The Role of β-Catenin and c-Myc Dysregulation in Acute Myeloid Leukemia: A Study of Egyptian Patients

Acute Myeloid Leukemia (AML) is a treatable but aggressive hematologic malignancy attributed to both genetic and epigenetic mutations in hematopoietic stem cells (HSCs). The disease is highly genetically heterogeneous with mutations in important genes like FLT3, NPM1 and TP53. Wnt/β-catenin dysregulated signaling pathways3839 are implicated in the majority of AML pathogenesis as they promote tumor progression and cancer stem cell-like properties also inhibit normal haemopoiesis. One of the crucial mediators of Wnt pathway, β-catenin plays a pivotal role in regulating HSC self-renewal, differentiation, and expression of oncogenes such as c-Myc. Dysregulation of c-Myc, often observed in AML, is associated with poor prognosis and chemoresistance.The present study aimed to investigate the expression of β-catenin and c-Myc mRNA in Egyptian patients with acute myeloid leukemia (AML), and its relationship to clinical parameters as well as AML subtypes. Clinical characteristics of AML patients were analyzed in our cohort relative to healthy controls, we demonstrated that kidney and liver dysfunction were frequent manifestations among AML patients which showed significantly higher serum creatinine, urea, ALT and AST levels compared with healthy individuals.Plasma β-catenin levels were significantly lower in AML patients, particularly in the M4/M5 subtypes characterized by monocytic differentiation. In contrast, no significant difference in β-catenin levels was observed between M0-M2 subtypes and controls. Age and FAB subtypes influenced β-catenin levels, with lower levels common in middle-aged patients (30–45 years) and the M5 subtype, while higher levels were associated with younger patients (18–30 years) and the M1 subtype.Expression of c-Myc mRNA did not differ significantly between overall AML patients and controls. However, subgroup analysis revealed substantially lower c-Myc expression in M4/M5 subtypes compared to M0-M2 subtypes and controls