The HemAtlas 2.0 project embarks on a groundbreaking multi-omics journey to unravel
the complexities of pediatric acute myeloid leukemia (AML), incorporating a diverse
range of 241 pediatric cases plus 158 healthy donor samples, representing the normal
hematopoiesis. Integrating genomic, transcriptomic, and epigenetic data with clinical
insights, our work advances AML subtype classification and elucidates the impact of
somatic mutations on prognosis, especially impacting overall and event-free survival.
This integration highlights the importance of mutational networks over individual
aberrations in disease progression and therapeutic response. Through Multi-Omics Factor
Analysis (MOFA), we uncover intricate molecular interactions that define AML's
heterogeneity. This provides deep insights into AML's pathogenesis identifying
therapy targets. Our findings underscore the benefits of multi-omics integration in
enhancing disease understanding, improving classification and prognosis, and paving
the way for precision oncology in AML. The HemAtlas 2.0 project highlights the potential
of combining diverse omic layers and clinical data to refine patient care strategies.
