ArticleBlood2014
IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Nilotinib-induced bone marrow CD34+/lin-Ph+ cells early clearance in newly diagnosed CP-Chronic Myeloid Leukemia: Final report of the PhilosoPhi34 study.European journal of haematology · 2021Trial
- Pathway incompatibility between NF-κB and RAS signaling constrains oncogenicity in B-cell leukemia.The Journal of biological chemistry · 2026Article
- Understanding drug resistance in chronic myeloid leukemia through the lens of leukemic stem cell states: insights from single-cell analyses.Haematologica · 2026Review
- Complementary and countervailing actions of Jak2 and Ikk2 in hematopoiesis in mice.Experimental hematology · 2023Article
- Siglec-15 Promotes Evasion of Adaptive Immunity in B-cell Acute Lymphoblastic Leukemia.Cancer research communications · 2023Article
- FBXW7β isoform drives transcriptional activation of the proinflammatory TNF cluster in human pro-B cells.Blood advances · 2023Article
- Targeting cytokine-induced leukemic stem cell persistence in chronic myeloid leukemia by IKK2-inhibition.Haematologica · 2023Article
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Eliminating chronic myeloid leukemia stem cells by IRAK1/4 inhibitors.Nature communications · 2022Article
- Article
- An aging mouse model of human chronic myeloid leukemia.Oncogene · 2021Article
- Inhibition of cystathionine β-synthase promotes apoptosis and reduces cell proliferation in chronic myeloid leukemia.Signal transduction and targeted therapy · 2021Article
- Therapeutic Vulnerabilities of Transcription Factors in AML.Molecular cancer therapeutics · 2021Review
- MNase Profiling of Promoter Chromatin inG3 (Bethesda, Md.) · 2020Article
- Novel Quinoline Compounds Active in Cancer Cells through Coupled DNA Methyltransferase Inhibition and Degradation.Cancers · 2020Article
- Infliximab therapy together with tyrosine kinase inhibition targets leukemic stem cells in chronic myeloid leukemia.BMC cancer · 2019Article
- Strategies For Targeting Chronic Myeloid Leukaemia Stem Cells.Blood and lymphatic cancer : targets and therapy · 2019Review
- Reactive Oxygen Species Are Involved in the Development of Gastric Cancer and Gastric Cancer-Related Depression through ABL1-Mediated Inflammation Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- Novel AF1q/MLLT11 favorably affects imatinib resistance and cell survival in chronic myeloid leukemia.Cell death & disease · 2018Article
- Stabilization of NF-κB-Inducing Kinase Suppresses MLL-AF9-Induced Acute Myeloid Leukemia.Cell reports · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The product of the Ph chromosome, the BCR-ABL1 tyrosine kinase activates diverse signaling pathways in leukemic cells from patients with chronic myeloid leukemia (CML) and Ph(+) B-cell acute lymphoblastic leukemia (B-ALL). Previous studies showed that nuclear factor κB (NF-κB) is activated in BCR-ABL1-expressing cells, but the mechanism of activation and importance of NF-κB to the pathogenesis of BCR-ABL1-positive myeloid and lymphoid leukemias are unknown. Coexpression of BCR-ABL1 and a superrepressor mutant of inhibitory NF-κB α (IκBαSR) blocked nuclear p65/RelA expression and inhibited the proliferation of Ba/F3 cells and primary BCR-ABL1-transformed B lymphoblasts without affecting cell survival. In retroviral mouse models of CML and B-ALL, coexpression of IκBαSR attenuated leukemogenesis, prolonged survival, and reduced myeloid leukemic stem cells. Coexpression of dominant-negative mutants of IκB kinase α (IKKα)/IKK1 or IKKβ/IKK2 also inhibited lymphoid and myeloid leukemogenesis by BCR-ABL1. Blockade of NF-κB decreased expression of the NF-κB targets c-MYC and BCL-X and increased the sensitivity of BCR-ABL1-transformed lymphoblasts to ABL1 kinase inhibitors. These results demonstrate that NF-κB is activated through the canonical IKK pathway and plays distinct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, validating NF-κB and IKKs as targets for therapy of Ph(+) leukemias.
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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.