ReviewCancer science2008
Roles of the histone acetyltransferase monocytic leukemia zinc finger protein in normal and malignant hematopoiesis.
Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
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- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Decoding the Implications of Zinc in the Development and Therapy of Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Panel-based RNA fusion sequencing improves diagnostics of pediatric acute myeloid leukemia.Leukemia · 2024Article
- Small-molecule TIP60 inhibitors enhance regulatory T cell induction through TIP60-P300 acetylation crosstalk.iScience · 2023Article
- HEY1-NCOA2 expression modulates chondrogenic differentiation and induces mesenchymal chondrosarcoma in mice.JCI insight · 2023Article
- Emerging Roles of Epigenetic Regulators in Maintaining Hematopoietic Stem Cell Homeostasis.Advances in experimental medicine and biology · 2023Article
- Regulome analysis in B-acute lymphoblastic leukemia exposes Core Binding Factor addiction as a therapeutic vulnerability.Nature communications · 2022Article
- MOZ is critical for the development of MOZ/MLL fusion-induced leukemia through regulation of Hoxa9/Meis1 expression.Blood advances · 2022Article
- Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022Review
- Inflammation, epigenetics, and metabolism converge to cell senescence and ageing: the regulation and intervention.Signal transduction and targeted therapy · 2021Review
- The Biological Significance of Targeting Acetylation-Mediated Gene Regulation for Designing New Mechanistic Tools and Potential Therapeutics.Biomolecules · 2021Review
- Zinc Metalloproteins in Epigenetics and Their Crosstalk.Life (Basel, Switzerland) · 2021Review
- Mechanisms and rejuvenation strategies for aged hematopoietic stem cells.Journal of hematology & oncology · 2020Review
- The genomics of acute myeloid leukemia in children.Cancer metastasis reviews · 2020Review
- Epigenetic Changes as a Target in Aging Haematopoietic Stem Cells and Age-Related Malignancies.Cells · 2019Review
- Epigenetic regulation of hematopoietic stem cell homeostasis.Blood science (Baltimore, Md.) · 2019Review
- Losing Sense of Self and Surroundings: Hematopoietic Stem Cell Aging and Leukemic Transformation.Trends in molecular medicine · 2019Review
- Investigation of the changes in the expression levels ofJournal of gastrointestinal oncology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone-modified enzymes are involved in various cell functions, including proliferation, differentiation, cell death and carcinogenesis. The protein MOZ (monocytic leukemia zinc finger protein) is a Myst (MOZ, Ybf2 (Sas3), Sas2, Tip60)-type histone acetyltranseferase (HAT) that generates fusion genes, such as MOZ-TIF2, MOZ-CBP and MOZ-p300, in acute myeloid leukemia (AML) by chromosomal translocation. MOZ associates with AML1 (RUNX1), PU.1, and p53, and cooperatively activates target gene transcription. Gene targeting in mice has revealed that MOZ is essential for the generation and maintenance of hematopoietic stem cells (HSC) and for the appropriate development of myeloid, erythroid and B-lineage cell progenitors. In AML, MOZ fusion genes lead to repressed differentiation, hyper-proliferation, and self-renewal of myeloid progenitors through deregulation of MOZ-regulated target gene expression. It is therefore necessary to analyze the roles of MOZ and MOZ fusion genes in normal and malignant hematopoiesis to elucidate the mechanisms underlying and develop therapies for MOZ-related AML.
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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.