Shared Genetic and Regulatory Mechanisms in Acute Myeloid Leukaemia and Blast Crisis Chronic Myeloid Leukaemia

Acute Myeloid Leukemia (AML) and Blast Crisis Chronic Myeloid Leukemia (BC CML) share several clinical characteristics, including the accumulation of immature myeloid cells and disrupted hematopoiesis. Despite the similarities, the two diseases exhibit different genetic profiles, contributing to distinct disease progressions and therapeutic outcomes. In this study, we perform a comparative analysis using bioinformatics and systems biology approaches to explore shared and unique mutational signatures, transcriptional networks, and molecular regulators in AML and BC CML. Our analysis identifies 29 genes common to both diseases, which are involved in key biological processes such as cell proliferation, cell death regulation, and transcriptional control. A subsequent pathway enrichment highlights common pathways, including the PI3K-AKT signaling and cytokine-mediated signaling, that may contribute to disease progression and resistance to therapy. Additionally, we construct a protein-protein interaction network and a transcription factor-miRNA coregulatory network, revealing key hub genes such as TP53, RUNX1, and BCL2. These genes could be potential shared therapeutic targets for treating AML and BC CML. Therefore, our analysis offers insights into the molecular underpinnings of these aggressive hematological malignancies.