ArticleScientific reports2015
Improving chemotherapeutic efficiency in acute myeloid leukemia treatments by chemically synthesized peptide interfering with CXCR4/CXCL12 axis.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 42 citations in OpenAlex.
- CXCR4 as a therapeutic target in acute myeloid leukemia.Leukemia · 2024Review
- A Nucleus-Targeting WT1 Antagonistic Peptide Encapsulated in Polymeric Nanomicelles Combats Refractory Chronic Myeloid Leukemia.Pharmaceutics · 2023Article
- Peptide-assembled nanoparticles targeting tumor cells and tumor microenvironment for cancer therapy.Frontiers in chemistry · 2023Review
- A biomimetic nanocomposite with enzyme-like activities and CXCR4 antagonism efficiently enhances the therapeutic efficacy of acute myeloid leukemia.Bioactive materials · 2022Article
- Bone Marrow Aging and the Leukaemia-Induced Senescence of Mesenchymal Stem/Stromal Cells: Exploring Similarities.Journal of personalized medicine · 2022Review
- Role of CXCR4 in the progression and therapy of acute leukaemia.Cell proliferation · 2021Review
- Therapeutic Targeting of the Leukaemia Microenvironment.International journal of molecular sciences · 2021Review
- Insights Into Bone Marrow Niche Stability: An Adhesion and Metabolism Route.Frontiers in cell and developmental biology · 2021Review
- Significance of CXCL12/CXCR4 Ligand/Receptor Axis in Various Aspects of Acute Myeloid Leukemia.Cancer management and research · 2020Review
- Targeting CXCR4 in AML and ALL.Frontiers in oncology · 2020Review
- The Bone Marrow Niche - The Tumor Microenvironment That Ensures Leukemia Progression.Advances in experimental medicine and biology · 2020Review
- Relationship between CXC chemokine receptor 4 expression and prognostic significance in acute myeloid leukemia.Medicine · 2019Article
- Cotargeting BCL-2 and PI3K Induces BAX-Dependent Mitochondrial Apoptosis in AML Cells.Cancer research · 2018Article
- Targeting murine leukemic stem cells by antibody functionalized mesoporous silica nanoparticles.Scientific reports · 2018Article
- A novel CXCR4 antagonist IgG1 antibody (PF-06747143) for the treatment of hematologic malignancies.Blood advances · 2017Article
- Article
- The Interaction Between Niche and Hematopoietic Stem Cells.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2016Review
- Article
- Targeting the CXCR4/CXCL12 axis with the peptide antagonist E5 to inhibit breast tumor progression.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone marrow stroma can protect acute myeloid leukemia (AML) cells against chemotherapeutic agents and provide anti-apoptosis and chemoresistance signals through secreting chemokine CXCL12 to activate its receptor CXCR4 on AML cells, resulting in minimal residual leukemia and relapse. Therefore disrupting the CXCR4/CXCL12 axis with antagonists is of great significance for improving chemosensitivity and decreasing relapse rate. In a previous study, we reported a novel synthetic peptide E5 with its remarkable effect on inhibiting CXCR4/CXCL12-mediated adhesion and migration of AML cells. Here we presented E5's capacity of enhancing the therapeutic efficiency of various chemotherapeutics on AML in vitro and in vivo. Results showed that E5 can diminish bone marrow stromal cell-provided protection to leukemia cells, significantly increasing the apoptosis induced by various chemotherapeutics in multiple AML cell lines. In an AML mouse xenograft model, E5 induced 1.84-fold increase of circulating AML cells out of protective stroma niche. Combined with vincristine or cyclophosphamide, E5 inhibited infiltration of AML cells into bone marrow, liver and spleen, as well as prolonged the lifespan of AML mice compared with mice treated with chemotherapy alone. In addition, E5 presented no toxicity in vivo according to the histological analysis and routine clinical parameters of serum analysis.
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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.