Galectin-3 and galectin-3-binding site expression in human adult astrocytic tumours and related angiogenesis

Citation
L. Gordower et al., Galectin-3 and galectin-3-binding site expression in human adult astrocytic tumours and related angiogenesis, NEUROP AP N, 25(4), 1999, pp. 319-330
Citations number
58
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
ISSN journal
03051846 → ACNP
Volume
25
Issue
4
Year of publication
1999
Pages
319 - 330
Database
ISI
SICI code
0305-1846(199908)25:4<319:GAGSEI>2.0.ZU;2-D
Abstract
Using computer-assisted microscopy, the present work aimed to quantitativel y characterize the level of the histochemically detectable expression of ga lectin-3 and galectin-3-binding sites in sections of a series of 84 astrocy tic tumours (including 22 grade II, 21 grade III and 41,grade IV specimens) and seven non-tumoural specimens used as controls. The presence of galecti n-3 and reactive sites for this lectin were monitored by means of a specifi c polyclonal anti-galectin-3 antibody (aGal3) and biotinylated galectin-3 ( Gal3), respectively. The pattern of expression of galectin-3-binding sites is compared to the pattern of expression of laminin (a potential galectin-3 ligand) revealed using a biotinylated anti-laminin antibody (aLam). Three variables quantitatively characterizing histochemical staining reactions we re evaluated by means of computer-assisted microscopy for each of the 3 pro bes under study (aGal3, Gal3 and aLam), The labelling index (LI) is the per centage of tissue area specifically stained by a histochemical probe. The m ean optical density (MOD) denotes staining intensity. The concentration het erogeneity (CH) feature expresses the concentrational spread of individual fields. The data obtained in the present study show that: (i) white matter of a non-tumoural brain expresses galectin-3 (and also galectin-3-binding s ites); (ii) the level of galectin-3 expression significantly decreases in t he majority of tumour astrocytes from low to high grade astrocytic tumours; while (iii) some tumour cell clones expressing high amounts of galectin-3 emerged with increasing levels of malignancy; and (iv) the level of accessi ble galectin-3-binding sites was apparently not heavily modified in the cou rse of malignancy progression. In conclusion, the results obtained in the p resent study show that human astrocytic tumours are very heterogenous in th eir galectin-3 levels of expression. If high levels of galectin-3 determine the invasiveness potential of a tumour cell, then within a heterogenous tu mour the presence of even a small, but actively proliferating number of tum our cell clones expressing high levels of galectin-3 can be expected to lea d to tumour invasiveness.