KMT2A-rearranged pediatric acute myeloid leukemia (KMT2A-r pAML) is a diverse and clinically challenging leukemia. KMT2A, a transcriptional co-activator that modifies histones, is involved in gene fusions with more than 80 KMT2A partners. Of these, MLLT3, MLLT10, ELL, MLLT4 and MLLT1 account for ~70% of pAML cases. This diversity correlates with a range of clinical outcomes, with different rearrangement partners stratified into different risk categories. The mechanisms driving differences in treatment response remain under study. We aim to analyze the gene regulatory networks associated with KMT2A rearrangement partners at diagnosis and relapse. By comparing these networks at the single-cell level, we seek to understand whether different rearrangement partners manifest distinct gene regulatory networks, whether these networks converge on one or several pathways, how different rearrangement partners might influence treatment response, and whether modulating regulatory networks can shape responses, ideally leading to future improvements in patient outcomes.
Single-cell Multi-omic Analyses to Identify and Characterize Cell Populations in Patients with Primary and Relapsed Pediatric Acute Myeloid Leukemia
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