p53 is cytoplasmically sequestered in a subset of AML patients from a clinical population

Although healthy human white blood cells may become cancerous, molecular mechanisms exist to combat neoplasia. In this study, we investigate a clinical population of human acute myologenous leukemia cells (AML). In healthy white blood cells, the transcription factor p53 resides in the cytoplasm of blood cells where it translocates to the nucleus and induces apoptosis (programmed cellular death), thereby removing neoplastic cells. This defense keeps cancerous cells from proliferating and forming diffuse blood tumors or leukemia. In many cancerous cells, wild type p53 is sequestered in the cytoplasm and cannot move into the nucleus and promote apoptosis. Here we investigate samples from AML patients. Our research attempts to verify where p53 resides within the cells. This is accomplished by reanimation of the patient samples, separation of the cytoplasmic and nucleic fractions, running Western blots on these fractions using a monoclonal antibody for p53 and using immunocytochemistry to localize p53 within these AML cells. Previous studies in the lab show that p53 is sequestered in the cytoplasm in 46% of the patient samples. This defines a subset of AML patients with cytoplasmically sequestered p53. We are also investigating the role of the mitochondrial Hsp70 protein as a protein anchor involved in sequestration of p53