ArticleProceedings of the National Academy of Sciences of the United States of America2005
Polyclonality of familial murine adenomas: analyses of mouse chimeras with low tumor multiplicity suggest short-range interactions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Evaluation of tumor clonality with chemical carcinogenesis in a mouse model of visualized X chromosome inactivation.Journal of toxicologic pathology · 2026Article
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- Redefining familial adenomatous polyposis: competition, cooperation, and the path to monoclonality.Familial cancer · 2025Review
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- Interstitial deletion of the Apc locus in β-catenin-overexpressing cells is a signature of radiation-induced intestinal tumors in C3B6F1 ApcMin/+ mice†.Journal of radiation research · 2023Article
- Multi-ancestral origin of intestinal tumors: Impact on growth, progression, and drug efficacy.Cancer reports (Hoboken, N.J.) · 2022Article
- Surface microstructures are associated with mutational intratumoral heterogeneity in colorectal tumors.Journal of gastroenterology · 2018Article
- An evolutionary perspective on field cancerization.Nature reviews. Cancer · 2018Review
- Mutational Heterogeneity inClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- OncogenicGenes & development · 2017Article
- Understanding Intratumoral Heterogeneity: Lessons from the Analysis of At-Risk Tissue and Premalignant Lesions in the Colon.Cancer prevention research (Philadelphia, Pa.) · 2016Article
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- Occult progression by Apc-deficient intestinal crypts as a target for chemoprevention.Carcinogenesis · 2014Article
- Transformation of epithelial cells through recruitment leads to polyclonal intestinal tumors.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Regulated Expression of Chromobox Homolog 5 Revealed in Tumors of Apc(Min) (/+) ROSA11 Gene Trap Mice.G3 (Bethesda, Md.) · 2012Article
- The many ways to open the gate to colon cancer.Cell cycle (Georgetown, Tex.) · 2012Article
- Monoallelic silencing and haploinsufficiency in early murine intestinal neoplasms.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Clonal structure of carcinogen-induced intestinal tumors in mice.Cancer prevention research (Philadelphia, Pa.) · 2011Article
- Stem cells and their implications for colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2011Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
In previous studies demonstrating the polyclonal structure of familial intestinal adenomas, high tumor multiplicity made it difficult to eliminate the possibility that polyclonality arose by the random collision of distinct initiated clones as opposed to some form of clonal interaction. We sought to test further the random collision hypothesis. Chimeric mice carrying the multiple intestinal neoplasia (Min) mutation of the adenomatous polyposis coli gene (Apc) and homozygous for the tumor resistance allele of the Mom1 locus were established. These chimeras also display a strong propensity for tumors of polyclonal structure, despite their markedly reduced tumor multiplicity. Considering tumor sizes and multiplicities, the observed fraction of overtly polyclonal heterotypic adenomas was significantly higher than predicted by the random collision hypothesis. This finding supports models of polyclonality involving interaction among multiple initiated clones. The extent of clonal interaction was assessed by statistical analyses that relate the observed frequency of overtly polyclonal heterotypic tumors to the geometry of the chimeric patches and the pattern of underlying crypts. These statistical calculations indicate that the familial adenomas of the Apc(Min/+) mouse may commonly form through interactions between clones as close as 1-2 crypt diameters apart.
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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.