ReviewCarcinogenesis2009
Mouse models for the study of colon carcinogenesis.
Review in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 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
190 citing papers in PubMed, 427 citations in OpenAlex.
- ACSS2 is required for colorectal cancer progression and a druggable target for colorectal cancer treatment.iScience · 2026Article
- IL-27 shapes NK cell heterogeneity and function in colorectal cancer.Journal for immunotherapy of cancer · 2026Article
- Frequent Detection of Abasic Sites andChemical research in toxicology · 2026Article
- NAPRT-mediated deamidated NAD biosynthesis enhances colon tissue resiliency and suppresses tumorigenesis.Nature communications · 2026Article
- Optimization of DMH-Induced Colorectal Carcinogenesis in Rats: A Systematic Meta-Review.Clinical and experimental gastroenterology · 2026Review
- Platelet activation, aspirin, and cancer: From basic science to clinical trials.Pharmacological reviews · 2026Review
- Mitochondrial DNA Damage and Histological Features in Liver Tissue of Azoxymethane-TreatedBiomolecules · 2025Article
- Development and Application of MiMouse, a Comprehensive Genomic Profiling Panel for Credentialing Mouse Tumor Models.Cancer research communications · 2025Article
- Review
- Model systems to study tumor-microbiome interactions in early-onset colorectal cancer.EMBO molecular medicine · 2025Review
- Rat Models of Breast Cancer.Advances in experimental medicine and biology · 2025Review
- The paradigm shift: re-evaluating preclinical animal models for colorectal cancer in the precision medicine era.Frontiers in immunology · 2025Review
- Mechanisms and applications of N-Methyl-N'-nitro-N-nitrosoguanidine in animal tumor models: current situation and challenges.Frontiers in oncology · 2025Review
- Genotoxic and Anti-Genotoxic Assessments of FermentedFoods (Basel, Switzerland) · 2024Article
- Exploring the protective effect of silverHeliyon · 2024Article
- Exploring the relationship between ulcerative colitis, colorectal cancer, and prostate cancer.Human cell · 2024Article
- Article
- Impact of Ascending HPV Infection on Colorectal Cancer Risk: Evidence from a Nationwide Study.Microorganisms · 2024Article
- Advancements in Research and Treatment Applications of Patient-Derived Tumor Organoids in Colorectal Cancer.Cancers · 2024Review
- KHK-A promotes fructose-dependent colorectal cancer liver metastasis by facilitating the phosphorylation and translocation of PKM2.Acta pharmaceutica Sinica. B · 2024Article
130 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 3 institutions in 2 countries.
Funding
Abstract
The study of experimental colon carcinogenesis in rodents has a long history, dating back almost 80 years. There are many advantages to studying the pathogenesis of carcinogen-induced colon cancer in mouse models, including rapid and reproducible tumor induction and the recapitulation of the adenoma-carcinoma sequence that occurs in humans. The availability of recombinant inbred mouse panels and the existence of transgenic, knock-out and knock-in genetic models further increase the value of these studies. In this review, we discuss the general mechanisms of tumor initiation elicited by commonly used chemical carcinogens and how genetic background influences the extent of disease. We will also describe the general features of lesions formed in response to carcinogen treatment, including the underlying molecular aberrations and how these changes may relate to the pathogenesis of human colorectal cancer.
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.