FGFR1 and WT1 are markers of human prostate cancer progression.

Elizabeth Devilard,Catherine Nguyen,Luc Xerri,Franck Bladou,Olivier Ramuz,François Bertucci,Gwenaëlle Gravis,Gilles Karsenty,Daniel Birnbaum,Jean-Philippe Dalès

doi:10.1186/1471-2407-6-272

Abstract

BackgroundAndrogen-independent prostate adenocarcinomas are responsible for about 6% of overall cancer deaths in men.MethodsWe used DNA microarrays to identify genes related to the transition between androgen-dependent and androgen-independent stages in the LuCaP 23.1 xenograft model of prostate adenocarcinoma. The expression of the proteins encoded by these genes was then assessed by immunohistochemistry on tissue microarrays (TMA) including human prostate carcinoma samples issued from 85 patients who had undergone radical prostatectomy.ResultsFGFR1, TACC1 and WT1 gene expression levels were associated with the androgen-independent stage in xenografts and human prostate carcinoma samples. MART1 protein expression was correlated with pT2 tumor stages.ConclusionOur results suggest that each of these four genes may play a role, or at least reflect a stage of prostate carcinoma growth/development/progression.

Highlights

Androgen-independent prostate adenocarcinomas are responsible for about 6% of overall cancer deaths in men
Most genes were expressed at the same level in hormone sensitive (HS) and hormone refractory (HR) stages, FGFR1 was clearly overexpressed in HR stage (Figure 1C)
Using three methods of analysis (DNA microarrays, tissue microarrays (TMA), and reverse-transcribed PCR (RT-PCR)), we have shown that FGFR1, TACC1 and WT1 have much higher levels of expression in human prostate carcinoma than in benign prostate tissue samples, at both mRNA and protein levels

Summary

Introduction

Androgen-independent prostate adenocarcinomas are responsible for about 6% of overall cancer deaths in men. Prostate adenocarcinoma is the most common cancer in men in western countries, and is responsible for about 6% of overall cancer deaths [1]. Tumor growth is dependent on androgen stimulus and androgen ablation may be used as a complementary therapy. The tumor progresses to an androgen-independent stage against which hormone therapy has no effect. There is no effective therapy against androgen-independent prostate cancer. GSTP1, PTEN, TP53, and androgen receptor (AR) are mutated or deregulated in sporadic prostate cancer [5] and may become targets for innovative therapies. Little is known about the progression from androgen-dependent to androgen-independent stages [2]

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Discussion

Conclusion