Prostate Cancer Scientific Abstracts - G

Welcome to the Prostate Cancer Guide scientific abstracts, author section G. Here you will find abstracts from the latest research being carried out in the field.

This section is recommended for people who have a scientific interest in prostate cancer. It is recommended that people without prior knowledge of prostate cancer visit the more general areas of the site (Prostate Cancer Guide).

Abstract Authors


Latest Prostate Cancer Abstract

Journal: International Journal of Molecular Medicine.

Issue: 2006, 17(6):1085-91.

Pubmed ID: 16685420

Authors: Gotanda T, Haraguchi M, Tachiwada T, Shinkura R, Koriyama C, Akiba S, Kawahara M, Nishiyama K, Sumizawa T, Furukawa T, Mimata H, Nomura Y, Akiyama S, Nakagawa M.

Title: Molecular basis for the involvement of thymidine phosphorylase in cancer invasion.

Thymidine phosphorylase, also known as platelet-derived endothelial cell growth factor, has been implicated in bladder cancer angiogenesis and invasion. However, the molecular basis of its role in invasion remains unclear. We investigated the expression of thymidine phosphorylase and 10 invasion-related genes in bladder cancers from 72 randomly selected patients by real-time two-step RT-PCR assay. We found that the expression levels of thymidine phosphorylase, MMP-9, uPA, and MMP-2 were significantly higher in invasive tumors than those in superficial tumors. Also, the expression level of thymidine phosphorylase significantly correlated with that of uPA, MMP-1, MMP-9, PAI-1 and VEGF. KK47/TP cells, bladder cancer cells that overexpress thymidine phosphorylase, had a higher expression of MMP-7 and MMP-9 than KK/CV cells that express lower level of TP in hypoxic condition. PC/thymidine phosphorylase cells, prostate cancer cells that overexpress thymidine phosphorylase, also had a higher expression of MMP-1 and MMP-7 than PC/CV cells that express no detectable thymidine phosphorylase. Taken together these data indicate that thymidine phosphorylase enhances the invasion of tumor cells through the induction of invasion-related genes.

Contact: Department of Urology, Field of Oncology, Course of Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8520, Japan.

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