ArticleGut2018
Differential preventive activity of sulindac and atorvastatin in Apc
Article in Gut, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Atorvastatin as a pleiotropic anticancer agent: mechanisms, evidence, and therapeutic repurposing potential.Frontiers in immunology · 2026Review
- Microbiota-derived tryptophan catabolites mediate the chemopreventive effects of statins on colorectal cancer.Nature microbiology · 2023Article
- The role of gut microbiota and drug interactions in the development of colorectal cancer.Frontiers in pharmacology · 2023Review
- Article
- Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC.Cancer research communications · 2022Article
- Alteration in the Immune Microenvironment Based on APC Status in MSS/pMMR Colon Cancer.Disease markers · 2022Article
- Suppression of Colon Tumorigenesis in MutantCancer prevention research (Philadelphia, Pa.) · 2021Article
- Celecoxib alleviates zinc deficiency-promoted colon tumorigenesis through suppressing inflammation.Aging · 2021Article
- High Variability in Cellular Proliferation, Gene Expression, and Cytokine Production in the Nonneoplastic Colonic Epithelium of YoungFrontiers in oncology · 2021Article
- Dysplastic Aberrant Crypt Foci: Biomarkers of Early Colorectal Neoplasia and Response to Preventive Intervention.Cancer prevention research (Philadelphia, Pa.) · 2020Review
- Review
- The application of ApcJournal of cancer research and clinical oncology · 2019Review
- Epidemiology of colorectal cancer: incidence, mortality, survival, and risk factors.Przeglad gastroenterologiczny · 2019Review
- Autophagic flux is essential for the downregulation of D-dopachrome tautomerase by atractylenolide I to ameliorate intestinal adenoma formation.Journal of cell communication and signaling · 2018Article
- Clinically Relevant Anti-Inflammatory Agents for Chemoprevention of Colorectal Cancer: New Perspectives.International journal of molecular sciences · 2018Review
- Calcium-Induced Differentiation of Human Colon Adenomas in Colonoid Culture: Calcium Alone versus Calcium with Additional Trace Elements.Cancer prevention research (Philadelphia, Pa.) · 2018Article
- The Reprimo Gene Family: A Novel Gene Lineage in Gastric Cancer with Tumor Suppressive Properties.International journal of molecular sciences · 2018Review
- Aspirin alone and combined with a statin suppresses eicosanoid formation in human colon tissue.Journal of lipid research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
objectiveThe response of subjects to preventive intervention is heterogeneous. The goal of this study was to determine if the efficacy of a chemopreventive agent differs in non-tumour-bearing animals versus those with colorectal tumours. Sulindac and/or atorvastatin was administered to Apc
designMale mice (6-8 weeks old) underwent colonoscopy and received control chow or chow with sulindac (300 ppm), atorvastatin (100 ppm) or sulindac/atorvastatin. Tissues were collected from mice treated for 14 weeks (histopathology) or 7 days (gene expression). Cell cycle analyses were performed on SW480 colon carcinoma cells treated with sulindac, atorvastatin or both.
resultsThe multiplicity of colorectal adenomas in untreated mice bearing tumours at baseline was 3.6-fold higher than that of mice that were tumour free at baseline (P=0.002). Atorvastatin completely inhibited the formation of microadenomas in mice that were tumour free at baseline (P=0.018) and altered the expression of genes associated with stem/progenitor cells. Treatment of tumour-bearing mice with sulindac/atorvastatin led to a 43% reduction in the multiplicity of colorectal adenomas versus untreated tumour-bearing mice (P=0.049). Sulindac/atorvastatin increased the expression of
conclusionsThe tumour status of animals at treatment initiation dictates response to therapeutic intervention. Atorvastatin eliminated microadenomas in tumour-free mice. The tumour inhibition observed with Sul/Atorva in tumour-bearing mice was greater than that achieved with each agent.
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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.