ArticlePLoS genetics2022
Understanding a high-risk acute myeloid leukemia by analyzing the interactome of its major driver mutation.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- DEK facilitates bortezomib resistance of multiple myeloma by modulating ferroptosis.Clinical and experimental medicine · 2025Article
- DEK-nucleosome structure shows DEK modulates H3K27me3 and stem cell fate.Nature structural & molecular biology · 2025Article
- XPO1-dependency of DEK::NUP214 leukemia.Leukemia · 2025Article
- Bioinformatics analysis identifies ZBTB16 as a potential immune biomarker for lung cancer and pan-cancer.Frontiers in genetics · 2025Article
- DEK regulates B-cell proliferative capacity and is associated with aggressive disease in low-grade B-cell lymphomas.Blood cancer journal · 2024Article
- The Role of Epithelial-to-Mesenchymal Transition Transcription Factors (EMT-TFs) in Acute Myeloid Leukemia Progression.Biomedicines · 2024Review
- The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia.Experimental hematology · 2023Review
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The WHO classifies t(6;9)-positive acute myeloid leukemia (AML) as a subgroup of high-risk AML because of its clinical and biological peculiarities, such as young age and therapy resistance. t(6;9) encodes the DEK/NUP214 fusion oncoprotein that targets only a small subpopulation of bone marrow progenitors for leukemic transformation. This distinguishes DEK/NUP214 from other fusion oncoproteins, such as PML/RARα, RUNX1/ETO, or MLL/AF9, which have a broad target population they block differentiation and increase stem cell capacity. A common theme among most leukemogenic fusion proteins is their aberrant localization compared to their wild-type counterparts. Although the actual consequences are widely unknown, it seems to contribute to leukemogenesis most likely by a sequester of interaction partners. Thus, we applied a global approach to studying the consequences of the aberrant localization of t(6;9)-DEK/NUP214 for its interactome. This study aimed to disclose the role of localization of DEK/NUP214 and the related sequester of proteins interacting with DEK/NUP214 for the determination of the biology of t(6;9)-AML. Here we show the complexity of the biological consequences of the expression of DEK/NUP214 by an in-depth bioinformatic analysis of the interactome of DEK/NUP214 and its biologically dead mutants. DEK/NUP214's interactome points to an essential role for aberrant RNA-regulation and aberrant regulation of apoptosis and leukocyte activation as a significant determinant of the phenotype of t(6;9)-AML. Taken together, we provide evidence that the interactome contributes to the aberrant biology of an oncoprotein, providing opportunities for developing novel targeted therapy approaches.
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