TCGA competent samples had at the very least one modification within the RAS or PI3K/AKT pathways or within RB1. Nevertheless, as opposed to the cell lines where point mutations in these pathway genes were predominant, copy number changes dominated the gene alterations found in the primary tumors. For example, primary ovarian met inhibitor tumors usually harbored amplification activities encompassing the BRAF, KRAS, and PIK3CA loci, while mutations in these genes were rarely observed. We evaluated the mRNA expression of select genes as a function of copy number status, to further define the importance of the gene amplifications recognized. KRAS and BRAF amplifications were usually major events and highly correlated with mRNA overexpression. as modified at the PIK3CA locus generally exhibited broader gains in 3q though tumors classified, the clear presence of gene amplification neuroendocrine system still strongly correlated with overexpression of the PIK3CA gene product. On the other hand, there was no strict correlation between AKT3 mRNA overexpression and the degree of amplification, nor were there any focal AKT3 amplification events. Improved AKT3 mRNA appearance, nevertheless, was noticed in 80x-speed of tumors, including those recognized as diploid in the AKT3 locus. This implies that gene amplification isn’t the main determinant of AKT3 expression in serous ovarian cancers. This does not hold true for AKT2, for which focal amplification was popular and strongly correlated with mRNA overexpression. Therefore, while AKT2 overexpression is secondary to a genetic function in certain ovarian cancers, the etiology of AKT3 overexpression is unknown and may be caused by yet to be elucidated epigenetic factors. Among the removal events present in the TCGA dataset, homozygous loss of PTEN, RB1, and NF1 were common. These deletions were generally central and were clearly related to loss in mRNA expression in every three instances. We assessed PTEN expression and AKT activation deubiquitination assay by immunohistochemistry in 52 of the 316 TCGA tumors and correlated these with GISTIC based genotype calls and mRNA expression, to gain insight into the functional relevance of these activities. In ten of 52 cancers, PTEN protein expression was absent in most areas of the tumor. All 8 of those cases demonstrated PTEN copy number loss, with 5 as homozygous deleted by three and GISTIC as hemizygous loss in the PTEN locus scored. Of the latter 3, one taste harbored a frameshift mutation in PTEN. Six of the 8 tumors had correspondingly paid down log2 mRNA values less-than 1. 2. Consistent with the IHC information, PTEN homozygous removal was also associated with low protein levels by reverse phase proteomic selection analysis. High degrees of AKT phosphorylation by IHC and by RPPA research also linked with PTEN homozygous deletion. On the other hand, notably lower levels of AKT phosphorylation were found in PTEN diploid/gain cohorts and the PTENhemizygous reduction, with no big difference found between these latter two groups.