ReviewFrontiers in oncology2015
Targeting the innate immune system as immunotherapy for acute myeloid leukemia.
Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 40 citations in OpenAlex.
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- Monitoring of (Leukemia-Specific) Immune Cells in Stages, Treatment Groups and in the Course of Disease and Therapy Contributes to Qualify Antileukemic Potential and Survival in Patients with AML.International journal of molecular sciences · 2025Article
- Review
- Role of Toll-Like Receptors in Myeloid Neoplasms: Focuses on the Molecular Mechanisms and Clinical Impact on Myelodysplastic Syndromes, Acute Myeloid Leukemia, and Chronic Myeloid Leukemia.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025Review
- Identification and functional analysis ofTranslational cancer research · 2025Article
- Bi-functional CpG-STAT3 decoy oligonucleotide triggers multilineage differentiation of acute myeloid leukemia in mice.Molecular therapy. Nucleic acids · 2024Article
- Analysis of action of 1,4-naphthoquinone scaffold-derived compounds against acute myeloid leukemia based on network pharmacology, molecular docking and molecular dynamics simulation.Scientific reports · 2024Article
- Review
- Identification of Nonfunctional Alternatively Spliced Isoforms of STING in Human Acute Myeloid Leukemia.Cancer research communications · 2024Article
- Article
- The role of IL-33/ST2 signaling in the tumor microenvironment and Treg immunotherapy.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Transcriptional profiling demonstrates altered characteristics of CD8Cancer medicine · 2022Article
- m6A-related lncRNAs predict prognosis and indicate immune microenvironment in acute myeloid leukemia.Scientific reports · 2022Article
- Establishment of a risk model correlated with metabolism based on RNA-binding proteins associated with cell pyroptosis in acute myeloid leukemia.Frontiers in oncology · 2022Article
- Article
- Immunotherapy for acute myeloid leukemia: from allogeneic stem cell transplant to novel therapeutics.Leukemia & lymphoma · 2019Review
- The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox.International journal of molecular sciences · 2019Review
- Mutational spectrum and associations with clinical features in patients with acute myeloid leukaemia based on next‑generation sequencing.Molecular medicine reports · 2019Article
- Immune Checkpoint Inhibitors in Acute Myeloid Leukemia: Novel Combinations and Therapeutic Targets.Current oncology reports · 2019Review
- Potentiating Tissue-Resident Type 2 Innate Lymphoid Cells by IL-33 to Prevent Renal Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2018Article
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 at 1 institution in 1 country.
Funding
Abstract
Because of its disseminated nature and lack of tumor-draining lymph nodes, acute myeloid leukemia (AML) likely employs unique immune evasion strategies as compared to solid malignancies. Targeting these unique mechanisms may result in improved immunotherapeutic approaches. Emerging data suggest that a specific dendritic cell (DC) subset, CD8α DCs, may be responsible for mediating tolerance in AML and thus targeting the innate immune system may be of benefit in this disease. Promising immune targets include the toll-like receptors, calreticulin/CD47, the stimulator of interferon genes pathway, and signal transducer and activator of transcription 3 (STAT3). However, it is becoming clear that compensatory mechanisms may limit the efficacy of these agents alone and thus rationale combinations of immunotherapies are warranted. This review discusses the potential immune evasion strategies in AML, as well as discussion of the promising innate immune targets, both alone and in combination, for this disease.
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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.