ReviewFrontiers in immunology2022
The cytokine network in acute myeloid leukemia.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 71 citations in OpenAlex.
- Single-cell chromatin profiling reveals relapse-related priming in pediatric acute myeloid leukemia.Life science alliance · 2026Article
- Retinal Microvascular Changes Associated with Concurrent Morphologic/Hematologic Response to Induction Therapy in Acute Leukemia: An Exploratory Prospective Wide-Field Swept-Source OCT Angiography Study.Diagnostics (Basel, Switzerland) · 2026Article
- Exploring the Role of Macrophage Marker CD68 in Pediatric Acute Myeloid Leukemia.International journal of molecular sciences · 2026Article
- Prognostic significance of inflammatory cytokine polymorphisms in AML: a study of IFNG, TNFA, and IL1B polymorphisms.BMC immunology · 2026Article
- Immune-Genomic Evolution in AML Spontaneous Remission: A 66-Patient Pooled Analysis and Longitudinal Clonal Tracking.Cancers · 2026Article
- Neuroinflammatory changes in acute myeloid leukemia: Evidence for blood-brain barrier disruption and glial activation.HemaSphere · 2026Article
- Modulation of Leukemic Blasts into Dendritic Cells (DCCancers · 2026Article
- The tumor microenvironment in hematologic malignancies: immune evasion, metabolic reprogramming, and therapeutic resistance.Blood science (Baltimore, Md.) · 2026Review
- Targeting IL-1/IRAK1/4 signaling in acute myeloid leukemia stem cells following treatment and relapse.Leukemia · 2026Article
- Role of p38 MAPK in the cytokine reprogramming of a human leukemic cell line with a drug-resistant phenotype.Cell communication and signaling : CCS · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- The transformative potential of lipid nanoparticles tailored for acute myeloid leukemia immunotherapy.Frontiers in immunology · 2026Review
- Bone marrow plasma cytokine composition indicates acute myeloid leukemia progression and treatment response.Frontiers in cell and developmental biology · 2026Article
- IL-1 signaling and inflammasomes in acute myeloid leukemia: mechanisms and therapeutic opportunities.Cellular and molecular life sciences : CMLS · 2025Review
- Article
- Mitochondrial Dysfunction in Apoptosis-Resistant Acute Myeloid Leukemia Cells During a Sterile Inflammatory Response.Biomolecules · 2025Article
- Acute myeloid leukemia after CAR T-cell therapy: role of pre-existing clonal hematopoiesis and inflammation in leukemogenesis.Bone marrow transplantation · 2025Article
- Longitudinal single-cell analysis reveals treatment-resistant stem and mast cells with potential treatments for pediatric AML.Leukemia · 2025Article
- The Imbalanced Patterns and Clinical Significance of Cytokines in Acute Myeloid Leukemia Microenvironment.Immunity, inflammation and disease · 2025Article
- Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia.Cancer research communications · 2025Article
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
Acute myeloid leukemia (AML) is a highly heterogeneous malignancy of the blood and bone marrow, characterized by clonal expansion of myeloid stem and progenitor cells and rapid disease progression. Chemotherapy has been the first-line treatment for AML for more than 30 years. Application of recent high-throughput next-generation sequencing technologies has revealed significant molecular heterogeneity to AML, which in turn has motivated efforts to develop new, targeted therapies. However, due to the high complexity of this disease, including multiple driver mutations and the coexistence of multiple competing tumorigenic clones, the successful incorporation of these new agents into clinical practice remains challenging. These continuing difficulties call for the identification of innovative therapeutic approaches that are effective for a larger cohort of AML patients. Recent studies suggest that chronic immune stimulation and aberrant cytokine signaling act as triggers for AML initiation and progression, facets of the disease which might be exploited as promising targets in AML treatment. However, despite the greater appreciation of cytokine profiles in AML, the exact functions of cytokines in AML pathogenesis are not fully understood. Therefore, unravelling the molecular basis of the complex cytokine networks in AML is a prerequisite to develop new therapeutic alternatives based on targeting cytokines and their receptors.
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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.