ArticleCancer prevention research (Philadelphia, Pa.)2011
Clonal structure of carcinogen-induced intestinal tumors in mice.
Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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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.
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Who cites it
12 citing papers in PubMed, 17 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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- o-Aminoazotoluene, 7,12-dimethylbenz[a]anthracene, and N-ethyl-N-nitrosourea, which are mutagenic but not carcinogenic in the colon, rapidly induce colonic tumors in mice with dextran sulfate sodium-induced colitis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Multi-ancestral origin of intestinal tumors: Impact on growth, progression, and drug efficacy.Cancer reports (Hoboken, N.J.) · 2022Article
- Mutational Heterogeneity inClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
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- Mammalian models of chemically induced primary malignancies exploitable for imaging-based preclinical theragnostic research.Quantitative imaging in medicine and surgery · 2015Review
- 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
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Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have shown that intestinal tumors from Apc(Min)(/+) (Min) mice and familial adenomatous polyposis (FAP) patients are often polyclonal. We sought to determine whether polyclonality is unique to tumors arising from hereditary predispositions or, instead, is a common feature of intestinal tumorigenesis in other pathways to tumorigenesis. Ethylnitrosourea-induced intestinal tumors from mice wild type at the Apc locus and chimeric for the Rosa26 lineage marker were analyzed. Many were overtly polyclonal, being composed of a mixture of Rosa26(+) and Rosa26(-) neoplastic cells. Statistical analyses revealed that polyclonality could be explained by interactions between two initiated clones separated by a very short distance. The frequency of overtly polyclonal tumors and the range of interactions estimated in this model are similar to those observed when analyzing familial tumors from Min mice. Thus, polyclonality does not depend on the familial pathway to tumorigenesis. Interactions between two initiated clones might provide a selective advantage during the early stages of intestinal tumorigenesis.
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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.