ArticleProceedings of the National Academy of Sciences of the United States of America2020
Reversible suppression of T cell function in the bone marrow microenvironment of acute myeloid leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- Review
- T-cell miR-155 regulates the response to tumor-specific mRNA vaccines in a murine model of acute myeloid leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Off-target anti-leukemic effects of antibiotics: mechanisms and therapeutic insights.Cancer chemotherapy and pharmacology · 2026Review
- An Immune Dysfunction Signature Score Predicts Survival in MDS Patients: Insights From a Longitudinal, Multicenter Study.Cancer science · 2026Article
- Mining single-cell transcriptomic data reveals distinct T-cell population in pediatric B-ALL and AML at diagnosis.Blood advances · 2026Article
- Azacytidine restores T cell function in AML by modulating DNA methylation.bioRxiv : the preprint server for biology · 2026Article
- Measurable residual disease testing in acute myeloid leukemia: current state, foundational models, and tools for future development.Cancer metastasis reviews · 2026Review
- Article
- T-Cell Responses and T-Cell-Based Therapy in Acute Myeloid Leukemia.Current medical science · 2025Review
- Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.Nature cancer · 2025Article
- Article
- Single-cell sequencing reveals the expansion and diversity of T cell subsets in the bone marrow microenvironment of chronic myeloid leukemia.Genes & diseases · 2025Article
- Combining antigen specific T-cells with T-cell engager therapy induces a molecular signature that favors T-cell fitness.Blood immunology & cellular therapy · 2025Article
- SOCS1 Protects Acute Myeloid Leukemia against Allogeneic T Cell-Mediated Cytotoxicity.Blood cancer discovery · 2025Article
- Blockade of TIGAR prevents CD8Cancer immunology, immunotherapy : CII · 2025Article
- Immunogenic shift of arginine metabolism triggers systemic metabolic and immunological reprogramming to suppress HER2 + breast cancer.Cancer & metabolism · 2025Article
- The Emerging Role of CD8Cancers · 2025Review
- Characterization of the Bone Marrow Lymphoid Microenvironment and Discovery of Prognostic Immune-Related Factors in Acute Myeloid Leukemia.International journal of molecular sciences · 2024Article
- Immunosuppressive microenvironment in acute myeloid leukemia: overview, therapeutic targets and corresponding strategies.Annals of hematology · 2024Review
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is the most common acute leukemia in adults, with approximately four new cases per 100,000 persons per year. Standard treatment for AML consists of induction chemotherapy with remission achieved in 50 to 75% of cases. Unfortunately, most patients will relapse and die from their disease, as 5-y survival is roughly 29%. Therefore, other treatment options are urgently needed. In recent years, immune-based therapies have led to unprecedented rates of survival among patients with some advanced cancers. Suppression of T cell function in the tumor microenvironment is commonly observed and may play a role in AML. We found that there is a significant association between T cell infiltration in the bone marrow microenvironment of newly diagnosed patients with AML and increased overall survival. Functional studies aimed at establishing the degree of T cell suppression in patients with AML revealed impaired T cell function in many patients. In most cases, T cell proliferation could be restored by blocking the immune checkpoint molecules PD-1, CTLA-4, or TIM3. Our data demonstrate that AML establishes an immune suppressive environment in the bone marrow, in part through T cell checkpoint function.
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