ReviewFrontiers in immunology2014
IL-1 Receptor-Associated Kinase Signaling and Its Role in Inflammation, Cancer Progression, and Therapy Resistance.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 4 of them syntheses that pooled it.
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
96 citing papers in PubMed, 4 syntheses or guidelines pooled it, 171 citations in OpenAlex.
- Pooled it
- Meta-analysis of gene signatures and key pathways indicates suppression of JNK pathway as a regulator of chemo-resistance in AML.Scientific reports · 2021Pooled it
- Pooled it
- Pooled it
- IRAK-M Knockout Exacerbates Inflammation in Mice Infected withMicroorganisms · 2026Article
- Interleukin-1 receptor-associated kinase 1 controls chemoresistance and immuno-killing in non-small cell lung cancer.Signal transduction and targeted therapy · 2026Article
- Activation of MyD88/IRAK1 axis and downstream proinflammatory signaling in healthy adult and neonatal African American skin.JID innovations : skin science from molecules to population health · 2026Article
- IL-36 activates neutrophil extracellular traps and exacerbates LPS-induced ARDS in mice.Scientific reports · 2026Article
- Probiotic bacteria Bifidobacterium bifidum upregulation of intestinal epithelial tight junction barrier is mediated by TLR-2/TLR-6 receptor complex activation of occludin gene.NPJ biofilms and microbiomes · 2026Article
- Host Responses to SARS-CoV-2 with an Emphasis on Cytokines.International journal of molecular sciences · 2026Review
- Phosphoregulation of interleukin-1 receptor-associated kinase 1 in inflammatory signaling.Frontiers in immunology · 2026Review
- BCTI: a Bayesian network-based method for revealing critical transitions in complex biological systems.PeerJ · 2026Article
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- A novel approach to metabolic profiling in case models of MECP2-related disorders.Metabolic brain disease · 2025Article
- Review
- UBE2N Is Essential for Maintenance of Skin Homeostasis and Suppression of Inflammation.The Journal of investigative dermatology · 2024Article
- Emerging interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors or degraders as therapeutic agents for autoimmune diseases and cancer.Acta pharmaceutica Sinica. B · 2024Review
- Review
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- A highly sensitive reporter system to monitor endogenous YAP1/TAZ activity and its application in various human cells.Cancer science · 2024Article
36 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic inflammation has long been associated with the development of cancer. Among the various signaling pathways within cancer cells that can incite the expression of inflammatory molecules are those that activate IL-1 receptor-associated kinases (IRAK). The IRAK family is comprised of four family members, IRAK-1, IRAK-2, IRAK-3 (also known as IRAK-M), and IRAK-4, which play important roles in both positively and negatively regulating the expression of inflammatory molecules. The wide array of inflammatory molecules that are expressed in response to IRAK signaling within the tumor microenvironment regulate the production of factors which promote tumor growth, metastasis, immune suppression, and chemotherapy resistance. Based on published reports we propose that dysregulated activation of the IRAK signaling pathway in cancer cells contributes to disease progression by creating a highly inflammatory tumor environment. In this article, we present both theoretical arguments and reference experimental data in support of this hypothesis.
Indexed as
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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.