Dissecting the transcriptional regulation of infant and childhood acute myeloid leukemia

Abstract

Pediatric acute myeloid leukemia (AML) exhibits distinct characteristics between infants and children, manifested by variations in clinical features, cytogenetic abnormalities, and molecular aberrations. While most studies have focused on the associations between genomic abnormalities, age groups, and disease status, the transcriptional profiles and gene regulatory mechanisms underlying these differences remain underexplored. In this study, through differential gene expression analysis and Weighted Gene Co-expression Network Analysis, I have identified gene groups associated with AML and further categorized them by infant and childhood subgroups. The findings reveal three distinct gene groups with age- and tissue-specific expression patterns. Additionally, I propose a gene regulatory circuitry that elucidates the differences between infant and childhood AML. Several novel markers demonstrating significant expression changes in tumors were identified. Moreover, a comprehensive gene regulatory network for pediatric AML was constructed using differentially expressed transcription factors and protein-gene interaction data. This study highlights new gene regulation mechanisms in pediatric AML and offers potential avenues for developing novel biomarkers and therapeutic strategies.