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The use of thyroglobulin concentration in washout fluid of fine-needle aspiration (FNA-Tg) is a procedure advocated by international guidelines to diagnose metastatic LN in papillary thyroid cancer. With the increasing use of active follow-up or lobectomy alone for low-risk thyroid cancers, the determination of the diagnostic performance of FNA-Tg in the detection of metastatic PTC when the thyroid is in situ is paramount. Prospective study with measurement of Tg in washout fluid obtained from intraoperative fine needle aspiration (FNA) cytology in order to avoid contamination from thyroid tissue and rigorously isolated punctured nodes. Receiver-operating characteristic (ROC) curve and area under the curve (AUC), optimal threshold to discriminate benign and malignant LN, sensitivity and specificity were provided. Results: a total of 58 lymph nodes from 32 patients were analyzed. ROC analysis defined the optimal cutoff values of FNA-Tg at 60 ng/ml for the diagnosis of malignant LNs in patients with a thyroid in situ. Sensitivity and specificity were 75% (95% confidence interval 57.89–86.75) and 87.5% (95%CI: 69–95.66), respectively. Our results support the hypothesis that the Tg-FNA threshold for a safe diagnosis of LN metastasis in PTC is higher in presence of a thyroid gland in situ. The use of lower thresholds could result in false positive results and lead to unnecessary surgery. [ABSTRACT FROM AUTHOR]

Autophagy is a degradation process of cytoplasmic cellular constituents, which serves as a survival mechanism in starving cells, and it is characterized by sequestration of bulk cytoplasm and organelles in double-membrane vesicles called autophagosomes. Autophagy has been linked to a variety of pathological processes such as neurodegenerative diseases and tumorigenesis, which highlights its biological and medical importance. We have previously characterized the vacuole membrane protein 1 (VMP1) gene, which is highly activated in acute pancreatitis, a disease associated with morphological changes resembling autophagy. Here we show that VMP1 expression triggers autophagy in mammalian cells. VMP1 expression induces the formation of ultrastructural features of autophagy and recruitment of the microtubule-associated protein 1 light-chain 3 (LC3), which is inhibited after treatment with the autophagy inhibitor 3-methiladenine. VMP1 is induced by starvation and rapamycin treatments. Its expression is necessary for autophagy, because VMP1 small interfering RNA inhibits autophagosome formation under both autophagic stimuli. VMP1 is a transmembrane protein that co-localizes with LC3, a marker of the autophagosomes. It interacts with Beclin 1, a mammalian autophagy initiator, through the VMP1-Atg domain, which is essential for autophagosome formation. VMP1 endogenous expression co-localizes with LC3 in pancreas tissue undergoing pancreatitis-induced autophagy. Finally, VMP1 stable expression targeted to pancreas acinar cell in transgenic mice induces autophagosome formation. Our results identify VMP1 as a novel autophagy-related membrane protein involved in the initial steps of the mammalian cell autophagic process. [ABSTRACT FROM AUTHOR]