ArticleLeukemia2002
Bcr-abl-positive cells secrete angiogenic factors including matrix metalloproteinases and stimulate angiogenesis in vivo in Matrigel implants.
Article in Leukemia, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 92 citations in OpenAlex.
- Trial
- Decoding the Implications of Zinc in the Development and Therapy of Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- 8-Hydroxydaidzein Downregulates JAK/STAT, MMP, Oxidative Phosphorylation, and PI3K/AKT Pathways in K562 Cells.Biomedicines · 2021Article
- Aberrantly reduced expression of miR-342-5p contributes to CCND1-associated chronic myeloid leukemia progression and imatinib resistance.Cell death & disease · 2021Article
- VEGFA's distal enhancer regulates its alternative splicing in CML.NAR cancer · 2021Article
- Selectively-Packaged Proteins in Breast Cancer Extracellular Vesicles Involved in Metastasis.International journal of molecular sciences · 2020Article
- Article
- Bone marrow microenvironment: The guardian of leukemia stem cells.World journal of stem cells · 2019Review
- The underestimated role of basophils in PhEuropean journal of clinical investigation · 2018Review
- Healing of a Large Long-Bone Defect through Serum-Free In Vitro Priming of Human Periosteum-Derived Cells.Stem cell reports · 2017Article
- [Regulation of Ruxolitinib on matrix metalloproteinase in JAK2V617F positive myeloroliferative neoplasms cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2017Article
- Association of Vascular Endothelial Growth Factor A (VEGFA) and its Receptor (VEGFR2) Gene Polymorphisms with Risk of Chronic Myeloid Leukemia and Influence on Clinical Outcome.Molecular diagnosis & therapy · 2016Article
- BCR/ABL oncogene-induced PI3K signaling pathway leads to chronic myeloid leukemia pathogenesis by impairing immuno-modulatory function of hemangioblasts.Cancer gene therapy · 2015Article
- Molecular biological characteristics of the recruitment of hematopoietic stem cells from bone marrow niche in chronic myeloid leukemia.International journal of clinical and experimental pathology · 2015Article
- Cytokine Regulation of Microenvironmental Cells in Myeloproliferative Neoplasms.Mediators of inflammation · 2015Review
- Reduced miR-3127-5p expression promotes NSCLC proliferation/invasion and contributes to dasatinib sensitivity via the c-Abl/Ras/ERK pathway.Scientific reports · 2014Article
- The malignancy suppression role of miR-23a by targeting the BCR/ABL oncogene in chromic myeloid leukemia.Cancer gene therapy · 2014Article
- The Hepatocyte Growth Factor (HGF)/Met Axis: A Neglected Target in the Treatment of Chronic Myeloproliferative Neoplasms?Cancers · 2014Review
- Studies on microRNAs that are correlated with the cancer stem cells in chronic myeloid leukemia.Molecular and cellular biochemistry · 2014Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
To further elucidate the role of angiogenesis in the pathogenesis of chronic myelogenous leukemia (CML) we evaluated the effects of the bcr-abl translocation on the secretion of the angiogenic factors VEGF, FGF-2, HGF, IL-8 and matrix metalloproteinases (MMPs) as well as on the angiogenic potential in vivo of bcr-abl+ cells. First, we examined murine FL5.12 cells transfected with the bcr-abl constructs p185, p210 and p230 and found that the transfected cells secreted as much as four-fold more VEGF (p185 > p210 >p230) than wild-type (wt) cells, as well as MMP-9 and MMP-2. When Matrigel fragments containing these bcr-abl+ cells were implanted subcutaneously in SCID or Balb-C mice they became significantly more vascularized and hemoglobinized than implants containing normal or wt cells (p185 > p210 > p230). Similarly, we found that myeloblasts expanded from bone marrow (BM) CD34+ cells derived from Philadelphia-positive CML patients secreted up to 10 times more VEGF, FGF-2, HGF and IL-8 compared to myeloblasts derived from normal donors' BM CD34+ cells and that BM mononuclear cells (MNC) isolated from CML patients induced vascularization of Matrigel implants in mice. Moreover, we found that peripheral blood MNC expressed MMP-2 and membrane-type (MT)1-MMP in about 50% of CML patients studied, and MMP-9 in all of them. Furthermore, VEGF stimulated the secretion of MMP-9 in these primary CML cells. We conclude that stimulation of angiogenesis by angiogenic factors, including MMPs, could play an important role in the pathogenesis of CML, suggesting that therapies targeting the newly formed endothelium could be developed for CML.
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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.