Expression of Glut-1 and HK-II in Pancreatic Cancer and Their Impact on Prognosis and FDG Accumulation.

OBJECTIVE: The purpose of this article is to analyze the expression of Glut-1 and HK-II, the association between their expression and 18F-FDG accumulation in pancreatic cancer. METHODS: Fifty patients with histologically proven pancreatic cancer were included in this preliminary study, all of whom received 18F-FDG PET/CT performance before surgery. Immunohistochemical staining of tumor tissue and adjacent normal tissue was performed for Glut-1 and HK-II. By combining proportions and intensity of immunochemical staining, we obtained the modified immunohistological scores for Glut-1 and HK-II respectively. The relationship between expression of Glut-1, HK-II and series of parameters was analyzed, i.e. clinicopathological characteristics, prognosis of patients and SUVmax of PET-CT. RESULTS: Compared with normal tissue, the Glut-1 and HK-II expression in pancreatic cancer tissue was significantly increased (P<.001). There was no correlation between expression of Glut-1, HK-II and age, gender, tumor size, tumor location, tumor histological type, tumor differentiation, the nerve infiltration, vascular invasion, local infiltration, lymph node metastasis or tumor staging in pancreatic cancer (P>.05). During the follow-up period, the survival curves of low Glut-1 group and high Glut-1 group were statistically different (P=.049). Multivariate analysis (Cox regression) revealed that Glut-1 expression was not associated with mortality (P>.05). No statistical difference was found in the survival curves of negative HK-II group and positive HK-II group (P=.545). There was no correlation between 18F-FDG uptake and expression of Glut-1 and HK-II(P>.05). CONCLUSION: The Glut-1 and HK-II expression in pancreatic cancer tissue was significantly increased. There was no correlation between expression of Glut-1, HK-II and clinicopathological characteristics, prognosis and 18F-FDG uptake.

The value of 18F-FDG positron emission tomography/computed tomography on the pre-operative staging and the management of patients with pancreatic carcinoma.

BACKGROUND/AIMS: To evaluate the value of FDG-PET/CT on the pre-operative staging of pancreatic cancer and its impact on clinical management. METHODOLOGY: From December 2006 to January 2013, data of pancreatic carcinoma patients who underwent surgical treatment at our center was collected retrospectively. MDCT and FDGPET/CT were used separately to diagnose and stage the tumor. Pre-operation staging by MDCT with chest x-ray and by FDG-PET/CT was compared according to the final pathological staging. RESULTS: A total of 79 histologically proven pancreatic cancer patients were enrolled in this study. FDG-PET/CT was more accurate in the detection of tumor (PET/CT vs. MDCT: 93.67% vs. 88.61%, p=0.402). The SE (60.00% vs. 24.00%, p=0.01) and accuracy (87.81% vs. 76.83%, p=0.015) of PET/CT to detect distant metastasis is significantly higher than those of MDCT. FDG-PET/CT also showed advantage over CT in the detection of metastatic lymph nodes (52.83% vs. 16.98%, p<0.001; accuracy: 66.67% vs. 41.33, p=0.002). The extra staging information PET/CT provided could have skipped eight patients (10.13%) of unnecessary surgical exploration. CONCLUSION: FDG-PET/CT is an important staging procedure and helps to make the clinical decision for the patients with pancreatic carcinoma.

Metabolic imaging of deep brain stimulation in anorexia nervosa: a 18F-FDG PET/CT study.

OBJECTIVES: Anorexia nervosa (AN), a disorder of unknown etiology, has the highest mortality rate of any psychiatric disorder. Drawing the brain metabolic pattern of AN may help to target the core biological and psychological features of the disorder and to perfect the diagnosis and recovery criteria. In this study, we used 18F-FDG PET to show brain metabolic network for AN. METHODS: Glucose metabolism in 6 AN patients and 12 age-matched healthy controls was studied using 18F-FDG PET. SPM2 was used to compare brain metabolism in AN patients with that in healthy controls. Four of 6 AN patients took deep brain stimulation (DBS) targeted in nucleus accumbens (NAcc). About 3 to 6 months after the surgery, the 4 AN patients took another 18F-FDG PET scan to assess the change in brain glucose metabolism. RESULTS: The SPM (statistical parametric mapping ) analysis showed hypermetabolism in the frontal lobe (bilateral, BA10, BA11, BA47), the limbic lobe (bilateral, hippocampus, and amygdala), lentiform nucleus (bilateral), left insula (BA13), and left subcallosal gyrus (BA25). It also showed hypometabolism in the parietal lobe (bilateral, BA7, BA40). The hypermetabolism in frontal lobe, hippocampus, and lentiform nucleus decreased after NAcc-DBS. CONCLUSIONS: The changes in brain glucose metabolism illustrated the brain metabolic pattern in AN patients. Furthermore, the pattern can be modulated by NAcc-DBS, which confirmed specificity of the pattern. The regions with altered metabolism could interconnect to form a network and integrate information related to appetite. Our study may provide information for targeting the potential candidate brain regions for understanding the pathophysiology of AN and assessing the effects of existing and future treatment approaches.

Targeting the kynurenine pathway as a potential strategy to prevent and treat Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the elderly accounting for the vast majority of dementia. Recently, many studies have implicated the role of inflammatory response, especially neuroinflammatory response in the development and progression of AD. However, the underlying mechanism of how inflammatory response induces AD is unknown. Kynurenine pathway is a major route of the amino acid tryptophan catabolism, resulting in the production of nicotine adenine dinucleotide and other neuroactive intermediates: quinolinic acid (QA) and kynurenic acid (KA). QA exerts different toxic effects, including over-activation of N-methyl-d-aspartate (NMDA) receptor and excitotoxicity, synaptic dysfunction and neuronal death. On the other hand, KA is identified as the only endogenous NMDA receptor antagonist and could modulate neurotoxic effects of QA. We hypothesize that an activated kynurenine pathway induced by inflammatory cytokines would generate more neurotoxic metabolites, which could be closely related to the pathogenesis of AD in elderly patients. Moreover, some measures, which facilitate KA synthesis and reduce the formation of QA, may emerge as a new therapeutic strategy against AD.