ReviewFrontiers in immunology2016
Underground Adaptation to a Hostile Environment: Acute Myeloid Leukemia vs. Natural Killer Cells.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Immunotherapy in acute myeloid leukemia: The antibodies, TriKEs, and CARs on the arduous road to cure.Blood reviews · 2026Review
- NKG2A gene variant predicts outcome of immunotherapy in AML and modulates the repertoire and function of NK cells.Journal for immunotherapy of cancer · 2023Article
- Myelodysplastic Syndrome associated TET2 mutations affect NK cell function and genome methylation.Nature communications · 2023Article
- Molecular Systems Architecture of Interactome in the Acute Myeloid Leukemia Microenvironment.Cancers · 2022Review
- Increased TIGIT expressing NK cells with dysfunctional phenotype in AML patients correlated with poor prognosis.Cancer immunology, immunotherapy : CII · 2022Article
- Acute lymphoblastic leukemia-derived exosome inhibits cytotoxicity of natural killer cells by TGF-β signaling pathway.3 Biotech · 2021Article
- High-dimensional mass cytometry analysis of NK cell alterations in AML identifies a subgroup with adverse clinical outcome.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Natural Killer Cell Subpopulations and Inhibitory Receptor Dynamics in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Frontiers in immunology · 2021Article
- Circulating and Tumor-Infiltrating NK Cells From Clear Cell Renal Cell Carcinoma Patients Exhibit a Predominantly Inhibitory Phenotype Characterized by Overexpression of CD85j, CD45, CD48 and PD-1.Frontiers in immunology · 2021Article
- Chronic IL-15 Stimulation and Impaired mTOR Signaling and Metabolism in Natural Killer Cells During Acute Myeloid Leukemia.Frontiers in immunology · 2021Article
- Review
- CD56 as a marker of an ILC1-like population with NK cell properties that is functionally impaired in AML.Blood advances · 2019Article
- NK Cells in the Treatment of Hematological Malignancies.Journal of clinical medicine · 2019Review
- NK Cell Hyporesponsiveness: More Is Not Always Better.International journal of molecular sciences · 2019Review
- Natural killer receptor ligand expression on acute myeloid leukemia impacts survival and relapse after chemotherapy.Blood advances · 2018Article
- Dextran Enhances the Lentiviral Transduction Efficiency of Murine and Human Primary NK Cells.Journal of visualized experiments : JoVE · 2018Article
- NKp30 expression is a prognostic immune biomarker for stratification of patients with intermediate-risk acute myeloid leukemia.Oncotarget · 2017Article
- Natural Killer Defective Maturation Is Associated with Adverse Clinical Outcome in Patients with Acute Myeloid Leukemia.Frontiers in immunology · 2017Article
- CD19-specific triplebody SPM-1 engages NK and γδ T cells for rapid and efficient lysis of malignant B-lymphoid cells.Oncotarget · 2016Article
- Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a heterogeneous group of malignancies which incidence increases with age. The disease affects the differentiation of hematopoietic stem or precursor cells in the bone marrow and can be related to abnormal cytogenetic and/or specific mutational patterns. AML blasts can be sensitive to natural killer (NK) cell antitumor response. However, NK cells are frequently defective in AML patients leading to tumor escape. NK cell defects affect not only the expression of the activating NK receptors, including the natural cytotoxicity receptors, the NK group 2, member D, and the DNAX accessory molecule-1, but also cytotoxicity and IFN-γ release. Such perturbations in NK cell physiology could be related to the adaptation of the AML to the immune pressure and more generally to patient's clinical features. Various mechanisms are potentially involved in the inhibition of NK-cell functions in AML, including defects in the normal lymphopoiesis, reduced expression of activating receptors through cell-to-cell contacts, and production of immunosuppressive soluble agents by leukemic blasts. Therefore, the continuous cross-talk between AML and NK cells participates to the leukemia immune escape and eventually to patient's relapse. Methods to restore or stimulate NK cells seem to be attractive strategies to treat patients once the complete remission is achieved. Moreover, our capacity in stimulating the NK cell functions could lead to the development of preemptive strategies to eliminate leukemia-initiating cells before the emergence of the disease in elderly individuals presenting preleukemic mutations in hematopoietic stem cells.
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