ArticleMolecular and cellular biology1999
The oncoprotein E2A-Pbx1a collaborates with Hoxa9 to acutely transform primary bone marrow cells.
Article in Molecular and cellular biology, 1999. 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, 78 citations in OpenAlex.
- A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene.PLoS genetics · 2021Article
- Oligomeric self-association contributes to E2A-PBX1-mediated oncogenesis.Scientific reports · 2019Article
- Comparative genomics reveals multistep pathogenesis of E2A-PBX1 acute lymphoblastic leukemia.The Journal of clinical investigation · 2015Article
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- Isolated Hoxa9 overexpression predisposes to the development of lymphoid but not myeloid leukemia.Experimental hematology · 2013Article
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- MYC and PIM2 co-expression in mouse bone marrow cells readily establishes permanent myeloid cell lines that can induce lethal myeloid sarcoma in vivo.Molecules and cells · 2012Article
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- Transformation by Tribbles homolog 2 (Trib2) requires both the Trib2 kinase domain and COP1 binding.Blood · 2010Article
- Novel methods to identify biologically relevant genes for leukemia and prostate cancer from gene expression profiles.BMC genomics · 2010Article
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- Review: genetic models of acute myeloid leukaemia.Oncogene · 2008Review
- Critical role for a single leucine residue in leukemia induction by E2A-PBX1.Molecular and cellular biology · 2006Article
- EN2 is a candidate oncogene in human breast cancer.Oncogene · 2005Article
- Animal models of acute myelogenous leukaemia - development, application and future perspectives.Leukemia · 2005Review
- High incidence of proviral integrations in the Hoxa locus in a new model of E2a-PBX1-induced B-cell leukemia.Genes & development · 2005Article
- Protein kinase C-mediated phosphorylation of the leukemia-associated HOXA9 protein impairs its DNA binding ability and induces myeloid differentiation.Molecular and cellular biology · 2004Article
- Differential and common leukemogenic potentials of multiple NUP98-Hox fusion proteins alone or with Meis1.Molecular and cellular biology · 2004Article
- A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A recurrent translocation between chromosome 1 (Pbx1) and 19 (E2A) leading to the expression of the E2A-Pbx1 fusion oncoprotein occurs in approximately 5 to 10% of acute leukemias in humans. It has been proposed that some of the oncogenic potential of E2A-Pbx1 could be mediated through heterocomplex formation with Hox proteins, which are also involved in human and mouse leukemias. To directly test this possibility, mouse bone marrow cells were engineered by retroviral gene transfer to overexpress E2A-Pbx1a together with Hoxa9. The results obtained demonstrated a strong synergistic interaction between E2A-Pbx1a and Hoxa9 in inducing growth factor-independent proliferation of transduced bone marrow cells in vitro and leukemic growth in vivo in only 39 +/- 2 days. The leukemic blasts which coexpress E2A-Pbx1a and Hoxa9 showed little differentiation and produced cytokines such as interleukin-3, granulocyte colony-stimulating factor, and Steel. Together, these studies demonstrate that the Hoxa9 and E2A-Pbx1a gene products collaborate to produce a highly aggressive acute leukemic disease.
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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.