ArticleCell reports2018
Stabilization of NF-κB-Inducing Kinase Suppresses MLL-AF9-Induced Acute Myeloid Leukemia.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
29 citing papers in PubMed, 39 citations in OpenAlex.
- NF-κB inducing kinase (NIK) deletion accelerates KRAS-driven pancreatic cancer in association with tumor microenvironment remodeling.Cell death & disease · 2026Article
- Construction of a prognostic risk model for acute myeloid leukemia based on exosomal genes and analysis of immune microenvironment characteristics.Scientific reports · 2025Article
- Integrative multi-omic analysis of NLRP3 inflammasome dysregulation and subtyping for personalized treatment in acute myeloid leukemia.Discover oncology · 2025Article
- TIFAB modulates metabolic pathways in KMT2A::MLLT3-induced AML through HNF4A.Blood advances · 2025Article
- Not just for lymphoid cells: the role of the noncanonical NF-κB signaling pathway in early and late myelopoiesis with a focus on hypereosinophilic disorders.Journal of leukocyte biology · 2024Review
- Anti-Inflammatory and Cancer-Preventive Potential of Chamomile (Biomedicines · 2024Article
- Nanotechnology in leukemia: diagnosis, efficient-targeted drug delivery, and clinical trials.European journal of medical research · 2023Review
- RETRACTED: TRIM10 Is Downregulated in Acute Myeloid Leukemia and Plays a Tumor Suppressive Role via Regulating NF-κB Pathway.Cancers · 2023Article
- Identification of curaxin as a potential new therapeutic for JAK2 V617F mutant patients.PloS one · 2023Article
- HSF1 is a driver of leukemia stem cell self-renewal in acute myeloid leukemia.Nature communications · 2022Article
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Targeting metabolism: A potential strategy for hematological cancer therapy.World journal of clinical cases · 2022Review
- TIFAB accelerates MLL-AF9-Induced acute myeloid leukemia through upregulation of HOXA9.iScience · 2021Article
- Therapeutic Vulnerabilities of Transcription Factors in AML.Molecular cancer therapeutics · 2021Review
- Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms.Frontiers in immunology · 2021Review
- Article
- Sphingosine-1-phosphate receptor 3 potentiates inflammatory programs in normal and leukemia stem cells to promote differentiation.Blood cancer discovery · 2021Article
- Drug Repurposing for Targeting Acute Leukemia WithFrontiers in pharmacology · 2021Review
- Targeting NF-κB-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer.International journal of molecular sciences · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Canonical NF-κB signaling is constitutively activated in acute myeloid leukemia (AML) stem cells and is required for maintenance of the self-renewal of leukemia stem cells (LSCs). However, any potential role for NF-κB non-canonical signaling in AML has been largely overlooked. Here, we report that stabilization of NF-κB-inducing kinase (NIK) suppresses AML. Mechanistically, stabilization of NIK activates NF-κB non-canonical signaling and represses NF-κB canonical signaling. In addition, stabilization of NIK-induced activation of NF-κB non-canonical signaling upregulates Dnmt3a and downregulates Mef2c, which suppresses and promotes AML development, respectively. Importantly, by querying the connectivity MAP using up- and downregulated genes that are present exclusively in NIK-stabilized LSCs, we discovered that verteporfin has anti-AML effects, suggesting that repurposing verteporfin to target myeloid leukemia is worth testing clinically. Our data provide a scientific rationale for developing small molecules to stabilize NIK specifically in myeloid leukemias as an attractive therapeutic option.
Indexed as
Identifiers
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.