ArticleJournal of hematology & oncology2013
IGF binding protein 2 is a cell-autonomous factor supporting survival and migration of acute leukemia cells.
Article in Journal of hematology & oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Prognostic value of IGFBP2 in various cancers: a systematic review and meta-analysis.Cancer medicine · 2022Pooled it
- Rewiring the tumor microenvironment: IGFBP2 at the Nexus of remodeling and therapy resistance?Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
- IGFBP2 alteration contributes to prostate cancer progression by modulating prostate stroma activation.Cell communication and signaling : CCS · 2025Article
- NIPA1 depletion in tumor-associated macrophages via IGFBP2/EGFR attenuates acute myeloid leukemia progression and chemoresistance.Annals of hematology · 2025Article
- Advances in the role of the IGF signaling system in myelodysplastic syndromes and acute myeloid leukemia.Frontiers in oncology · 2025Review
- The role of IGF/IGF-1R signaling in the regulation of cancer stem cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Extracellular vesicles from type-2 macrophages increase the survival of chronic lymphocytic leukemia cells ex vivo.Cancer gene therapy · 2024Article
- A machine learning model identifies M3-like subtype in AML based on PML/RARα targets.iScience · 2024Article
- A novel AML1-ETO/FTO positive feedback loop promotes leukemogenesis and Ara-C resistance via stabilizing IGFBP2 in t(8;21) acute myeloid leukemia.Experimental hematology & oncology · 2024Article
- Secreted insulin-like growth factor binding protein 5 functions as a tumor suppressor and chemosensitizer through inhibiting insulin-like growth factor 1 receptor/protein kinase B pathway in acute myeloid leukemia.Neoplasia (New York, N.Y.) · 2024Article
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4Cell reports · 2023Article
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4bioRxiv : the preprint server for biology · 2023Article
- RHOA-regulated IGFBP2 promotes invasion and drives progression of BCR-ABL1 chronic myeloid leukemia.Haematologica · 2023Article
- Article
- Hymeglusin Enhances the Pro-Apoptotic Effects of Venetoclax in Acute Myeloid Leukemia.Frontiers in oncology · 2022Article
- Article
- IGFBP-2 acts as a tumour suppressor and plays a role in determining chemosensitivity in bladder cancer cells.Oncotarget · 2019Article
- Gene expression signature that predicts early molecular response failure in chronic-phase CML patients on frontline imatinib.Blood advances · 2019Article
- IGFBP2 promotes vasculogenic mimicry formation via regulating CD144 and MMP2 expression in glioma.Oncogene · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe role of IGF binding protein 2 (IGFBP2) in cancer development is intriguing. Previously we identified IGFBP2 as an extrinsic factor that supports the activity of hematopoietic stem cells (HSCs). METHODS AND
resultsHere we investigated the role of IGFBP2 in in human leukemia cells and in the retroviral AML1-ETO9a transplantation acute myeloid leukemia (AML) mouse model.
resultsIGFBP2 is highly expressed in certain human AML and acute lymphoblastic leukemia (ALL) cells. Inhibition of expression of endogenous IGFBP2 in human leukemia cells led to elevated apoptosis and decreased migration and, consistently, to decreased activation of AKT and other signaling molecules. We also studied the effects of IGFBP2 knockout in the retroviral AML1-ETO9a transplantation AML mouse model. The deletion of IGFBP2 in donor AML cells significantly decreased leukemia development in transplanted mice. Lack of IGFBP2 resulted in upregulation of PTEN expression and downregulation of AKT activation, in the mouse AML cells. The treatment of IGFBP2 deficient AML cells with a PTEN inhibitor restored the wild-type colony forming ability. The deletion of IGFBP2 also led to decreased AML infiltration into peripheral organs and tissues, suggesting that IGFBP2 is required for the migration of AML cells out of bone marrow.
conclusionIGFBP2 is a critical cell-autonomous factor that promotes the survival and migration of acute leukemia cells.
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Registered trials
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