ArticleJournal of hematology & oncology2018
CAMKs support development of acute myeloid leukemia.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The trial behind it
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
27 citing papers in PubMed, 46 citations in OpenAlex.
- Sintilimab plus decitabine for higher-risk treatment-naïve myelodysplastic syndromes: efficacy, safety, and biomarker analysis of a phase II, single-arm trial.Journal for immunotherapy of cancer · 2024Trial
- ANGPTL8 induces the aging of hematopoietic stem/progenitor cells.Biogerontology · 2026Article
- Longitudinal localization of leukaemic stem cells between the metaphysis and central marrow governs their behaviour.Nature cell biology · 2026Article
- scDIAGRAM: detecting chromatin compartments from individual single-cell Hi-C matrix without imputation or reference features.Briefings in bioinformatics · 2026Article
- Nonionotropic action of an acid-sensing ion channel inhibits leukemogenesis in the acidic bone marrow niche.The Journal of clinical investigation · 2025Article
- CaMKK2 as a therapeutic target to combat metastasis in glioblastoma.Molecular biology reports · 2025Review
- Cholesterol metabolism regulated by CAMKK2-CREB signaling promotes castration-resistant prostate cancer.Cell reports · 2025Article
- Eph Receptors Activate Myeloid Checkpoint Receptor LILRB5 to Support Tumor Development.Cancer immunology research · 2025Article
- Angiopoietin-like protein 2 inhibits thrombus formation.Molecular and cellular biochemistry · 2025Article
- The Anti-Leukemic Potential of Bee Venom.International journal of general medicine · 2025Review
- LILRB2 promotes immune escape in breast cancer cells via enhanced HLA-A degradation.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Inhibiting AGTR1 reduces AML burden and protects the heart from cardiotoxicity in mouse models.Science translational medicine · 2024Article
- Leukocyte immunoglobulin-like receptor B2 overexpression as a promising therapeutic target and noninvasive screening biomarker for colorectal cancer.World journal of gastroenterology · 2023Article
- Repair of Limb Ischemia Is Dependent on Hematopoietic Stem Cell Specific-SHP-1 Regulation of TGF-β1.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Review
- Regulation and role of CAMKK2 in prostate cancer.Nature reviews. Urology · 2022Review
- Put in a "CaCells · 2022Review
- Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential.Frontiers in oncology · 2022Review
- Hinge Binder Scaffold Hopping Identifies Potent Calcium/Calmodulin-Dependent Protein Kinase Kinase 2 (CAMKK2) Inhibitor Chemotypes.Journal of medicinal chemistry · 2021Article
- Article
Corrections and comments
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Authors and funding
15 authors at 9 institutions in 2 countries.
Funding
Abstract
backgroundWe recently identified the human leukocyte immunoglobulin-like receptor B2 (LILRB2) and its mouse ortholog-paired Ig-like receptor (PirB) as receptors for several angiopoietin-like proteins (Angptls). We also demonstrated that PirB is important for the development of acute myeloid leukemia (AML), but exactly how an inhibitory receptor such as PirB can support cancer development is intriguing.
resultsHere, we showed that the activation of Ca (2+)/calmodulin-dependent protein kinases (CAMKs) is coupled with PirB signaling in AML cells. High expression of CAMKs is associated with a poor overall survival probability in patients with AML. Knockdown of CAMKI or CAMKIV decreased human acute leukemia development in vitro and in vivo. Mouse AML cells that are defective in PirB signaling had decreased activation of CAMKs, and the forced expression of CAMK partially rescued the PirB-defective phenotype in the MLL-AF9 AML mouse model. The inhibition of CAMK kinase activity or deletion of CAMKIV significantly slowed AML development and decreased the AML stem cell activity. We also found that CAMKIV acts through the phosphorylation of one of its well-known target (CREB) in AML cells.
conclusionCAMKs are essential for the growth of human and mouse AML. The inhibition of CAMK signaling may become an effective strategy for treating leukemia.
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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.