ArticleBlood advances2024
Differential inflammatory conditioning of the bone marrow by acute myeloid leukemia and its impact on progression.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Modulation of the bone marrow microenvironment by acute B-cell lymphoblastic leukemia-derived large oncosomes.Blood advances · 2026Article
- Exploring the Bone Marrow Microenvironment as a Therapeutic Barrier and Targetable Source of Crosstalk in Acute Myeloid Leukemia.Blood and lymphatic cancer : targets and therapy · 2026Review
- Co-operative epigenetic remodelling by Setd2 deficiency and Kras mutation drives juvenile myelomonocytic leukaemia development and MEK inhibitor sensitivity.British journal of haematology · 2025Article
- HDAC3-YY1-RAB5A axis remodels AML-supportive niche by modulating mitochondrial homeostasis in bone marrow stromal cells.Cell death & disease · 2025Article
- The causal relationship between circulating inflammatory proteins, gut microbiotas, immune cells and leukemia: a bidirectional Mendelian randomization study.Discover oncology · 2025Article
- An integrated machine learning framework for developing and validating a prognostic risk model of gastric cancer based on endoplasmic reticulum stress-associated genes.Biochemistry and biophysics reports · 2025Article
- Annexin A: Cell Death, Inflammation, and Translational Medicine.Journal of inflammation research · 2025Review
- SPOP enhances FADD degradation and decreases the activeness of the NF-κB signaling pathway in prostate cancer: anTranslational andrology and urology · 2024Article
- Exploitation of the fibrinolytic system by B-cell acute lymphoblastic leukemia and its therapeutic targeting.Nature communications · 2024Article
- Acute Myeloid Leukemia in Older Patients: From New Biological Insights to Targeted Therapies.Current oncology (Toronto, Ont.) · 2024Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractInflammation promotes solid tumor progression, but how regulatory mechanisms of inflammation may affect leukemia is less well studied. Using annexin A5 (ANXA5), a calcium-binding protein known for apoptosis, which we discovered to be differentially expressed in the bone marrow microenvironment (BMM) of mice with acute myeloid (AML) vs chronic myeloid leukemia, as a model system, we unravel here a circuit in which AML-derived tumor necrosis factor α (TNF-α) dose-dependently reduces ANXA5 in the BMM. This creates an inflammatory BMM via elevated levels of prostaglandin E2 (PGE2). Via binding to its EP4 receptor, PGE2 increases β-catenin and hypoxia-inducible factor 1α signaling in AML cells, thereby accelerating PGE2-sensitive AML. Human trephine biopsies may show lower ANXA5 expression and higher PGE2 expression in AML than other hematologic malignancies. Furthermore, syngeneic and xenogeneic transplantation models suggest a survival benefit after treatment with the inhibitor of prostaglandin-endoperoxide synthase 2 (cyclooxygenase 2 [COX2]), celecoxib, plus cytarabine in those AML types highly sensitive to PGE2 compared with cytarabine alone. Taken together, TNF-α/ANXA5/NF-κB/COX2/PGE2-mediated inflammation influences AML course in a highly differential and circular manner, and patients with AML with "inflammatory AML" may benefit from antiphlogistic agents as adjunct therapy.
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