ArticleOncogene2016
Transformation of human CD34+ hematopoietic progenitor cells with DEK-NUP214 induces AML in an immunocompromised mouse model.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Rapid epigenomic classification of acute leukemia.Nature genetics · 2025Article
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Structural insights into how DEK nucleosome binding facilitates H3K27 trimethylation in chromatin.Nature structural & molecular biology · 2025Article
- XPO1-dependency of DEK::NUP214 leukemia.Leukemia · 2025Article
- The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia.Experimental hematology · 2023Review
- Progress in construction of mouse models to investigate the pathogenesis and immune therapy of human hematological malignancy.Frontiers in immunology · 2023Review
- Molecular Classification and Overcoming Therapy Resistance for Acute Myeloid Leukemia with Adverse Genetic Factors.International journal of molecular sciences · 2022Review
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- DEK-AFF2 fusion-associated papillary squamous cell carcinoma of the sinonasal tract: clinicopathologic characterization of seven cases with deceptively bland morphology.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Acute Myeloid Leukemia in Children: Emerging Paradigms in Genetics and New Approaches to Therapy.Current oncology reports · 2021Review
- MG132 inhibits the expression of PBX3 through miRNAs by targeting Argonaute2 in hepatoma cells.Saudi journal of biological sciences · 2020Article
- KLF1/EKLF expression in acute leukemia is correlated with chromosomal abnormalities.Blood cells, molecules & diseases · 2020Article
- Humanized mouse models of genetic immune disorders and hematological malignancies.Biochemical pharmacology · 2020Review
- The genomics of acute myeloid leukemia in children.Cancer metastasis reviews · 2020Review
- The SQSTM1-NUP214 fusion protein interacts with Crm1, activates Hoxa and Meis1 genes, and drives leukemogenesis in mice.PloS one · 2020Article
- Immunogenic neoantigens derived from gene fusions stimulate T cell responses.Nature medicine · 2019Article
- NUP214 in Leukemia: It's More than Transport.Cells · 2019Review
- Myeloid Disease Mutations of Splicing Factor SRSF2 Cause G2-M Arrest and Skewed Differentiation of Human Hematopoietic Stem and Progenitor Cells.Stem cells (Dayton, Ohio) · 2018Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Acute myeloid leukemia (AML) is a heterogeneous disease comprising a large number of subtypes defined by specific chromosome abnormalities. One such subtype carries the t(6;9)(p22;q34) chromosome rearrangement, which leads to expression of the DEK-NUP214 chimeric gene, and has a particularly poor outcome. To provide a better understanding of the molecular etiology of these relatively rare individual AML variants, it is necessary to generate in vivo models, which can also serve as a means to evaluate targeted therapies based on their specific genetic abnormalities. Here, we describe the development of a human cell AML, generated in CD34+ human hematopoietic progenitor cells xenografted into immunocompromised mice that express human myeloid cell growth factors. Within 6 months, these mice develop a human cell AML with phenotypic characteristics of the primary t(6;9) disease and a CD45+CD13+CD34+CD38+ immunophenotype. Gene expression studies show that members of the HOX family of genes (HOXA9, 10, B3, B4 and PBX3) are highly upregulated in the AML from this mouse model as well as from primary human t(6;9) AML. Gene expression analysis also identified several other significantly disregulated pathways involving KRAS, BRCA1 and ALK, for example. This is the first report of a humanized model of the DEK-NUP214 disease and provides a means to study the development and treatment of this particular subtype of AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.