Fas and Fas ligand expression is elevated in prostatic intraepithelial neoplasia and prostatic adenocarcinoma

✍ Scribed by Jiazhong Jiang; Thomas M. Ulbright; Shaobo Zhang; George J. Eckert; Chinghai Kao; Thomas A. Gardner; Michael O. Koch; John N. Eble; Liang Cheng

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 690 KB
• Volume: 95
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/cncr.10674

✦ Synopsis

Abstract

BACKGROUND

Fas is a Type I membrane receptor of the tumor necrosis factor/nerve growth factor family. On binding to Fas ligand, a Type II transmembrane protein, the Fas/Fas ligand complex, induces apoptosis in target cells. Dysregulation of Fas and Fas ligand expression has been found in some malignant neoplasms.

METHODS

Using immunohistochemical analysis, the authors studied the expression of Fas and Fas ligand in prostatic adenocarcinoma, high‐grade prostatic intraepithelial neoplasia (PIN), and adjacent benign prostate tissue from 95 radical prostatectomy specimens.

RESULTS

The percentage of cells that stained positively with Fas in benign prostate tissue (mean, 2%) was statistically significantly lower compared with that in prostatic intraepithelial neoplasia (mean, 13%; P = 0.0014) and prostatic adenocarcinoma (mean, 31%; P = 0.0001). The staining intensity of Fas was significantly less in benign prostate tissue compared with the staining intensity in PIN and prostatic adenocarcinoma. The percentage of cells that stained positively with Fas ligand in benign prostate tissue (mean, 13%) was statistically significantly lower compared with that in PIN (mean, 47%; P = 0.0001) and in prostatic adenocarcinoma (mean, 53%; P = 0.0001). The staining intensity of Fas ligand was significantly less in benign prostate tissue compared with that in PIN and prostatic adenocarcinoma.

CONCLUSIONS

Data from the current study indicate that Fas/Fas ligand is elevated in prostatic malignancy, suggesting that Fas‐mediated apoptosis may be a potential target for therapeutic intervention. Cancer 2002;95:296–300. © 2002 American Cancer Society.

DOI 10.1002/cncr.10674