ArticleThe EMBO journal1998
Hoxa9 transforms primary bone marrow cells through specific collaboration with Meis1a but not Pbx1b.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 337 papers.
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Who cites it
337 citing papers in PubMed, 637 citations in OpenAlex.
- Trial
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- Targeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.International journal of cancer · 2026Review
- Posttranscriptional activity of eIF4E contributes to HoxA9-driven leukemogenesis.Blood neoplasia · 2025Article
- KMT2A-rearranged leukemia: from mechanism to drug development.Experimental hematology · 2025Review
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- The proto-oncogenic miR-106a-363 cluster enhances adverse risk acute myeloid leukemia through mitochondrial activation.Leukemia · 2025Article
- Transcriptomic characterisation of acute myeloid leukemia cell lines bearing the same t(9;11) driver mutation reveals different molecular signatures.BMC genomics · 2025Article
- The role of tribbles homolog 2 in cell proliferation.Cell communication and signaling : CCS · 2025Review
- The E3 ubiquitin ligase Herc1 modulates the response to nucleoside analogs in acute myeloid leukemia.Blood advances · 2024Article
- PHF6 suppresses self-renewal of leukemic stem cells in AML.Leukemia · 2024Article
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- Regulation of HOX gene expression in AML.Blood cancer journal · 2024Review
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- PHF6 suppresses self-renewal of leukemic stem cells in AML.bioRxiv : the preprint server for biology · 2024Article
- Twist family BHLH transcription factor 1 is required for the maintenance of leukemia stem cell in MLL-AF9Haematologica · 2024Article
277 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hoxa9, Meis1 and Pbx1 encode homeodomaincontaining proteins implicated in leukemic transformation in both mice and humans. Hoxa9, Meis1 and Pbx1 proteins have been shown to physically interact with each other, as Hoxa9 cooperatively binds consensus DNA sequences with Meis1 and with Pbx1, while Meis1 and Pbx1 form heterodimers in both the presence and absence of DNA. In this study, we sought to determine if Hoxa9 could transform hemopoietic cells in collaboration with either Pbx1 or Meis1. Primary bone marrow cells, retrovirally engineered to overexpress Hoxa9 and Meis1a simultaneously, induced growth factor-dependent oligoclonal acute myeloid leukemia in <3 months when transplanted into syngenic mice. In contrast, overexpression of Hoxa9, Meis1a or Pbx1b alone, or the combination of Hoxa9 and Pbx1b failed to transform these cells acutely within 6 months post-transplantation. Similar results were obtained when FDC-P1 cells, engineered to overexpress these genes, were transplanted to syngenic recipients. Thus, these studies demonstrate a selective collaboration between a member of the Hox family and one of its DNA-binding partners in transformation of hemopoietic cells.
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