AI Article Synopsis
- Acute myeloid leukemia (AML) is a serious blood cancer with a complex genetic background, particularly affecting children through specific gene rearrangements associated with poor treatment outcomes.
- * In AML, translocations involving the NUP98 gene create fusion proteins that disrupt normal cell functions, leading to abnormal cell growth and structure.
- * This review explores the roles of NUP98 fusion proteins in AML and discusses potential new treatment strategies targeting these specific genetic alterations.
Article Abstract
Acute myeloid leukemia (AML) is an aggressive hematological malignancy with a heterogeneous molecular landscape. In the pediatric context, the gene is a frequent target of chromosomal rearrangements that are linked to poor prognosis and unfavorable treatment outcomes in different AML subtypes. The translocations fuse to a diverse array of partner genes, resulting in fusion proteins with novel functions. NUP98 fusion oncoproteins induce aberrant biomolecular condensation, abnormal gene expression programs, and re-wired protein interactions which ultimately cause alterations in the cell cycle and changes in cellular structures, all of which contribute to leukemia development. The extent of these effects is steered by the functional domains of the fusion partners and the influence of concomitant somatic mutations. In this review, we discuss the complex characteristics of NUP98 fusion proteins and potential novel therapeutic approaches for NUP98 fusion-driven AML.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11423334 | PMC |
| http://dx.doi.org/10.1002/hem3.70013 | DOI Listing |
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