ArticleNature communications2019
Synthetic modeling reveals HOXB genes are critical for the initiation and maintenance of human leukemia.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Human iPSCs-based modeling unveils SETBP1 as a driver of chromatin rewiring in GATA2 deficiency.Nature communications · 2025Article
- NOTCH1 dimeric signaling is essential for T-cell leukemogenesis and leukemia maintenance.Blood · 2025Article
- Identification and validation ofFrontiers in immunology · 2025Article
- The circadian clock circuitry modulates leukemia initiating cell activity in T-cell acute lymphoblastic leukemia.Journal of experimental & clinical cancer research : CR · 2023Article
- Notch Partners in the Long Journey of T-ALL Pathogenesis.International journal of molecular sciences · 2023Review
- Tcf1 is essential for initiation of oncogenic Notch1-driven chromatin topology in T-ALL.Blood · 2022Article
- RNA-binding protein IGF2BP1 maintains leukemia stem cell properties by regulating HOXB4, MYB, and ALDH1A1.Leukemia · 2020Article
- Humanized Rodent Models for Cancer Research.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanistic studies in human cancer have relied heavily on cell lines and mouse models, but are limited by in vitro adaptation and species context issues, respectively. More recent efforts have utilized patient-derived xenografts; however, these are hampered by variable genetic background, inability to study early events, and practical issues with availability/reproducibility. We report here an efficient, reproducible model of T-cell leukemia in which lentiviral transduction of normal human cord blood yields aggressive leukemia that appears indistinguishable from natural disease. We utilize this synthetic model to uncover a role for oncogene-induced HOXB activation which is operative in leukemia cells-of-origin and persists in established tumors where it defines a novel subset of patients distinct from other known genetic subtypes and with poor clinical outcome. We show further that anterior HOXB genes are specifically activated in human T-ALL by an epigenetic mechanism and confer growth advantage in both pre-leukemia cells and established clones.
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