The complete coding region of AURORA A was sequenced in most breast cancer lines shown in Figure 3A. However, three cell lines showed the increasing loss of one copy of the Aurora A gene, just like the situation noticed in tumors from p53 mice. All three tumors showing decreased copy number also had low levels of AURORA A protein, as did some tumors with typical gene copy number. We conclude that some human breast Enzalutamide manufacturer cancers display reduced gene copy number and protein levels of Aurora A, like the lymphomas from p53 mice. Obviously, these human cancers cannot have developed from p53 normal cells, but it can be done that mutations ultimately causing loss of p53 function occurred fairly early in the tumorigenesis process, exerting selective pressure for loss rather than gain of Aurora A. As was also observed for the mouse tumors, no mutations were discovered which may affect the conclusions from these experiments. As it has demonstrated an ability that genetic changes at the Aurora A locus in mouse lymphomas were p53 dependent, we examined the relationship between the quantities of P53 and AURORA A in human breast cancer cell lines by Affymetrix microarray evaluation Organism and western blotting. Genome large expression array analysis using the Affymetrix platform has been carried out on a large section of human breast cancer cell lines. Evaluation of these variety data showed that there clearly was a statistically significant relationship between the RNA levels of AURORA A and protein levels of p53. Cyst cell lines were separated in to two groups based on the presence or absence of p53 detectable by western blotting. The association between p53 protein status and Aurora A RNA levels was statistically significant Celecoxib price using two separate probe sets for Aurora A. We also found a significant association between AURORA A and P53 at the protein level. Western blotting using AURORA A antibodies demonstrated a substantial relationship between RNA expression and protein levels. The info indicated that p53 good tumors, as defined in the Experimental Procedures, had on average greater levels of Aurora A than tumors with low levels of p53. Eventually, we sought out further confirmation of the observations in a independent group of Affymetrix RNA expression array information on primary breast cancers. Although western blots of the tumors for p53 were not available, there clearly was a very significant association between tumors designated as p53 positive or negative by immunohistochemistry and RNA levels of AURORA A. In spite of the complexity of genetic changes in human tumors, as opposed to the controlled condition investigated in the mouse, we conclude that quantities of p53 and AURORA A are somewhat correlated in human breast cancer cell lines and primary tumors.