ArticleBlood2014
Immune evasion by oncogenic proteins of acute myeloid leukemia.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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
36 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- Dual Regulatory Functions and Therapeutic Potential of CD48 in Tumor Immunity.Oncology research · 2026Review
- Upregulation of YY1/EZH2 and MLH1 as Therapeutic Targets for Adult T-Cell Leukemia/Lymphoma.Cancer science · 2025Article
- VISTA is a potential target for immunotherapy in B-cell acute lymphoblastic leukemia in children.Scientific reports · 2025Article
- Genetic Risk Profiling Reveals Altered Glycosyltransferase Expression as a Predictor for Patient Outcome in Neuroblastoma.Journal of clinical medicine · 2025Article
- Unveiling mitochondrial and ribosomal gene deregulation and tumor microenvironment dynamics in acute myeloid leukemia.Cancer gene therapy · 2024Article
- The KIR2DL family serves as prognostic biomarkers and correlates with immune infiltrates in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2024Article
- Epigenetic regulation of CD38/CD48 by KDM6A mediates NK cell response in multiple myeloma.Nature communications · 2024Article
- STAT3 in acute myeloid leukemia facilitates natural killer cell-mediated surveillance.Frontiers in immunology · 2024Article
- Immunotherapy in leukaemia.Acta biochimica et biophysica Sinica · 2023Review
- Article
- Heme oxygenase 1 overexpression induces immune evasion of acute myeloid leukemia against natural killer cells by inhibiting CD48.Journal of translational medicine · 2022Article
- Microenvironmental Features Driving Immune Evasion in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Diseases (Basel, Switzerland) · 2022Review
- Chidamide-based 3-drug combination regimen reverses molecular relapse post transplantation in AML1-ETO-positive acute myeloid leukemia.Frontiers in pharmacology · 2022Article
- Engineered type 1 regulatory T cells designed for clinical use kill primary pediatric acute myeloid leukemia cells.Haematologica · 2021Article
- Chimeric antigen receptor (CAR) natural killer (NK)-cell therapy: leveraging the power of innate immunity.British journal of haematology · 2021Review
- Syngeneic leukemia models using lentiviral transgenics.Cell death & disease · 2021Article
- Single-Cell Technologies to Decipher the Immune Microenvironment in Myeloid Neoplasms: Perspectives and Opportunities.Frontiers in oncology · 2021Review
- Immune escape and immunotherapy of acute myeloid leukemia.The Journal of clinical investigation · 2020Review
- Targeting transcription factors in cancer - from undruggable to reality.Nature reviews. Cancer · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
PML-RARA and AML1-ETO are important oncogenic fusion proteins that play a central role in transformation to acute myeloid leukemia (AML). Whether these fusion proteins render the tumor cells with immune evasion properties is unknown. Here we show that both oncogenic proteins specifically downregulate the expression of CD48, a ligand of the natural killer (NK) cell activating receptor 2B4, thereby leading to decreased killing by NK cells. We demonstrate that this process is histone deacetylase (HDAC)-dependent, that it is mediated through the downregulation of CD48 messenger RNA, and that treatment with HDAC inhibitors (HDACi) restores the expression of CD48. Furthermore, by using chromatin immunoprecepitation (ChIP) experiments, we show that AML1-ETO directly interacts with CD48. Finally, we show that AML patients who are carrying these specific translocations have low expression of CD48.
Indexed as
Identifiers
What OpenQuestion holds
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.