Abstract CN01-01: Genetic and epigenetic changes in prostate cancer as targets for prevention

CN01-01

Prostate cancer cells are known to carry a variety of genetic defects, including gene translocations (eg. TMPRSS-ERG1), amplifications (eg. AR), mutations, and deletions. These changes are thought to endow the prostate cancer cells with new capabilities for dysregulated proliferation, inappropriate survival, tissue invasion and destruction, immune system evasion, and metastasis. In addition, cancer cells also carry epigenetic defects, manifest as changes in CpG dinucleotide methylation patterns and in chromatin structure and organization (eg. at GSTP1 and many others), which are equivalent to genetic changes in promoting malignant phenotypes. During the pathogenesis of prostate cancer, the somatic epigenetic alterations tend appear earlier during cancer development than genetic changes, as well as more commonly and consistently. For this presentation, new data concerning the mechanism(s) by which androgen action might promote translocations at AR target genes, and by which inflammatory processes might trigger CpG island hypermethylation, in prostate cells will be presented. These new insights into the formation of somatic genetic and epigenetic changes will provide new molecular biomarkers to aid in prostate cancer detection and diagnosis, and may lead to new opportunities for prostate cancer prevention and treatment.

Citation Information: Cancer Prev Res 2008;1(7 Suppl):CN01-01.