ArticleScientific reports2017
De novo AML exhibits greater microenvironment dysregulation compared to AML with myelodysplasia-related changes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- Defining alteration in bone marrow mesenchymal stem cells (MSC) from acute myeloid leukemia and exploring cultured MSC-conditioned media as a novel anti-leukemia therapy agent.Cancer immunology, immunotherapy : CII · 2026Article
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- Constructing a tumor immune microenvironment-driven prognostic model in acute myeloid leukemia using bioinformatics and validation data.Scientific reports · 2025Article
- Mesenchymal stem cells in the bone marrow microenvironment: a double-edged sword for AML.Journal of cancer research and clinical oncology · 2025Review
- Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.Cancer cell international · 2025Review
- Acute myeloid leukemia-derived bone marrow mesenchymal cells exhibit improved support for leukemic cell proliferation.Hematology, transfusion and cell therapy · 2024Article
- Mesenchymal Stem Cells in Myelodysplastic Syndromes and Leukaemia.Biomedicines · 2024Review
- The role of bone marrow microenvironment (BMM) cells in acute myeloid leukemia (AML) progression: immune checkpoints, metabolic checkpoints, and signaling pathways.Cell communication and signaling : CCS · 2023Review
- Acute myeloid leukemia (AML)-derived mesenchymal stem cells induce chemoresistance and epithelial-mesenchymal transition-like program in AML through IL-6/JAK2/STAT3 signaling.Cancer science · 2023Article
- Checkpoint Inhibitors in Acute Myeloid Leukemia.Biomedicines · 2023Review
- Mesenchymal stromal cell senescence in haematological malignancies.Cancer metastasis reviews · 2023Review
- Review
- Bone marrow stroma cells promote induction of a chemoresistant and prognostic unfavorable S100A8/A9high AML cell subset.Blood advances · 2022Article
- Microenvironmental Features Driving Immune Evasion in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Diseases (Basel, Switzerland) · 2022Review
- Bone Marrow Aging and the Leukaemia-Induced Senescence of Mesenchymal Stem/Stromal Cells: Exploring Similarities.Journal of personalized medicine · 2022Review
- Characteristics and regulation of mesenchymal stem cell plasticity by the microenvironmentGenes & diseases · 2022Review
- Review
- Arhgap21 Deficiency Results in Increase of Osteoblastic Lineage Cells in the Murine Bone Marrow Microenvironment.Frontiers in cell and developmental biology · 2021Article
- Location First: Targeting Acute Myeloid Leukemia Within Its Niche.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction between the bone marrow microenvironment and malignant hematopoietic cells can result in the protection of leukemia cells from chemotherapy in both myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). We, herein, characterized the changes in cytokine expression and the function of mesenchymal stromal cells (MSC) in patients with MDS, AML with myelodysplasia-related changes (MRC), a well-recognized clinical subtype of secondary AML, and de novo AML. We observed a significant inhibitory effect of MDS-MSC on T lymphocyte proliferation and no significant differences in any of the cytokines tested. AML-MSC inhibited T-cell proliferation only at a very low MSC/T cell ratio. When compared to the control, AML-MRCderived MSC presented a significant increase in IL6 expression, whereas de novo AML MSC presented a significant increase in the expression levels of VEGFA, CXCL12, RPGE2, IDO, IL1β, IL6 and IL32, followed by a decrease in IL10 expression. Furthermore, data indicate that IL-32 regulates stromal cell proliferation, has a chemotactic potential and participates in stromal cell crosstalk with leukemia cells, which could result in chemoresistance. Our results suggest that the differences between AML-MRC and de novo AML also extend into the leukemic stem cell niche and that IL-32 can participate in the regulation of the bone marrow cytokine milieu.
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