Ions of other genes, may be of 104 Side CCI-779 Temsirolimus effects. It’s worth the idea that the sample explained after three months of therapy, a Gro Part of the side effects Ren k Nnte were collected. The closing date t the early androgen responsive genes and found that the long-term targets AR. In addition, ARBSs derived H3K4 methylation and gene expression data by DHT stimulation models of prostate cancer cell lines. Thus, it is m Possible that some of these genes can be the direct targets AR 104 in prostate tissues. Momomethylation H3K4 has been shown that the binding of transcription enhancers, and demethylation with TSS and two amplifier Assigned AMPLIFIERS. In this study we used data from the methylation of histone two independent Identify studies ngigen m Possible areas of the amplifier to Rkers. Although areas of potential activators were found, they are not strictly regulate the expression of the gene N Chsten, and thus the possibility M Of false positives and false negatives exist. A reporter and analyzed chromatin conformation could reliably identify, precious metals, to correct the areas of target genes enhancer. Sun reliably To recognize SSIG AR target genes, we combined the data of methylation with ARBS and DHT-induced expression of data. Since the endocrine treatment is not curative and closing the disease Lich f Filled, we examined genes downregulated after endocrine therapy and reactivated at the level of castration are. These genes have k Nnten potential biomarkers for response to hormonal treatment. We found a trend toward increased Hten TMEFF2 and DHCR24 expression and a significant overexpression of TPD52 and NEDD4L in CRPC when compared to F Ll of BPH. The expression of TPD52, DHCR24 and TMEFF2 havepreviously has been shown that androgen-regulated. In addition, NEDD4L has brought in AR signaling in combination. In addition, the expression of TPD52 and TMEFF2 were shown, increases are ht, especially in CRPC in prostate cancer. We also assessed the influence of the TMPRSS2: ERG fusion gene expression in both untreated and treated F ll the endocrine system. It seems that the ERG-sensitized cells to hormone therapy, because the genes were 8.7 times more displaced NgTE after endocrine therapy in F cases, Compared to F Cases, F F. Both ERGBSs ARBSs and were significantly regions near genes enriched suppressed. It is noteworthy that the majority of the repressed genes have the same genes whose expression was observed in cases F, Compared to FF case in the control group increased Ht. Therefore, the endocrine therapy, especially the genes cases high in the F, F were expressed affected and reduced the differences between tumors and F. F. It has been found that increased expression of ERG by androgens in the cell line VCAP ht is. This may also in our data with an increased Hten expression of putative target genes in ERG F Cases in Group F to see the hormone did ï contr The fifth. In our data reduce the endocrine treatment, the expression of genes in 601 F F cases, but only 69 genes in F. These 601 genes are likely direct targets of ERG, because the nature of androgen-dependent Ngigen expression makes the TMPRSS2 gene under control The molten ERG. Tats Chlich had 86% of these genes ERGBS their TSS on the northern chsten.