ReviewCytokine2023
The duality of STAT2 mediated type I interferon signaling in the tumor microenvironment and chemoresistance.
Review in Cytokine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 19 citations in OpenAlex.
- Global Proteomic Analysis Reveals Inflammatory Pathway Modulation Associated with miR-146a in LPS-Stimulated Macrophages.International journal of molecular sciences · 2026Article
- Review
- Article
- Loss of XRCC1 promotes cGAS/STING mediated innate immune signaling in gastric cancer.Molecular medicine (Cambridge, Mass.) · 2026Article
- Integrative Multi-Omics and Experimental Analyses Identify TAPBP as a Key Mediator Linking Genetic Susceptibility to Melanocyte Dysfunction in Vitiligo.Clinical, cosmetic and investigational dermatology · 2026Article
- Development of translational read-through-inducing drugs as novel therapeutic options for patients with Fanconi anemia.Cell death discovery · 2025Article
- Integrating gene expression, genomic, and phosphoproteomic data to infer transcription factor activity in lung cancer.NAR genomics and bioinformatics · 2025Article
- The role of TLR-4 in chemoresistance of cancer.Discover oncology · 2025Review
- cGAS/STING-Independent Induction of Type I Interferon by Inhibitors of the Histone Methylase KDM5B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- USP5 motivates immunosuppressive microenvironment in multiple myeloma by activating STAT2-PFKFB4-mediated glycolysis.Cancer immunology, immunotherapy : CII · 2025Article
- IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer.Molecular cancer · 2025Article
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Article
- Oncogenic STAT Transcription Factors as Targets for Cancer Therapy: Innovative Strategies and Clinical Translation.Cancers · 2024Review
- 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The tumor microenvironment consists of tumor cells, extracellular matrix, blood vessels, and non-tumor cells such as fibroblasts and immune cells. Crosstalk among components of this cellular ecosystem can transform non-malignant cells and promote tumor invasion and metastasis. Evidence is accumulating that the transcription factor STAT2, a downstream effector of type I interferon (IFN-I) signaling, can either inhibit or promote tumorigenesis depending on the unique environment presented by each type of cancer. STAT2 has long been associated with the canonical JAK/STAT pathway involved in various biological processes including reshaping of the tumor microenvironment and in antitumor immunity. This dichotomous tendency of STAT2 to both inhibit and worsen tumor formation makes the protein a curious, and yet relatively ill-defined player in many cancer pathways involving IFN-I. In this review, we discuss the role of STAT2 in contributing to either a tumorigenic or anti-tumorigenic microenvironment as well as chemoresistance.
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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.