ArticleGut2004
Development of colonic neoplasia in p53 deficient mice with experimental colitis induced by dextran sulphate sodium.
Article in Gut, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Gut microbiota and epigenetic inheritance: implications for the development of IBD.Gut microbes · 2025Review
- Defining the mucosal ecosystem: epithelial-mesenchymal interdependence in gastrointestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- p53 terminates the regenerative fetal-like state after colitis-associated injury.Science advances · 2024Article
- Trp53 Deletion Promotes Exacerbated Colitis, Facilitates Lgr5+ Cancer Stem Cell Expansion, and Fuels Tumorigenesis in AOM/DSS-Induced Colorectal Cancer.International journal of molecular sciences · 2024Article
- MAD1 upregulation sensitizes to inflammation-mediated tumor formation.PLoS genetics · 2024Article
- MicroRNA-200 Loaded Lipid Nanoparticles Promote Intestinal Epithelium Regeneration in Canonical MicroRNA-Deficient Mice.ACS nano · 2023Article
- Sleeping Beauty transposon mutagenesis identified genes and pathways involved in inflammation-associated colon tumor development.Nature communications · 2023Article
- Reelin Protects against Colon Pathology via p53 and May Be a Biomarker for Colon Cancer Progression.Biology · 2022Article
- Emerging Pathological Engagement of Ferroptosis in Gut Diseases.Oxidative medicine and cellular longevity · 2021Review
- Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.Cell death and differentiation · 2020Article
- Therapeutic Ablation of Gain-of-Function Mutant p53 in Colorectal Cancer Inhibits Stat3-Mediated Tumor Growth and Invasion.Cancer cell · 2018Article
- In Inflamed Intestinal Tissues and Epithelial Cells, Interleukin 22 Signaling Increases Expression of H19 Long Noncoding RNA, Which Promotes Mucosal Regeneration.Gastroenterology · 2018Article
- Absent in melanoma 2 proteins in the development of cancer.Cellular and molecular life sciences : CMLS · 2016Review
- Characterisation of colonic dysplasia-like epithelial atypia in murine colitis.World journal of gastroenterology · 2016Article
- Reduction of p53 by knockdown of theCellular and molecular gastroenterology and hepatology · 2016Article
- Recent advancement in understanding colitis-associated tumorigenesis.Inflammatory bowel diseases · 2014Review
- Kimchi protects against azoxymethane/dextran sulfate sodium-induced colorectal carcinogenesis in mice.Journal of medicinal food · 2014Article
- The gut microbiota in mouse models of inflammatory bowel disease.Frontiers in cellular and infection microbiology · 2014Review
- An EGFR targeted PET imaging probe for the detection of colonic adenocarcinomas in the setting of colitis.Theranostics · 2014Article
- Chemistry meets biology in colitis-associated carcinogenesis.Free radical research · 2013Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral animal models for human ulcerative colitis (UC) associated neoplasia have been reported. However, most neoplasias developed in these models have morphological and genetic characteristics different from UC associated neoplasia.
aimsTo establish a new colitis associated neoplasia model in p53 deficient mice by treatment with dextran sulphate sodium (DSS).
methodsDSS colitis was induced in homozygous p53 deficient mice (p53(-/-)-DSS), heterozygous p53 deficient mice (p53(+/-)-DSS) and wild-type mice (p53+/+-DSS) by treatment with 4% DSS. Numbers of developed neoplasias were compared among the experimental groups, and macroscopic and microscopic features of the neoplasias were analysed. Furthermore, K-ras mutation and beta-catenin expression were assessed.
resultsp53(-/-)-DSS mice showed 100% incidence of neoplasias whereas the incidences in p53(+/-)-DSS and p53+/+-DSS mice were 46.2% and 13.3%, respectively. No neoplasias were observed in the control groups. The mean numbers of total neoplasias per mouse were 5.0 (p53(-/-)-DSS), 0.62 (p53(+/-)-DSS), and 0.2 (p53+/+-DSS). The number of neoplasias per mouse in the p53(-/-)-DSS group was significantly higher than that in the other DSS groups. The incidences of superficial type neoplasias were 91.7% in p53(-/-)-DSS mice, 75.0% in p53(+/-)-DSS mice, and 33.3% in p53+/+-DSS mice. The K-ras mutation was not detected in any of the neoplasias tested. Translocation of beta-catenin from the cell membrane to the cytoplasm or nucleus was observed in 19 of 23 (82.6%) neoplasias.
conclusionsThe p53(-/-)-DSS mice is an excellent animal model of UC associated neoplasia because the morphological features and molecular genetics are similar to those of UC associated neoplasia. Therefore, this model will contribute to the analysis of tumorigenesis related to human UC associated neoplasia and the development of chemopreventive agents.
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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.