Presentation description

Acute Myeloid Leukemia (AML), is one of the most common types of cancer in adults, effecting every 1 in 3 diagnosed with leukemia. AML causes rapid division of CMP (common myeloid progenitors) which negatively impacts one's level of functional erythrocytes and thrombocytes. The ubiquitin-proteasome system (UPS) plays a critical role in cancer by regulating the degradation of key proteins involved in cell cycle control, DNA repair, apoptosis, and signaling pathways, making it a crucial mechanism for maintaining cellular homeostasis and preventing tumor development and progression. The expression levels of various F-box ubiquitin E3 ligase correlates with patient survival in several types of cancer, suggesting a role in tumorigenesis. However, the role of FBXO28 in hematopoietic cancers and malignancies, namely AML, has not been studied extensively to this point. Previous research has shown that certain cytogenetics, primarily partial or complete deletions on chromosomes 5 and 7, have consistently poorer prognoses. The focus of this project is to assess the role of FBXO28 through the utilization of spin transfections, colony formation assays, flow cytometry, and western blots. We expect that under expression of FBXO28 will increase the likelihood of developing AML. Understanding how F-box expression influences the development and aggression of AML may serve as a point of therapeutic intervention to improve cancer treatments and therapies.