ArticleLeukemia research2015
Endothelial cell derived angiocrine support of acute myeloid leukemia targeted by receptor tyrosine kinase inhibition.
Article in Leukemia research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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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
14 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring the Bone Marrow Microenvironment as a Therapeutic Barrier and Targetable Source of Crosstalk in Acute Myeloid Leukemia.Blood and lymphatic cancer : targets and therapy · 2026Review
- Harnessing upregulated E-selectin while enhancing SDF-1α sensing redirects infused NK cells to the AML-perturbed bone marrow.Leukemia · 2024Article
- Modelling acute myeloid leukemia (AML): What's new? A transition from the classical to the modern.Drug delivery and translational research · 2023Review
- Conversation before crossing: dissecting metastatic tumor-vascular interactions in microphysiological systems.American journal of physiology. Cell physiology · 2022Review
- Understanding the Immune-Stroma Microenvironment in B Cell Malignancies for Effective Immunotherapy.Frontiers in oncology · 2021Review
- 7‑Difluoromethyl‑5,4'‑dimethoxygenistein exerts anti‑angiogenic effects on acute promyelocytic leukemia HL‑60 cells by inhibiting the TLR4/NF‑κB signaling pathway.Molecular medicine reports · 2020Article
- Endothelial cells produce angiocrine factors to regulate bone and cartilage via versatile mechanisms.Theranostics · 2020Review
- Article
- The phenotype of vascular smooth muscle cells co-cultured with endothelial cells is modulated by PDGFR-β/IQGAP1 signaling in LPS-induced intravascular injury.International journal of medical sciences · 2019Article
- Targeting tumour microenvironment by tyrosine kinase inhibitor.Molecular cancer · 2018Review
- Myeloid malignancies and the microenvironment.Blood · 2017Article
- Bone Marrow Blood Vessels: Normal and Neoplastic Niche.Oncology reviews · 2016Review
- Mesenchymal Stem and Progenitor Cells in Normal and Dysplastic Hematopoiesis-Masters of Survival and Clonality?International journal of molecular sciences · 2016Review
- XBP1 splicing triggers miR-150 transfer from smooth muscle cells to endothelial cells via extracellular vesicles.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In acute myeloid leukemia (AML), refractory disease is a major challenge and the leukemia microenvironment may harbor refractory disease. Human AML cell lines KG-1 and HL-60 expressed receptors also found on endothelial cells (ECs) such as VEGFRs, PDGFRs, and cKit. When human AML cells were co-cultured with human umbilical vein endothelial cells (HUVECs) and primary bone marrow endothelial cell (BMECs), the AML cells were more resistant to cytarabine chemotherapy, even in transwell co-culture suggesting angiocrine regulation. Primary BMECs secreted significantly increased levels of VEGF-A and PDGF-AB after exposure to cytarabine. Pazopanib, a receptor tyrosine kinase inhibitor (RTKI) of VEGFRs, PDGFRs, and cKit, removed EC protection of AML cells and enhanced AML cell sensitivity to cytarabine. Xenograft modeling showed significant regression of AML cells and abrogation of BM hypervascularity in RTKI treated cohorts. Together, these results show direct cytotoxicity of RTKIs on AML cells and reversal of EC protection. Combining RTKIs with chemotherapy may serve as promising therapeutic strategy for patients with AML.
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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.