ArticleCancer research2023
CD36 Drives Metastasis and Relapse in Acute Myeloid Leukemia.
Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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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.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
- Molecular biomarkers as key determinants of outcome in mantle cell lymphoma: results from the FIL V-RBAC trial.Blood advances · 2026Trial
- Article
- Single cell transcriptional evolution of myeloid leukemia of Down syndrome.Nature communications · 2026Article
- Integrative transcriptomics defines CD36 as a key regulator of immunometabolic signaling in acute myeloid leukemia.Genes & genomics · 2026Article
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- Metformin induces ferroptosis associated with lipidomic remodeling in AML.Blood advances · 2026Article
- The role of thrombospondin-1 in dermatological conditions.Frontiers in medicine · 2026Review
- Single cell Raman spectroscopic profiles predict treatment responses in patients withFrontiers in cell and developmental biology · 2026Article
- Lipid metabolic plasticity in glioblastoma: mechanisms, tumor microenvironment remodeling, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Structural Insights into Recognition and Translocation of Oxidized Phospholipid by CD36 Using Mass Spectrometry, Molecular Docking, Dynamics, and Metadynamics Simulations.Journal of the American Chemical Society · 2025Article
- High CD36 Expression Predicts Aggressive Invasion and Recurrence in Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- Identification of New CD36 Antagonists by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- The dual role of CD36 in cancer: from lipid metabolism to tumor microenvironment regulation.Molecular biology reports · 2025Review
- The Landscape of Cancer Metabolism as a Therapeutic Target.Pathology international · 2025Review
- Analyzing the Blueprint: Exploring the Molecular Profile of Metastasis and Therapeutic Resistance.International journal of molecular sciences · 2025Review
- Expression of Aldehyde Dehydrogenase 1A1 in Relapse-Associated Cells in Acute Myeloid Leukemia.Cells · 2025Review
- Unraveling lipid metabolism for acute myeloid leukemia therapy.Current opinion in hematology · 2025Review
- Ang-1 and VEGF: central regulators of angiogenesis.Molecular and cellular biochemistry · 2025Review
- Suppression of thrombospondin-1-mediated inflammaging prolongs hematopoietic health span.Science immunology · 2025Article
- Discovery andFrontiers in immunology · 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
31 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and relapse in acute myeloid leukemia (AML). In a cohort of 1,273 AML patients, we uncovered that the multifunctional scavenger receptor CD36 was positively associated with extramedullary dissemination of leukemic blasts, increased risk of relapse after intensive chemotherapy, and reduced event-free and overall survival. CD36 was dispensable for lipid uptake but fostered blast migration through its binding with thrombospondin-1. CD36-expressing blasts, which were largely enriched after chemotherapy, exhibited a senescent-like phenotype while maintaining their migratory ability. In xenograft mouse models, CD36 inhibition reduced metastasis of blasts and prolonged survival of chemotherapy-treated mice. These results pave the way for the development of CD36 as an independent marker of poor prognosis in AML patients and a promising actionable target to improve the outcome of patients. SIGNIFICANCE: CD36 promotes blast migration and extramedullary disease in acute myeloid leukemia and represents a critical target that can be exploited for clinical prognosis and patient treatment.
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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.