The loss of lectin reactivity from human endometrium is a feature of malignant change.
Changes in the cell surface glycoproteins were investigated in endometrial adenocarcinomas using eight biotin-labelled lectins (Con A, LCA, WGA, e-PHA, l-PHA, SBA, PNA, LTA) which select for the major classes of N-linked and O-linked oligosaccharides. The tissues studied were 14 normal endometria, 20 cases of simple hyperplasia and 30 endometrial adenocarcinomas. Sections were cut at 5 microns from formalin fixed paraffin embedded blocks and were stained with an avidin-peroxidase method. All normal and hyperplastic endometria contained the full range of expected saccharides (positive staining for Con A, LCA, WGA, SBA, PNA, LTA, e-PHA and l-PHA). By contrast, over half of the endometrial adenocarcinomas exhibited a loss of galactosamine (56.7%) and over a third of them failed to reveal galactose (36.7%) and fucose (30.0%) (negative staining for SBA, PNA and LTA, respectively). Interestingly, following neuraminidase treatment, galactose was identified in all adenocarcinomas studied, but the expression of galactosamine and fucose was unaffected. There was a discrete linear staining at the level of the basement membranes in a proportion of endometrial glands treated with e-PHA, l-PHA and LCA; this was continuous in normal and hyperplastic endometria, while it was fragmentary in endometrial adenocarcinomas. The loss of galactosamine reactivity from endometrial adenocarcinomas was significantly correlated with high grade differentiation, and also with the more frequent occurrence of a poor oestrogen (ER) and progesterone (PR) receptor status and with an unfavourable 5-year survival. No relationship was found between fucose reactivity and tumour differentiation, stage of disease, hormone receptor status or prognosis. It is concluded that galactosamine loss, together with reduced fucose expression, is a common feature of endometrial malignancy, and that galactosamine deficient tumours may reflect a more aggressive biological behaviour.
Sivridis
E
E
Department of Pathology, Democritus University of Thrace, Alexandroupolis, Greece.
Agnantis
N
N
D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000032:analysis; D002240:Carbohydrate Sequence; D002471:Cell Transformation, Neoplastic / Q000378:metabolism* / Q000473:pathology*; D016889:Endometrial Neoplasms / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D037102:Lectins / Q000378:metabolism*; D008969:Molecular Sequence Data; D011485:Protein Binding / Q000276:immunology
D015415:Biomarkers; D037102:Lectins