ArticleExperimental hematology2012
Gene expression profiling and candidate gene resequencing identifies pathways and mutations important for malignant transformation caused by leukemogenic fusion genes.
Article in Experimental hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Ptpn1 deficiency collaborates with a NUP98::HOXD13 fusion gene to generate B cell precursor acute lymphoblastic leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Disruption of normal stem cell function and transmission of myelodysplastic syndrome by self-renewal of committed myeloid lineage cells.Stem cell reports · 2025Article
- Evaluation of HOTAIRM1, miR-196b, and HOXA9 as Oncogenic Markers in Patients with Acute Myeloblastic Leukemia.Iranian journal of pathology · 2025Article
- Therapeutic targeting in pediatric acute myeloid leukemia with aberrant HOX/MEIS1 expression.European journal of medical genetics · 2023Review
- Childhood acute myeloid leukemia with 5q deletion and HNRNPH1-MLLT10 fusion: the first case report.Blood advances · 2022Article
- Review
- Acute Myelogenous Leukemia with the t(7;7)(p15;p22) Translocation, a Novel Simple Variant of t(7;11)(p15;p15) Translocation: First Description.Case reports in hematology · 2021Article
- Article
- PBX3 in Cancer.Cancers · 2020Review
- Direct and Indirect Targeting of HOXA9 Transcription Factor in Acute Myeloid Leukemia.Cancers · 2019Review
- Somatic mutations in murine models of leukemia and lymphoma: Disease specificity and clinical relevance.Genes, chromosomes & cancer · 2017Article
- Deregulation of the HOXA9/MEIS1 axis in acute leukemia.Current opinion in hematology · 2016Review
- The target cell of transformation is distinct from the leukemia stem cell in murine CALM/AF10 leukemia models.Leukemia · 2016Article
- Review
- PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells.Nature communications · 2015Article
- C/EBPα is an essential collaborator in Hoxa9/Meis1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The fusion partner specifies the oncogenic potential of NUP98 fusion proteins.Leukemia research · 2013Article
- Isolated Hoxa9 overexpression predisposes to the development of lymphoid but not myeloid leukemia.Experimental hematology · 2013Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
NUP98-HOXD13 (NHD13) and CALM-AF10 (CA10) are oncogenic fusion proteins produced by recurrent chromosomal translocations in patients with acute myeloid leukemia (AML). Transgenic mice that express these fusions develop AML with a long latency and incomplete penetrance, suggesting that collaborating genetic events are required for leukemic transformation. We employed genetic techniques to identify both preleukemic abnormalities in healthy transgenic mice as well as collaborating events leading to leukemic transformation. Candidate gene resequencing revealed that 6 of 27 (22%) CA10 AMLs spontaneously acquired a Ras pathway mutation and 8 of 27 (30%) acquired an Flt3 mutation. Two CA10 AMLs acquired an Flt3 internal-tandem duplication, demonstrating that these mutations can be acquired in murine as well as human AML. Gene expression profiles revealed a marked upregulation of Hox genes, particularly Hoxa5, Hoxa9, and Hoxa10 in both NHD13 and CA10 mice. Furthermore, mir196b, which is embedded within the Hoxa locus, was overexpressed in both CA10 and NHD13 samples. In contrast, the Hox cofactors Meis1 and Pbx3 were differentially expressed; Meis1 was increased in CA10 AMLs but not NHD13 AMLs, whereas Pbx3 was consistently increased in NHD13 but not CA10 AMLs. Silencing of Pbx3 in NHD13 cells led to decreased proliferation, increased apoptosis, and decreased colony formation in vitro, suggesting a previously unexpected role for Pbx3 in leukemic transformation.
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