ArticleCancer research2016
Eradication of Acute Myeloid Leukemia with FLT3 Ligand-Targeted miR-150 Nanoparticles.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 66 citations in OpenAlex.
- Overcoming therapeutic challenges in acute myeloid leukemia: active targeting strategies by nano-drug delivery systems.Journal of translational medicine · 2026Review
- TET1 as a master regulator controlling GPX4-dependent and -independent ferroptosis surveillance in acute myeloid leukemia.Nature communications · 2026Article
- miR-150-5p at the Interface of Cancer Biology and Immune Regulation: Dual Roles, Mechanisms, and Therapeutic Opportunities.Journal of Cancer · 2026Review
- The miRNA Landscape of Leukemia - Cellular Actions to Therapy through Molecular Mechanisms.Cell biochemistry and biophysics · 2025Review
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
- RNA activation ofMolecular therapy. Nucleic acids · 2025Article
- A review of common immunotherapy and nano immunotherapy for acute myeloid leukemia.Frontiers in immunology · 2025Review
- Antisense oligonucleotides as a targeted therapeutic approach in model of acute myeloid leukemia.Molecular biology reports · 2024Article
- Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC.International journal of molecular sciences · 2024Review
- Current advance of nanotechnology in diagnosis and treatment for malignant tumors.Signal transduction and targeted therapy · 2024Review
- Homoharringtonine enhances cytarabine-induced apoptosis in acute myeloid leukaemia by regulating the p38 MAPK/H2AX/Mcl-1 axis.BMC cancer · 2024Article
- Targeting ferroptosis for leukemia therapy: exploring novel strategies from its mechanisms and role in leukemia based on nanotechnology.European journal of medical research · 2024Review
- RNA mGenes & diseases · 2024Article
- MicroRNAs in T Cell-Immunotherapy.International journal of molecular sciences · 2022Review
- Protocol to establish a stableSTAR protocols · 2022Article
- Hierarchically Multivalent Peptide-Nanoparticle Architectures: A Systematic Approach to Engineer Surface Adhesion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- mRNA therapy for myocardial infarction: A review of targets and delivery vehicles.Frontiers in bioengineering and biotechnology · 2022Review
- Article
- The role of EVI1 gene quantification in AML patients with 11q23/MLL rearrangement after allogeneic hematopoietic stem cell transplantation.Bone marrow transplantation · 2021Article
- The impact of molecular tumor profiling on the design strategies for targeting myeloid leukemia and EGFR/CD44-positive solid tumors.Beilstein journal of nanotechnology · 2021Review
Corrections and comments
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Authors and funding
25 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is a common and fatal form of hematopoietic malignancy. Overexpression and/or mutations of FLT3 have been shown to occur in the majority of cases of AML. Our analysis of a large-scale AML patient cohort (N = 562) indicates that FLT3 is particularly highly expressed in some subtypes of AML, such as AML with t(11q23)/MLL-rearrangements or FLT3-ITD. Such AML subtypes are known to be associated with unfavorable prognosis. To treat FLT3-overexpressing AML, we developed a novel targeted nanoparticle system: FLT3 ligand (FLT3L)-conjugated G7 poly(amidoamine) (PAMAM) nanosized dendriplex encapsulating miR-150, a pivotal tumor suppressor and negative regulator of FLT3 We show that the FLT3L-guided miR-150 nanoparticles selectively and efficiently target FLT3-overexpressing AML cells and significantly inhibit viability/growth and promote apoptosis of the AML cells. Our proof-of-concept animal model studies demonstrate that the FLT3L-guided miR-150 nanoparticles tend to concentrate in bone marrow, and significantly inhibit progression of FLT3-overexpressing AML in vivo, while exhibiting no obvious side effects on normal hematopoiesis. Collectively, we have developed a novel targeted therapeutic strategy, using FLT3L-guided miR-150-based nanoparticles, to treat FLT3-overexpressing AML with high efficacy and minimal side effects. Cancer Res; 76(15); 4470-80. ©2016 AACR.
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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.