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Context:Few prospective studies have evaluated the role of 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) in the characterization of adrenal masses.Objective:To assess the performance of 18F-FDG PET/CT in the malignancy diagnosis of adrenal masses in noncancer patients.Design:Prospective multicenter study.Material and Methods:The study population consisted of 87 patients (87 adrenal masses) referred to endocrine surgeons: 56 with mass diameter ≥40 mm and 31 with a diameter <40 mm and of indeterminate nature based on unenhanced and washout CT attenuation densities. Fourteen patients had hypercortisolism. Adrenal masses were characterized by 18F-FDG PET/CT. Histology was the gold standard for the diagnosis of malignancy. In the absence of pathological proof (n = 23), the nature of the lesion was based on the 12-month imaging follow-up.Results:Fifteen adrenal masses were classified as malignant (including 11 adrenocortical carcinomas) and 72 as benign. Compared with benign lesions, malignant lesions were larger in size (P = 0.003), had higher unenhanced densities (P = 0.002), lower relative washout values (P = 0.007), and higher 18F-FDG uptake parameters (P < 10−3). The optimal threshold value of (Tumor SUVmax:Liver SUVmax) the ratio for malignancy was >1.5 with sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 86.7%, 86.1%, 56.5%, 96.9%, and 86.2%, respectively.Conclusions:Our results show that 18F-FDG PET/CT complements adrenal washout CT in the evaluation of adrenal masses and should be recommended in the evaluation of large and/or indeterminate adrenal masses.We studied the performance of 18F-FDG PET/CT in the characterization of adrenal masses in noncancer patients and found that 18F-FDG PET/CT enabled accurate estimation of malignancy risk.

Pancreatic cancer cells generate metastases because they can survive the stress imposed by the new environment of the host tissue. To mimic this process, pancreatic cancer cells which are not stressed in standard culture conditions are injected into nude mice. Because they develop xenografts, they should have developed adequate stress response. Characterizing that response might provide new strategies to interfere with pancreatic cancer metastasis. In the human pancreatic cancer cell lines Panc-1, Mia-PaCa2, Capan-1, Capan-2 and BxPC3, we used Affymetrix DNA microarrays to compare the expressions of 22.000 genes in vitro and in the corresponding xenografts. We identified 228 genes overexpressed in xenografts and characterized the implication of one of them, WSB1, in the control of apoptosis and cell proliferation. WSB1 generates 3 alternatively spliced transcripts encoding distinct protein isoforms. In xenografts and in human pancreatic tumors, global expression of WSB1 mRNA is modestly increased whereas isoform 3 is strongly overexpressed and isoforms 1 and 2 are down-regulated. Treating Mia-PaCa2 cells with stress-inducing agents induced similar changes. Whereas retrovirus-forced expression of WSB1 isoforms 1 and 2 promoted cell growth and sensitized the cells to gemcitabine- and doxorubicin-induced apoptosis, WSB1 isoform 3 expression reduced cell proliferation and enhanced resistance to apoptosis, showing that stress-induced modulation of WSB1 alternative splicing increases resistance to apoptosis of pancreatic cancer cells. Data on WSB1 regulation support the hypothesis that activation of stress-response mechanisms helps cancer cells establishing metastases and suggest relevance to cancer development of other genes overexpressed in xenografts.