Acute myeloid leukemia (AML) is the progenitor and hematopoietic stem cell blood cancer. Chromosomal abnormalities include balanced translocations between two chromosomes like t[8;21] and t[15;17]) in malignant cells. The current study aimed to investigate AML with leukopenia and gene expression changes in high-white and low-white counts B-cell. The total number of samples used was ten. The raw gene expression profiles (ID: GSE20482) of bone marrow obtained from AML patients showed five high-white counts B-cell and five low-white counts B-cell expressed genes differentially expressed. Genes that corresponded to official gene symbols were selected for protein-protein interaction (PPI) and sub-network construction (score > 0.4). In addition, functional annotation of gene ontology (GO) and pathway analysis were performed for the genes involved in networking.
A total of 846 genes were identified as differentially expressed, and 406 genes were upregulated; and another 440 genes were downregulated. The remaining 14 genes that interacted with each other were significantly identified. The hub genes GNB4, LAMTOR2, ACTN4, HGSNAT, and TMED1 were upregulated while the downregulated DEGs forming hub nodes were UBR4, FBXO30, KLHL21, DCTN6, RNF123, RNF114. AML significantly affects the expression of genes involved in cell differentiation, apoptosis, cell signaling, and protein modification. AML cells enter the blood quickly and spread to the liver, spleen, and central nervous system. These are a total of thirteen pathways. They were enriched, and AML was found to significantly impact genes involved in oxidative phosphorylation, actin cytoskeleton regulation, endocytosis, phagocytosis, shigellosis, and epithelial cell signaling in helicobacter, adherent junction, pertussis, bile secretion, malaria, and African trypanosomiasis.
Hub genes like GNB4 and UBR4 provide a novel biomarker in AML.