ArticleThe Journal of cell biology1992
The Min (multiple intestinal neoplasia) mutation: its effect on gut epithelial cell differentiation and interaction with a modifier system.
Article in The Journal of cell biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
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
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.
- A systemic review of the role of enterotoxic Bacteroides fragilis in colorectal cancer.Neoplasia (New York, N.Y.) · 2022Pooled it
- IGF2BP3 is essential for the growth heterogeneity of colorectal adenoma cells by regulating MYC.iScience · 2026Article
- Human colonic organoids for understanding early events of familial adenomatous polyposis pathogenesis.The Journal of pathology · 2025Article
- Studying the Effect of the Host Genetic Background of Juvenile Polyposis Development Using Collaborative Cross andInternational journal of molecular sciences · 2024Article
- Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.Scientific reports · 2022Article
- Genetic Drivers of Ileal Neuroendocrine Tumors.Cancers · 2021Review
- High Variability in Cellular Proliferation, Gene Expression, and Cytokine Production in the Nonneoplastic Colonic Epithelium of YoungFrontiers in oncology · 2021Article
- Natural Killer T-Cell Agonist α-Galactosylceramide and PD-1 Blockade Synergize to Reduce Tumor Development in a Preclinical Model of Colon Cancer.Frontiers in immunology · 2020Article
- Modeling open surgery in mice to explore peritoneal damage, carbon dioxide humidification and desmoidogenesis.Pleura and peritoneum · 2019Article
- Human colon mucosal biofilms from healthy or colon cancer hosts are carcinogenic.The Journal of clinical investigation · 2019Article
- Conjugated Linoleic Acid Effects on Cancer, Obesity, and Atherosclerosis: A Review of Pre-Clinical and Human Trials with Current Perspectives.Nutrients · 2019Review
- Unraveling the role of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) expression in colon carcinogenesis.NPJ precision oncology · 2019Review
- Tumor suppressor APC is an attenuator of spindle-pulling forces duringProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains.Proceedings of the National Academy of Sciences of the United States of America · 2017Review
- Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis.Oncogene · 2017Article
- Insulin signaling regulates a functional interaction between adenomatous polyposis coli and cytoplasmic dynein.Molecular biology of the cell · 2017Article
- The genetic heterogeneity of colorectal cancer predisposition - guidelines for gene discovery.Cellular oncology (Dordrecht, Netherlands) · 2016Review
- Elevation of n-3/n-6 PUFAs ratio suppresses mTORC1 and prevents colorectal carcinogenesis associated with APC mutation.Oncotarget · 2016Article
- Increased variability in Apc(Min)/+ intestinal tissue can be measured with microultrasound.Scientific reports · 2016Article
- Lack of interferon-γ receptor results in a microenvironment favorable for intestinal tumorigenesis.Oncotarget · 2016Article
52 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Min is a fully penetrant dominant mutation that leads to the development of multiple intestinal adenomas throughout the duodenal-to-colonic axis. Min/+ C57BL6/J mice have an average life-span of 120 d. Multi-label immunocytochemical studies of these lesions demonstrate patches of differentiated enterocytes, and scattered enteroendocrine, goblet and Paneth cells. Expression of endogenous marker genes within these differentiated cells can be directly correlated with the position occupied by the adenoma along the duodenal-to-colonic axis and mirrors the regional differentiation of the normal gut epithelium. The presence of multiple lineages in adenomas together with their retention of spatial information suggests that tumorigenesis in Min/+ mice may be initiated in a multipotent stem cell normally located at the base of intestinal crypts. To study the time-dependent properties of these tumors, genetic conditions were sought in which Min/+ animals could survive for up to 300 d. Min is fully penetrant in hybrids with either AKR/J or MA/MyJ. However, the hybrids demonstrate a reduction in the number of intestinal adenomas. Preliminary backcross analysis is consistent with a single major modifier locus unlinked to Min in both the AKR/J and MA/MyJ strains. The increased lifespan of the hybrid animals is also associated with the development of invasive tumors. New tumors do not arise continuously over the lifespan of these animals; instead all adenomas appear to be established by 100 d of age or sooner. These studies indicate that the Min/+ mouse is a powerful model system for analyzing the mechanisms that establish and maintain a balance between proliferation and differentiation in the continuously renewing gut epithelium and for an assessment of the multi-step hypothesis of intestinal neoplasia.
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.