ArticleThe Journal of experimental medicine2014
Co-inhibition of NF-κB and JNK is synergistic in TNF-expressing human AML.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 93 citations in OpenAlex.
- TRMT6/61A-mediated tRNA m1A methylation promotes codon-dependent TAB2 translation and drives AML progression.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- HCX3 Mitigates LPS-Induced Inflammatory Responses in Macrophages by Suppressing the Activation of the NF-κB Signaling Pathway.Current issues in molecular biology · 2025Article
- Review
- JAK-STAT-activated, fratricide-resistant CAR-T cells targeting membrane-bound TNF effectively treat AML and solid tumors.Journal for immunotherapy of cancer · 2025Article
- Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.Cancer cell international · 2025Review
- Low Dose Methotrexate Has Divergent Effects on Cycling and Resting Human Hematopoietic Stem and Progenitor Cells.Clinical and translational science · 2025Article
- Clinical Potential of Misshapen/NIKs-Related Kinase (MINK) 1-A Many-Sided Element of Cell Physiology and Pathology.Current issues in molecular biology · 2024Review
- Bone marrow inflammation in haematological malignancies.Nature reviews. Immunology · 2024Review
- Distinct roles of hematopoietic cytokines in the regulation of leukemia stem cells in murine MLL-AF9 leukemia.Stem cell reports · 2024Article
- Complementary and countervailing actions of Jak2 and Ikk2 in hematopoiesis in mice.Experimental hematology · 2023Article
- Anti-inflammatory effects of extracellular vesicles from Morchella on LPS-stimulated RAW264.7 cells via the ROS-mediated p38 MAPK signaling pathway.Molecular and cellular biochemistry · 2023Article
- Influence of cytokines on early death and coagulopathy in newly diagnosed patients with acute promyelocytic leukemia.Frontiers in immunology · 2023Article
- Article
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Review
- Article
- Inflammatory Cytokines Shape an Altered Immune Response During Myeloid Malignancies.Frontiers in immunology · 2021Review
- Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms.Frontiers in immunology · 2021Review
- Clinical Implications of Inflammation in Acute Myeloid Leukemia.Frontiers in oncology · 2021Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
Abstract
Leukemic stem cells (LSCs) isolated from acute myeloid leukemia (AML) patients are more sensitive to nuclear factor κB (NF-κB) inhibition-induced cell death when compared with hematopoietic stem and progenitor cells (HSPCs) in in vitro culture. However, inadequate anti-leukemic activity of NF-κB inhibition in vivo suggests the presence of additional survival/proliferative signals that can compensate for NF-κB inhibition. AML subtypes M3, M4, and M5 cells produce endogenous tumor necrosis factor α (TNF). Although stimulating HSPC with TNF promotes necroptosis and apoptosis, similar treatment with AML cells (leukemic cells, LCs) results in an increase in survival and proliferation. We determined that TNF stimulation drives the JNK-AP1 pathway in a manner parallel to NF-κB, leading to the up-regulation of anti-apoptotic genes in LC. We found that we can significantly sensitize LC to NF-κB inhibitor treatment by blocking the TNF-JNK-AP1 signaling pathway. Our data suggest that co-inhibition of both TNF-JNK-AP1 and NF-κB signals may provide a more comprehensive treatment paradigm for AML patients with TNF-expressing LC.
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What OpenQuestion holds
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.