There are many possible alternative methods and thresholds for defining the oncogenic signatures that might have been used and which could have been considered equally valid. The author believes that any reasonable analytic approach for defining signatures that yielded numbers of genes comparable to those in Table 2 would have resulted in the same overall patterns of enrichment being observed between the signatures and the human tumors. In this study, several gene signatures of oncogenic pathways defined experimentally were found to be coordinately expressed with the single oncogene or biomarker corresponding to the pathway in human prostate tumors. These results demonstrate these signatures to be relevant to the study of human prostate cancer. These findings apply BKM120 PI3K inhibitor mainly for the sets of genes upregulated in the signatures, as the down-regulated genes by and large did not show expected correlation patterns. The gene-to-signature correlations of interest were observed in three of the four prostate tumor profiles datasets, but none were found in all four. The fact that no consistent patterns were found in all four datasets is curious but could be explained by a number of reasons, which could range from the technical to the biological. It should be emphasized that any association made between a gene and its corresponding signature for any one dataset was quite robust, the significance values testing against 1000 randomly-generated gene signature and 1000 permutations of the reference oncogene values. This study does underscore the value of the metaanalysis approach, as patterns that may be missed in one profile dataset could be repeatedly found in other datasets. In general, experimental data might be expected to show changes in gene expression that are merely artifacts of the model system, while human tumor data alone can show patterns of correlation but do not readily demonstrate cause-and-effect in the way experimental models can. For a given pathway, the intersection of the set of genes up-regulated by experimental activation of the pathway with the set of genes showing anticipated patterns of expression in human tumor tissue specimens would be a set of genes of potential interest to researchers. For the Myc, c- Src, HER2, EGFR, cyclin D1, Akt, and androgen pathways, this study provides the set of genes relevant to each pathway both experimentally and pathologically. Molecular biologists who study any one of these pathways may select candidate gene targets of these pathways uncovered by this study and validate the expression patterns both in experimental models and in human prostate tumor specimens. It is understood that a particular pathway may be Temozolomide company deregulated through a number of different genes, and so a measure of the ����end point���� of a signaling pathway at the transcription level may prove to be a better indicator of pathway deregulation over any single gene.