidine (18F-FLT)], aerobic metabolism (11C-acetate), cell membrane synthesis (11C-choline, 18F-fluorocholine), hypoxia [18F-fluoromisonidazole (18F-FMISO)], and amino acid transport (11C-methionine, anti-[18F]fluorocyclobutane carboxylic acid (anti-3-18F-FACBC)).


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