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Vessels in benign prostatic hyperplasia contain more binding sites for endostatin than vessels in normal prostate tissue.

作者信息

Schmidt Annette, Sommer Frank, Ozgür Enver, Klotz Theodor, Engelmann Udo, Addicks Klaus, Bloch Wilhelm

机构信息

Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Carl-Diem-Weg 6, 50933 Cologne, Germany.

出版信息

Eur Urol. 2004 Dec;46(6):765-7. doi: 10.1016/j.eururo.2004.07.027.

DOI:10.1016/j.eururo.2004.07.027
PMID:15548445
Abstract

OBJECTIVE

The angiogenic phenotype is an effect of a net balance of angiogenic and anti-angiogenic factors. Endostatin is one of a group of recently described matrix-derived inhibitors of tumour angiogenesis that have acquired increasing significance for tumour treatment. Endostatin's anti-angiogenic mechanism and the causes of its heterogenic influence on various tissue types have not yet been defined.

METHODS

We investigated the variations in endostatin's binding behaviour to vessels in benign prostatic hyperplasia (BPH) compared to endostatin binding to vessels in normal prostate tissue. Biotinylated endostatin was used and was detected using Extravidin CY3.

RESULTS

In BPH 89.12% +/- 10.72% of vessels showed endostatin binding. This was significantly more than observed for vessels in normal prostate tissue (1.66% +/- 1.66%).

CONCLUSION

The strongly proliferative tissue of BPH may be a growth-limited cause of significantly more endostatin binding sites. The investigation indicates endostatin as a possible new target for BPH treatment.

摘要

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