ArticleBlood cancer journal2015
Mesenchymal stromal cells derived from acute myeloid leukemia bone marrow exhibit aberrant cytogenetics and cytokine elaboration.
Article in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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
55 citing papers in PubMed, 104 citations in OpenAlex.
- 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
- Chromosomal abnormalities of mesenchymal stromal cells in hematological malignancies.Oncogene · 2025Review
- Impact of Acute Myeloid Leukemia Cells on the Metabolic Function of Bone Marrow Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- Changing landscape of hematopoietic and mesenchymal cells and their interactions during aging and in age-related skeletal pathologies.Mechanisms of ageing and development · 2025Review
- MMP14 from BM-MSCs facilitates progression and Ara-C resistance in acute myeloid leukemia via the JAK/STAT pathway.Experimental hematology & oncology · 2025Article
- CD73: a new immune checkpoint for leukemia treatment.Frontiers in immunology · 2025Review
- Bone marrow stromal cells enhance differentiation of acute myeloid leukemia induced by pyrimidine synthesis inhibitors.American journal of physiology. Cell physiology · 2024Article
- Review
- Proteomic profiling reveals ACSS2 facilitating metabolic support in acute myeloid leukemia.Cancer gene therapy · 2024Article
- Mesenchymal Stem Cells in Myelodysplastic Syndromes and Leukaemia.Biomedicines · 2024Review
- Review
- Article
- The emerging role of ectodermal neural cortex 1 in cancer.Scientific reports · 2024Review
- Review
- Abnormal adipogenic signaling in the bone marrow mesenchymal stem cells contributes to supportive microenvironment for leukemia development.Cell communication and signaling : CCS · 2023Article
- The Role of Inflammation in the Initiation and Progression of Myeloid Neoplasms.Blood cancer discovery · 2023Article
- Acute Myeloid Leukemia Causes Serious and Partially Irreversible Changes in Secretomes of Bone Marrow Multipotent Mesenchymal Stromal Cells.International journal of molecular sciences · 2023Article
- An Updated Overview of the Role of CYP450 during Xenobiotic Metabolization in Regulating the Acute Myeloid Leukemia Microenvironment.International journal of molecular sciences · 2023Review
- Epigenetic Modification of Mesenchymal Stromal Cells Derived from Bone Marrow and Embryonal Tumors to Facilitate Immunotherapeutic Approaches in Pediatric Malignancies.Current issues in molecular biology · 2023Article
- Mesenchymal stromal cells, metabolism, and mitochondrial transfer in bone marrow normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Bone marrow-derived mesenchymal stromal cells (BM-MSCs) play a fundamental role in the BM microenvironment (BME) and abnormalities of these cells may contribute to acute myeloid leukemia (AML) pathogenesis. The aim of the study was to characterize the cytokine and gene expression profile, immunophenotype and cytogenetics of BM-MSCs from AML patients compared to normal BM-MSCs from healthy donors. AML BM-MSCs showed decreased monocyte chemoattractant protein-1 levels compared to normal BM-MSCs. AML BM-MSCs expressed similar β1 integrin, CD44, CD73, CD90 and E-cadherin compared to normal BM-MSCs. Cytogenetic analysis revealed chromosomal aberrations in AML BM-MSCs, some overlapping with and others distinct from their corresponding AML blasts. No significant difference in gene expression was detected between AML BM-MSCs compared to normal BM-MSCs; however, comparing the differences between AML and MSCs from AML patients with the differences between normal hematopoietic cells and normal MSCs by Ingenuity pathway analysis showed key distinctions of the AML setting: (1) upstream gene regulation by transforming growth factor beta 1, tumor necrosis factor, tissue transglutaminase 2, CCAAT/enhancer binding protein alpha and SWItch/Sucrose NonFermentable related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4; (2) integrin and interleukin 8 signaling as overrepresented canonical pathways; and (3) upregulation of transcription factors FBJ murine osteosarcoma viral oncogene homolog and v-myb avian myeloblastosis viral oncogene homolog. Thus, phenotypic abnormalities of AML BM-MSCs highlight a dysfunctional BME that may impact AML survival and proliferation.
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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.