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Glycobiology Advance Access originally published online on May 12, 2004
Glycobiology 2004 14(9):783-792; doi:10.1093/glycob/cwh092
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Glycobiology vol. 14 no. 9 © Oxford University Press 2004; all rights reserved.

Cell surface overexpression of galectin-3 and the presence of its ligand 90k in the blood plasma as determinants in colon neoplastic lesions

Claudia Greco2, Rosa Vona2,3, Maurizio Cosimelli4, Paola Matarrese3,5, Elisabetta Straface3,5, Patrizia Scordati6, Diana Giannarelli7, Vincenzo Casale8, Daniela Assisi8, Marcella Mottolese6, Anna Moles9 and Walter Malorni1,2,3

2 Clinical Pathology Service, Polo Oncologico Regina Elena, Rome, Italy; 3 Laboratory of Ultrastructures, Istituto Superiore di Sanitá, Viale Regina Elena 299, 00161 Rome, Italy; 4 Surgical Department, Polo Oncologico Regina Elena, Rome, Italy; 5 Department of Drug Research and Evaluation, Istituto Superiore di Sanitá, Viale Regina Elena 299, 00161 Rome, Italy; 6 Pathological Anatomy Service, Polo Oncologico Regina Elena, Rome, Italy; 7 Service of Statistics, Polo Oncologico Regina Elena, Rome, Italy; 8 Digestive Endoscopy Service, Polo Oncologico Regina Elena, Rome, Italy; and 9 Institute of Neuroscience, National Research Council, Rome, Italy

Received on March 5, 2004; revised on April 23, 2004; accepted on April 27, 2004

Galectins are a family of beta-galactoside binding molecules involved in cell–extracellular matrix adhesion processes. Specifically, Galectin-3 (Gal-3), one of the members of this family of molecules plays a role in cell adhesion processes as well as in cell survival or apoptosis. Gal-3 was also hypothesized to represent a useful tool in tumor characterization, for example, in thyroid tumors. We report herein the results obtained by evaluating Gal-3 expression of colon cells from human adenomas and adenocarcinomas with two different methodologies: immunohistochemistry and flow cytometry of living dispersed cells. We found that (1) the expression of Gal-3 was significantly increased on the surface of cells from adenomas with respect to normal mucosa from the same patient; (2) Gal-3 ligand, 90k molecule, was increased in the blood plasma from patients with both adenomatous and adenocarcinomatous lesions; and (3) Gal-3 overexpression was not related with the presence of K-ras mutation. Altogether these results clearly indicate that the evaluation of Gal-3 expression (and of its ligand, 90k) can be of interest in the characterization of nonmalignant and malignant colon cancers.

1 To whom correspondence should be addressed; e-mail: malorni{at}iss.it


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