ArticleOncogene2012
Four proteins governing overangiogenic endothelial cell phenotype in patients with multiple myeloma are plausible therapeutic targets.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Mechanisms and intervention strategies of microenvironment-mediated drug resistance in multiple myeloma.Cancer cell international · 2026Review
- Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors.International journal of molecular sciences · 2024Article
- Alpha-B-Crystallin overexpression is sufficient to promote tumorigenesis and metastasis in mice.Experimental hematology & oncology · 2023Article
- Pathways of Angiogenic and Inflammatory Cytokines in Multiple Myeloma: Role in Plasma Cell Clonal Expansion and Drug Resistance.Journal of clinical medicine · 2022Review
- Natural Killer Cells in the Malignant Niche of Multiple Myeloma.Frontiers in immunology · 2021Review
- Anti-VEGF Drugs in the Treatment of Multiple Myeloma Patients.Journal of clinical medicine · 2020Review
- Bone Marrow Stromal Cells-Induced Drug Resistance in Multiple Myeloma.International journal of molecular sciences · 2020Review
- A Comprehensive Biological and Clinical Perspective Can Drive a Patient-Tailored Approach to Multiple Myeloma: Bridging the Gaps between the Plasma Cell and the Neoplastic Niche.Journal of oncology · 2020Review
- High-Risk Multiple Myeloma: Integrated Clinical and Omics Approach Dissects the Neoplastic Clone and the Tumor Microenvironment.Journal of clinical medicine · 2019Review
- Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas.International journal of medical sciences · 2019Review
- EphA3 targeting reduces in vitro adhesion and invasion and in vivo growth and angiogenesis of multiple myeloma cells.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- Epha3 acts as proangiogenic factor in multiple myeloma.Oncotarget · 2017Article
- High serum levels of extracellular vesicles expressing malignancy-related markers are released in patients with various types of hematological neoplastic disorders.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A.Oncogenesis · 2014Article
- Novel agents and new therapeutic approaches for treatment of multiple myeloma.World journal of methodology · 2014Review
- Bone marrow fibroblasts parallel multiple myeloma progression in patients and mice: in vitro and in vivo studies.Leukemia · 2014Article
- The dual role of filamin A in cancer: can't live with (too much of) it, can't live without it.Endocrine-related cancer · 2013Review
- The proteomics big challenge for biomarkers and new drug-targets discovery.International journal of molecular sciences · 2012Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone marrow (BM) angiogenesis has an important role in the initiation and progression of multiple myeloma (MM). We looked at novel mechanisms of vessel formation in patients with MM through a comparative proteomic analysis between BM endothelial cells (ECs) of patients with active MM (MMECs) and ECs of patients with monoclonal gammopathy of undetermined significance (MGECs) and of subjects with benign anemia (normal ECs). Four proteins were found overexpressed in MMECs: filamin A, vimentin, α-crystallin B and 14-3-3ζ/δ protein, not yet linked to overangiogenic phenotype. These proteins gave a typical distribution in the BM of MM patients and in MMECs versus MGECs, plausibly according to a different functional state. Their expression was enhanced by vascular endothelial growth factor, fibroblast growth factor 2, hepatocyte growth factor and MM plasma cell conditioned medium in step with enhancement of MMEC angiogenesis. Their silencing RNA knockdown affected critical MMEC angiogenesis-related functions, such as spreading, migration and tubular morphogenesis. A gradual stabilization of 14-3-3ζ/δ protein was observed, with transition from normal ECs to MGECs and MMECs that may be a critical step for the angiogenic switch in MMECs and maintenance of the cell overangiogenic phenotype. These proteins were substantially impacted by anti-MM drugs, such as bortezomib, lenalidomide and panobinostat. Results suggest that these four proteins could be new targets for the antiangiogenic management of MM patients.
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Registered trials
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