ArticleCellular and molecular gastroenterology and hepatology2018
Epithelial Smad4 Deletion Up-Regulates Inflammation and Promotes Inflammation-Associated Cancer.
Article in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Trial
- eQTL in diseased colon tissue identifies potential target genes associated with IBD.Nature communications · 2026Article
- Regulation and Function of Sox2 and CD44 Expression in the Stomach by Bone Morphogenetic Protein Signaling.Gastro hep advances · 2026Article
- Ulcerative colitis and colorectal cancer: Pathogenic insights and precision strategies for prevention and treatment.World journal of gastrointestinal oncology · 2025Review
- ACVR2A attenuation impacts lactate production and hyperglycolytic conditions attracting regulatory T cells in hepatocellular carcinoma.Cell reports. Medicine · 2025Article
- Epithelial-specific loss of Smad4 alleviates the fibrotic response in an acute colitis mouse model.Life science alliance · 2024Article
- Interaction of the tumor suppressor SMAD4 and WNT signaling in progression to oral squamous cell carcinoma.The Journal of pathology · 2024Article
- Single-cell RNA sequencing analysis of vestibular schwannoma reveals functionally distinct macrophage subsets.British journal of cancer · 2024Article
- Concordant B and T Cell Heterogeneity Inferred from the Multiomic Landscape of Peripheral Blood Mononuclear Cells in a Crohn's Disease Cohort.Journal of Crohn's & colitis · 2024Article
- Smad4 Deficiency in S100A4International journal of biological sciences · 2024Article
- CRISPR/Cas9: a powerful tool in colorectal cancer research.Journal of experimental & clinical cancer research : CR · 2023Review
- Innovative molecular subtypes of multiple signaling pathways in colon cancer and validation of FMOD as a prognostic-related marker.Journal of cancer research and clinical oncology · 2023Article
- Synthesis of Bis-Chalcones and Evaluation of Its Effect on Peroxide-Induced Cell Death and Lipopolysaccharide-Induced Cytokine Production.Molecules (Basel, Switzerland) · 2023Article
- Transforming Growth Factor Beta Promotes Inflammation and Tumorigenesis in Smad4-Deficient Intestinal Epithelium in a YAP-Dependent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Stem cell-derived intestinal organoids: a novel modality for IBD.Cell death discovery · 2023Review
- Ten Years of CRISPRing Cancers In Vitro.Cancers · 2022Review
- SMAD4 Suppresses Colitis-associated Carcinoma Through Inhibition of CCL20/CCR6-mediated Inflammation.Gastroenterology · 2022Article
- Patient-derived organoids for therapy personalization in inflammatory bowel diseases.World journal of gastroenterology · 2022Review
- From inflammatory bowel disease to colorectal cancer: what's the role of miRNAs?Cancer cell international · 2022Review
- Chemokines in progression, chemoresistance, diagnosis, and prognosis of colorectal cancer.Frontiers in immunology · 2022Review
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Authors and funding
24 authors at 3 institutions in 1 country.
Funding
Abstract
Background & Aims: Chronic inflammation is a predisposing condition for colorectal cancer. Many studies to date have focused on proinflammatory signaling pathways in the colon. Understanding the mechanisms that suppress inflammation, particularly in epithelial cells, is critical for developing therapeutic interventions. Here, we explored the roles of transforming growth factor β (TGFβ) family signaling through SMAD4 in colonic epithelial cells. Methods: The Results: Dextran sodium sulfate treatment was sufficient to drive carcinogenesis in mice lacking colonic Conclusions: TGFβ suppresses the expression of proinflammatory genes in the colon epithelium, and loss of its downstream mediator, SMAD4, is sufficient to initiate inflammation-driven colon cancer. Transcript profiling: GSE100082.
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What Socratic 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 Socratic graph.