ArticleNeoplasia (New York, N.Y.)2015
Endothelial progenitor cell dysfunction in myelodysplastic syndromes: possible contribution of a defective vascular niche to myelodysplasia.
Article in Neoplasia (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.Cells · 2026Review
- Endothelial dysfunction and proinflammatory state determine severe hematotoxicity and inferior outcome of CAR-T therapy.HemaSphere · 2025Article
- Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.Cancer cell international · 2025Review
- The vascular microenvironment and its stem cells regulate vascular homeostasis.Frontiers in cell and developmental biology · 2025Review
- Recent advances in endothelial colony-forming cells: from the transcriptomic perspective.Journal of translational medicine · 2024Review
- A Novel Morphological Parameter Predicting Fibrotic Evolution in Myeloproliferative Neoplasms: New Evidence and Molecular Insights.International journal of molecular sciences · 2022Review
- Dysfunctional bone marrow endothelial progenitor cells are involved in patients with myelodysplastic syndromes.Journal of translational medicine · 2022Article
- The immunological role of mesenchymal stromal cells in patients with myelodysplastic syndrome.Frontiers in immunology · 2022Review
- Myelodysplastic Syndromes and Metabolism.International journal of molecular sciences · 2021Review
- Nature or Nurture? Role of the Bone Marrow Microenvironment in the Genesis and Maintenance of Myelodysplastic Syndromes.Cancers · 2021Review
- Assessment of All-Cause Cancer Incidence Among Individuals With Preeclampsia or Eclampsia During First Pregnancy.JAMA network open · 2021Article
- The Dynamic Interface Between the Bone Marrow Vascular Niche and Hematopoietic Stem Cells in Myeloid Malignancy.Frontiers in cell and developmental biology · 2021Review
- Myelodysplastic syndrome patient-derived xenografts: from no options to many.Haematologica · 2020Article
- c-MYC Expression Is a Possible Keystone in the Colorectal Cancer Resistance to EGFR Inhibitors.Cancers · 2020Article
- Pre-Exposure to Defibrotide Prevents Endothelial Cell Activation by Lipopolysaccharide: An Ingenuity Pathway Analysis.Frontiers in immunology · 2020Article
- The bone-marrow niche in MDS and MGUS: implications for AML and MM.Nature reviews. Clinical oncology · 2018Review
- Mesenchymal Stem Cells in Myeloid Malignancies: A Focus on Immune Escaping and Therapeutic Implications.Stem cells international · 2017Review
- Mesenchymal Stem and Progenitor Cells in Normal and Dysplastic Hematopoiesis-Masters of Survival and Clonality?International journal of molecular sciences · 2016Review
- Article
- Endothelial progenitor cells in hematologic malignancies.Stem cell investigation · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We set a model to replicate the vascular bone marrow niche by using endothelial colony forming cells (ECFCs), and we used it to explore the vascular niche function in patients with low-risk myelodysplastic syndromes (MDS). Overall, we investigated 56 patients and we observed higher levels of ECFCs in MDS than in healthy controls; moreover, MDS ECFCs were found variably hypermethylated for p15INK4b DAPK1, CDH1, or SOCS1. MDS ECFCs exhibited a marked adhesive capacity to normal mononuclear cells. When normal CD34+ cells were co-cultured with MDS ECFCs, they generated significant lower amounts of CD11b+ and CD41+ cells than in co-culture with normal ECFCs. At gene expression profile, several genes involved in cell adhesion were upregulated in MDS ECFCs, while several members of the Wingless and int (Wnt) pathways were underexpressed. Furthermore, at miRNA expression profile, MDS ECFCs hypo-expressed various miRNAs involved in Wnt pathway regulation. The addition of Wnt3A reduced the expression of intercellular cell adhesion molecule-1 on MDS ECFCs and restored the defective expression of markers of differentiation. Overall, our data demonstrate that in low-risk MDS, ECFCs exhibit various primary abnormalities, including putative MDS signatures, and suggest the possible contribution of the vascular niche dysfunction to myelodysplasia.
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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.