KRAS sound was common in the tumors but only present in a single cell line, SKOV 8. SKOV 8 cells did express high levels of RAS GTP and were MEK dependent, and their reaction to MEK and AKT inhibitors was just like those of the OVCAR 5 cell line, which conveys IPA-3 concentration a KRAS G12V allele, a mutation present in significantly less than a huge number of serous ovarian cancers. Differences between KRAS amplification and mutation, however, may become apparent with further research and thus it’d be inappropriate to take into account OVCAR 5 as a representative model for the larger cohort of RAS modified ovarian tumors, most of which exhibit amplification of wild type KRAS. In summary, the data suggest that the currently available ovarian cancer cell lines only modestly reveal the genomic complexity of the human condition and that a panel of ovarian cancer cell lines with multiple representative examples derived from each genetic class is necessary. Our integrated evaluation of the cell line and tumor screen also shows the problem of using range based copy number data to recognize those patients with functional gene amplifications and deletions. Plastid In case of PTEN, copy number status as won by either the GISTIC or RAE methods correlated strongly with PTEN mRNA expression. Further, PTEN copynumber natural or homozygous deletion calls were excellent predictors of the presence or loss in PTEN protein and levels of p AKT expression by immunohistochemistry and reverse phase protein arrays. However, hemizygous loss of the PTEN gene didn’t easily correlate with functional loss of PTEN protein expression by IHC or downregulation of PTEN mRNA expression. These declare that in lack of homozygous deletion, content number data alone was inadequate to accurately characterize PTEN status. A heterogeneous ATP-competitive Aurora Kinase inhibitor pattern of PTEN expression by IHC was also common suggesting that clonal heterogeneity will prove to be one more hurdle to the use of array based platforms to precisely identify tumors with functional loss of PTEN. In summary, our data suggest that the game of AKT inhibitors will be restricted to tumors harboring genomic changes inside the pathway and that combination therapy will be asked to elicit a tumefaction response or regression in many tumors. On the basis of those data, we anticipate a low response rate with when such agents are used alone in ovarian cancers particular AKT process inhibitors. This fact might warrant the development of such substances originally in cohorts of patients from other cyst lineages in which the frequency of defined PI3K/AKT path alterations is high.