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Mixed-lineage leukemia (MLL) oncoproteins drive distinct leukemia programs. Dynamic chromatin binding by MLL oncoproteins may promote lineage switching and resistance to menin inhibitors.

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Area of Science:

  • * Hematologic Oncology
  • * Molecular Biology
  • * Gene Regulation

Background:

  • * Chromosomal translocations involving the mixed-lineage leukemia (MLL) locus produce potent oncogenic fusion proteins (oncoproteins).
  • * These MLL oncoproteins disrupt the regulation of developmental gene expression, leading to leukemia.
  • * The specific fusion partner influences the oncoprotein's target binding and oncogenic potential.

Purpose of the Study:

  • * To investigate the genomic enrichment and dynamic regulation of MLL oncoprotein-target sites in MLL-rearranged leukemia.
  • * To understand how MLL oncoproteins activate distinct acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML) programs.
  • * To explore the role of MLL oncoproteins in therapy-induced lineage switching and potential resistance mechanisms.

Main Methods:

  • * Profiling of oncoprotein-target sites in 36 MLL-rearranged leukemia samples.
  • * Analysis of samples with therapy-induced lymphoid-to-myeloid lineage switching.
  • * Assessment of oncoprotein levels and chromatin occupancy in relation to gene expression programs.

Main Results:

  • * MLL oncoprotein genomic enrichment is highly variable and dynamically regulated between samples.
  • * High oncoprotein levels activate either ALL (pro-B-cell genes) or AML (hematopoietic stem cell genes) programs, correlating with fusion partner prevalence.
  • * Lineage-switching samples show reduced oncoprotein levels and preferential activation of granulocyte-monocyte progenitor (GMP) genes.
  • * In one case, ENL persisted on target loci despite undetectable oncoprotein and menin levels during revumenib treatment.

Conclusions:

  • * MLL oncoproteins promote lineage-switching events via dynamic chromatin binding at lineage-specific target genes.
  • * Changes in chromatin occupancy may contribute to resistance against menin inhibitors.
  • * Understanding these mechanisms is crucial for developing targeted therapies for MLL-rearranged leukemias.