ArticleProceedings of the National Academy of Sciences of the United States of America2011
Paneth cell marker expression in intestinal villi and colon crypts characterizes dietary induced risk for mouse sporadic intestinal cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Paneth Cells: Recent Updates on Elucidating Therapeutic Implications in Gastroenterological Disease Management.Current medicinal chemistry · 2025Pooled it
- Paneth cells as orchestrators of epithelial barrier defense and emerging therapeutic targets in inflammatory bowel disease.Seminars in immunopathology · 2026Review
- A Distinct Host-Microbiome Signature Underlies the Accelerated Malignant Potential of Colorectal Laterally Spreading Tumors.Gastro hep advances · 2026Article
- Porcine intestinal organoids cultured in an organ-on-a-chip microphysiological system.Biochemistry and biophysics reports · 2025Article
- CTHRC1 is associated withBiomolecules & biomedicine · 2024Article
- Metastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties.eLife · 2024Article
- Metastasis of colon cancer requires Dickkopf-2 to generate cancer cells with Paneth cell properties.bioRxiv : the preprint server for biology · 2024Article
- Intestinal stem cells: guardians of homeostasis in health and aging amid environmental challenges.Experimental & molecular medicine · 2024Review
- Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.Frontiers in genetics · 2024Review
- Dynamic Intestinal Stem Cell Plasticity and Lineage Remodeling by a Nutritional Environment Relevant to Human Risk for Tumorigenesis.Molecular cancer research : MCR · 2023Article
- Crypt and Villus Transcriptomic Responses in Mouse Small Intestine Following Oral Exposure to Hexavalent Chromium.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- The Interplay between Nutrition, Innate Immunity, and the Commensal Microbiota in Adaptive Intestinal Morphogenesis.Nutrients · 2021Review
- Article
- Paneth cell-derived growth factors support tumorigenesis in the small intestine.Life science alliance · 2021Article
- Subversion of Niche-Signalling Pathways in Colorectal Cancer: What Makes and Breaks the Intestinal Stem Cell.Cancers · 2021Review
- Wnt and Vitamin D at the Crossroads in Solid Cancer.Cancers · 2020Review
- Article
- IDO1Communications biology · 2020Article
- Vitamin D and the nutritional environment in functions of intestinal stem cells: Implications for tumorigenesis and prevention.The Journal of steroid biochemistry and molecular biology · 2020Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Nutritional and genetic risk factors for intestinal tumors are additive on mouse tumor phenotype, establishing that diet and genetic factors impact risk by distinct combinatorial mechanisms. In a mouse model of dietary-induced sporadic small and large intestinal cancer in WT mice in which tumor etiology, lag, incidence, and frequency reflect >90% of intestinal cancer in Western societies, dietary-induced risk altered gene expression profiles predominantly in villus cells of the histologically normal mucosa, in contrast to targeting of crypt cells by inheritance of an Apc(1638N) allele or homozygous inactivation of p21(Waf1/cip1), and profiles induced by each risk factor were distinct at the gene or functional group level. The dietary-induced changes in villus cells encompassed ectopic expression of Paneth cell markers (a lineage normally confined to the bottom of small intestinal crypts), elevated expression of the Wnt receptor Fzd5 and of EphB2 (genes necessary for Paneth cell differentiation and localization to the crypt bottom), and increased Wnt signaling in villus cells. Ectopic elevation of these markers was also present in the colon crypts, which are also sites of sporadic tumors in the nutritional model. Elevating dietary vitamin D(3) and calcium, which prevents tumor development, abrogated these changes in the villus and colon cells. Thus, common intestinal cancer driven by diet involves mechanisms of tumor development distinct from those mechanisms that cause tumors induced by the rare inheritance of a mutant adenomatous polyposis coli (Apc) allele. This is fundamental for understanding how common sporadic tumors arise and in evaluating relative risk in the population.
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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.