ArticleProceedings of the National Academy of Sciences of the United States of America2011
Down-regulation of homeobox genes MEIS1 and HOXA in MLL-rearranged acute leukemia impairs engraftment and reduces proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Dysregulation of HOXA genes in acute myeloid leukemia and targeted therapy.NPJ precision oncology · 2025Review
- Article
- Direct functional HOXA9/DNA-binding competitors versus epigenetic inhibitors of HOXA9 expression on cell proliferation, death and differentiation processes in the model of MLL-rearranged acute myeloid leukemia.Investigational new drugs · 2025Article
- KMT2A degradation is observed in decitabine-responsive acute lymphoblastic leukemia cells.Molecular oncology · 2025Article
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- MiR-27a downregulates 14-3-3θ, RUNX1, AF4, and MLL-AF4, crucial drivers of blast transformation in t(4;11) leukemia cells.Cell biochemistry and function · 2022Article
- Panobinostat (LBH589) increase survival in adult xenografic model of acute lymphoblastic leukemia with t(4;11) but promotes antagonistic effects in combination with MTX and 6MP.Medical oncology (Northwood, London, England) · 2022Article
- A novel fatty acid metabolism-related signature identifies features of the tumor microenvironment and predicts clinical outcome in acute myeloid leukemia.Lipids in health and disease · 2022Article
- Genetic and Epigenetic Characterization of a DiscordantInternational journal of molecular sciences · 2021Article
- MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021Review
- Nuclear FGFR2 Interacts with the MLL-AF4 Oncogenic Chimera and Positively RegulatesInternational journal of molecular sciences · 2021Article
- Epigenetic Control of Infant B Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- Stem cell characteristics promote aggressiveness of diffuse large B-cell lymphoma.Scientific reports · 2020Article
- Expression of microRNA-181a and microRNA-196b in Egyptian Pediatric acute Lymphoblastic Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Identification of co-expressed genes associated with MLL rearrangement in pediatric acute lymphoblastic leukemia.Bioscience reports · 2020Article
- Crosstalk between MEIS1 and markers of different cell signaling pathways in esophageal squamous cell carcinoma.Molecular biology reports · 2020Article
- A Menin-MLL Inhibitor Induces Specific Chromatin Changes and Eradicates Disease in Models of MLL-Rearranged Leukemia.Cancer cell · 2019Article
- Crosstalk between 14-3-3θ and AF4 enhances MLL-AF4 activity and promotes leukemia cell proliferation.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE-30.Molecular genetics & genomic medicine · 2019Article
- A novel small molecule that kills a subset of MLL-rearranged leukemia cells by inducing mitochondrial dysfunction.Oncogene · 2019Article
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
Rearrangements of the MLL (ALL1) gene are very common in acute infant and therapy-associated leukemias. The rearrangements underlie the generation of MLL fusion proteins acting as potent oncogenes. Several most consistently up-regulated targets of MLL fusions, MEIS1, HOXA7, HOXA9, and HOXA10 are functionally related and have been implicated in other types of leukemias. Each of the four genes was knocked down separately in the human precursor B-cell leukemic line RS4;11 expressing MLL-AF4. The mutant and control cells were compared for engraftment in NOD/SCID mice. Engraftment of all mutants into the bone marrow (BM) was impaired. Although homing was similar, colonization by the knockdown cells was slowed. Initially, both types of cells were confined to the trabecular area; this was followed by a rapid spread of the WT cells to the compact bone area, contrasted with a significantly slower process for the mutants. In vitro and in vivo BrdU incorporation experiments indicated reduced proliferation of the mutant cells. In addition, the CXCR4/SDF-1 axis was hampered, as evidenced by reduced migration toward an SDF-1 gradient and loss of SDF-1-augmented proliferation in culture. The very similar phenotype shared by all mutant lines implies that all four genes are involved and required for expansion of MLL-AF4 associated leukemic cells in mice, and down-regulation of any of them is not compensated by the others.
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