ArticleBlood2014
Downregulation of Prdm16 mRNA is a specific antileukemic mechanism during HOXB4-mediated HSC expansion in vivo.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- PRDM16 expression is an independent prognostic factor in AML with the double-mutant NPM1/FLT3-ITD genotype.Annals of hematology · 2026Article
- Metabolic reprogramming by PRDM16 drives cytarabine resistance in acute myeloid leukemia.Haematologica · 2025Article
- Downstream of the HOX genes: Explaining conflicting tumour suppressor and oncogenic functions in cancer.International journal of cancer · 2022Review
- Integrative epigenomic and transcriptomic analysis reveals the requirement of JUNB for hematopoietic fate induction.Nature communications · 2022Article
- Developmental maturation of the hematopoietic system controlled by a Lin28b-let-7-Cbx2 axis.Cell reports · 2022Article
- Isolation, Maintenance and Expansion of Adult Hematopoietic Stem/Progenitor Cells and Leukemic Stem Cells.Cancers · 2022Review
- Repeated cell sorting ensures the homogeneity of ocular cell populations expressing a transgenic protein.PloS one · 2022Article
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Article
- Reprogramming mechanisms influence the maturation of hematopoietic progenitors from human pluripotent stem cells.Cell death & disease · 2018Article
- PRDM16 isoforms differentially regulate normal and leukemic hematopoiesis and inflammatory gene signature.The Journal of clinical investigation · 2018Article
- HOXC10 suppresses browning of white adipose tissues.Experimental & molecular medicine · 2017Article
- LECT2 drives haematopoietic stem cell expansion and mobilization via regulating the macrophages and osteolineage cells.Nature communications · 2016Article
- The IRX1/HOXA connection: insights into a novel t(4;11)- specific cancer mechanism.Oncotarget · 2016Article
- Evaluating the Safety of Retroviral Vectors Based on Insertional Oncogene Activation and Blocked Differentiation in Cultured Thymocytes.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- PRDM16 Suppresses MLL1r Leukemia via Intrinsic Histone Methyltransferase Activity.Molecular cell · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Overexpression of HOXB4 in hematopoietic stem cells (HSCs) leads to increased self-renewal without causing hematopoietic malignancies in transplanted mice. The molecular basis of HOXB4-mediated benign HSC expansion in vivo is not well understood. To gain further insight into the molecular events underlying HOXB4-mediated HSC expansion, we analyzed gene expression changes at multiple time points in Lin(-)Sca1(+)c-kit(+) cells from mice transplanted with bone marrow cells transduced with a MSCV-HOXB4-ires-YFP vector. A distinct HOXB4 transcriptional program was reproducibly induced and stabilized by 12 weeks after transplant. Dynamic expression changes were observed in genes critical for HSC self-renewal as well as in genes involved in myeloid and B-cell differentiation. Prdm16, a transcription factor associated with human acute myeloid leukemia, was markedly repressed by HOXB4 but upregulated by HOXA9 and HOXA10, suggesting that Prdm16 downregulation was involved in preventing leukemia in HOXB4 transplanted mice. Functional evidence to support this mechanism was obtained by enforcing coexpression of sPrdm16 and HOXB4, which led to enhanced self-renewal, myeloid expansion, and leukemia. Altogether, these studies define the transcriptional pathways involved in HOXB4 HSC expansion in vivo and identify repression of Prdm16 transcription as a mechanism by which expanding HSCs avoid leukemic transformation.
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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.