Increased expression of galectin-I in carcinoma-associated stroma predicts poor outcome in prostate carcinoma patients

被引:0
作者
van den Brûle, FA [1 ]
Waltregny, D [1 ]
Castronovo, V [1 ]
机构
[1] Univ Liege Hosp, Metastasis Res Lab, B-4000 Liege 1, Belgium
基金
英国惠康基金; 加拿大健康研究院; 欧盟地平线“2020”;
关键词
prostate carcinoma; expression; galectin-l; stroma; progression; prognosis;
D O I
10.1002/1096-9896(2000)9999:9999<::AID-PATH730>3.0.CO;2-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Galectin-1, a member of the beta -galactoside-binding galectin family, is a pleiotropic dimeric protein participating in a variety of normal and pathological processes, including cancer progression. Modulation of the interactions with the basement membrane glycoprotein lamimin and induction of apoptosis in activated T lymphocytes are well-known functions of this galectin, In this study, the expression of galectin-1 was examined in 148 human primary prostate carcinoma samples. Immunohistochemical staining of paraffin sections of prostate tissues revealed that galectin-1 was not detected in normal, PIN (prostatic intraepitheliar neoplasia) or carcinoma cells, but accumulated in the stroma and associated fibroblasts, Galectin-1 expression was significantly increased in the tumour-associated stroma compared with the nonneoplastic gland-associated stroma in 21.3% of the cases (Mantel-Haenszel test, p=0.001; Wilcoxon signed rank test, p<0.0001). Increased galectin-1 expression in the cancer-associated stroma compared to the normal gland-associated stroma (p=0.03) was identified by multivariate analysis as a strong independent predictor of prostate-specific antigen (PSA) recurrence, just after the pathological stage (p<0.0001). The association between accumulation of galectin-1 in the stroma of the malignant tissue and aggressiveness of the tumour adds weight to the body of evidence that identifies a role for galectin-1 in the acquisition of the. invasive phenotype, In addition to modulating cancer cell interactions with laminin, galectin-1 accumulated around the cancer cells may act as an immunological shield by inducing activated T-cell apoptosis. This exciting hypothesis warrants further investigation. Copyright (C) 2000 John Wiley & Sons, Ltd.
引用
收藏
页码:80 / 87
页数:8
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