ArticleNature communications2022
Eliminating chronic myeloid leukemia stem cells by IRAK1/4 inhibitors.
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Article in Nature communications, 2022. 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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0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Application of NanoString Technologies in Chronic Myeloid Leukemia, Essential Thrombocythemia, Primary Myelofibrosis, and Polycythemia Vera: A Pilot Study.Diagnostics (Basel, Switzerland) · 2026Article
- FBXO3-mediated DUSP9 ubiquitination promotes leukemia stem cell maintenance and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Cell reports. Medicine · 2026Article
- Recent Advances in FLT3-Based Dual Inhibitors: A Promising Strategy for the Treatment of Acute Myeloid Leukemia.Current medicinal chemistry · 2026Review
- Advancing our understanding of the influence of myeloid-derived suppressor cells in chronic myeloid leukemia.Journal of cancer research and clinical oncology · 2025Review
- Artificial intelligence-driven label-free detection of chronic myeloid leukemia cells using ghost cytometry.Scientific reports · 2025Article
- BCR::ABL1-induced mitochondrial morphological alterations as a potential clinical biomarker in chronic myeloid leukemia.Cancer science · 2025Article
- Chronic inflammation deters natural killer cell fitness and cytotoxicity in myeloid leukemia.Blood advances · 2025Article
- BAP1 Represses Sequential Activation of IRAKs and NF-κB Signaling in Pancreatic Cancer.International journal of biological sciences · 2025Article
- Mechanisms and signaling pathways of tyrosine kinase inhibitor resistance in chronic myeloid leukemia: A comprehensive review.Leukemia research reports · 2025Review
- Revolution in Cell Therapy: In Vivo Chimeric-Antigen-Receptor-T-Cell Therapy Breakthroughs and Promises for the Future.Research (Washington, D.C.) · 2025Review
- The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway.Cell death & disease · 2024Article
- Signaling pathways governing the behaviors of leukemia stem cells.Genes & diseases · 2024Review
- Chromatographic analysis of ponatinib and its impurities: method development, validation, and identification of new degradation product.Frontiers in chemistry · 2024Article
- The Bone Marrow Immune Microenvironment in CML: Treatment Responses, Treatment-Free Remission, and Therapeutic Vulnerabilities.Current hematologic malignancy reports · 2023Review
- Analysis of causes for poor persistence of CAR-T cell therapyFrontiers in immunology · 2023Review
- IRAK-4 inhibition: emavusertib for the treatment of lymphoid and myeloid malignancies.Frontiers in immunology · 2023Review
- Properties of Leukemic Stem Cells in Regulating Drug Resistance in Acute and Chronic Myeloid Leukemias.Biomedicines · 2022Review
- Article
- Dual-Targeted Therapy Circumvents Non-Genetic Drug Resistance to Targeted Therapy.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 2 countries.
Yosuke TanakaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan. ytims@ims.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-8538-0916
Reina TakedaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.ORCID http://orcid.org/0000-0002-4233-8806
Tsuyoshi FukushimaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Keiko MikamiDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Shun TsuchiyaDepartment of Hematology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Moe TamuraDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Keito AdachiDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Terumasa UmemotoInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0003-0423-9003
Shuhei AsadaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.ORCID http://orcid.org/0000-0001-6116-7996
Naoki WatanabeDepartment of Hematology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Soji MorishitaDepartment of Transfusion Medicine and Stem Cell Regulation, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.ORCID http://orcid.org/0000-0003-1081-0130
Misa ImaiDepartment of Transfusion Medicine and Stem Cell Regulation, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Masayoshi NagataDepartment of Urology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Marito ArakiDepartment of Transfusion Medicine and Stem Cell Regulation, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.ORCID http://orcid.org/0000-0002-3502-5000
Hitoshi TakizawaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0002-5276-5430
Tomofusa FukuyamaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.ORCID http://orcid.org/0000-0002-0709-3188
Chrystelle LamagnaRigel, South San Francisco, California, 94080, USA.
Esteban S MasudaRigel, South San Francisco, California, 94080, USA.
Ryoji ItoCentral Institute for Experimental Animals, Kanagawa, 210-0821, Japan.ORCID http://orcid.org/0000-0003-2903-2332
Susumu GoyamaDivision of Molecular Oncology Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, 108-8639, Japan.
Norio KomatsuDepartment of Hematology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Tomoiku TakakuDepartment of Hematology, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Toshio KitamuraDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan. kitamura@ims.u-tokyo.ac.jp.
The University of Tokyo · JPJuntendo University · JPKumamoto University · JPRigel (United States) · USCentral Institute for Experimental Animals · JP
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukemia stem cells (LSCs) in chronic myeloid leukemia (CML) are quiescent, insensitive to BCR-ABL1 tyrosine kinase inhibitors (TKIs) and responsible for CML relapse. Therefore, eradicating quiescent CML LSCs is a major goal in CML therapy. Here, using a G
Indexed as
AnimalsAntineoplastic AgentsChronic DiseaseDrug Resistance, NeoplasmFemaleFusion Proteins, bcr-ablHumansImatinib MesylateImmune Checkpoint InhibitorsInterleukin-1 Receptor-Associated KinasesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, MyeloidMaleMiceMiddle AgedNeoplastic Stem CellsAntineoplastic AgentsFusion Proteins, bcr-ablImatinib MesylateImmune Checkpoint InhibitorsInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseIrak4 protein, mouseProtein Kinase Inhibitors
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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.