Diagnostic role of galectin-3 in follicular thyroid tumors

Background Galectin-3 is a member of a growing family of beta-galactoside binding animal lectins. It is widely distributed in human tissue and cell types and has a different distribution within the cell, according to cell type and functional status, being either restricted to the nucleus or localized to the cytoplasm and/or the cell surface [1, 13]. Galectin-3 is physiologically produced by macrophages, endothelial cells and several epithelial cells (colon, breast, kidney). Its wide distribution is paralleled by a relatively wide spectrum of actions which have been associated to galectin-3 in both physiological and pathological conditions. In particular, it plays a role in cell-cell and cell matrix interactions, cell growth, neoplastic transformation, metastatization, cell-cycle regulation and apoptosis, cell damage and repair processes [1, 13]. Since galectin-3 expression is modulated by several oncogenic stimuli, it was shown to be upregulated in different human tumors, including large cell lymphoma, colorectal carcinoma, breast carcinoma, hepatocellular carcinoma, brain tumors, melanoma and finally thyroid carcinoma. In non-medullary thyroid tumors, galectin-3 expression was restricted to malignant follicular-derived tumors. In fact, neither normal nor fetal [17] thyroid cells were found to contain galectin-3 (as opposed to other galectins which can be expressed even in physiological conditions). In addition, hyperplastic lesions and benign thyroid tumors also lacked galectin-3 expression [1, 13], although these latter observations were not confirmed by all authors [9, 11] (see below).