ArticleOncogene1999
Dysregulated expression of beta-catenin marks early neoplastic change in Apc mutant mice, but not all lesions arising in Msh2 deficient mice.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 60 citations in OpenAlex.
- Protein and mRNA Expression in Uveal Melanoma Cell Lines Are Related to GNA and BAP1 Mutation Status.Investigative ophthalmology & visual science · 2024Article
- Exercise through Shaking Stimuli Suppresses Cancer Growth via the Wnt pathway in ApcMin/+ Mice.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Interplay between APC and ALDH1B1 in a newly developed mouse model of colorectal cancer.Chemico-biological interactions · 2020Article
- Review
- Establishment of a novel human cell line retaining the characteristics of the original pancreatic adenocarcinoma, and evaluation of MEK as a therapeutic target.International journal of oncology · 2020Article
- Tales from the crypt: intestinal niche signals in tissue renewal, plasticity and cancer.Open biology · 2018Review
- Microbial-derived butyrate: an oncometabolite or tumor-suppressive metabolite?Cell host & microbe · 2014Article
- Wnt signaling and the control of human stem cell fate.Stem cell reviews and reports · 2014Review
- Epigenetic regulation of DACH1, a novel Wnt signaling component in colorectal cancer.Epigenetics · 2013Article
- An APC:WNT Counter-Current-Like Mechanism Regulates Cell Division Along the Human Colonic Crypt Axis: A Mechanism That Explains How APC Mutations Induce Proliferative Abnormalities That Drive Colon Cancer Development.Frontiers in oncology · 2013Review
- Wnt signaling, stem cells, and cancer of the gastrointestinal tract.Cold Spring Harbor perspectives in biology · 2012Article
- Correlation of SATB1 overexpression with the progression of human rectal cancer.International journal of colorectal disease · 2012Article
- The inhibitory effects of 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone on human colon cancer cells.Molecular nutrition & food research · 2011Article
- Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor.Carcinogenesis · 2010Article
- Article
- Upregulation of colonic ion channels in APC ( Min/+ ) mice.Pflugers Archiv : European journal of physiology · 2008Article
- The what, where, when and how of Wnt/β-catenin signaling in pancreas development.Organogenesis · 2008Article
- LZTS2 is a novel beta-catenin-interacting protein and regulates the nuclear export of beta-catenin.Molecular and cellular biology · 2006Article
- A simple device to rapidly prepare whole mounts of murine intestine.Cell proliferation · 2006Article
- Developmental abnormalities in multiple proliferative tissues of Apc(Min/+) mice.International journal of experimental pathology · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have analysed the pattern of beta-catenin expression by immunohistochemistry in mice singly or multiply mutant for Apc, p53 and Msh2. We observed increased expression of beta-catenin in all intestinal lesions arising on an ApcMin+/- background. In all categories of lesion studied mosaic patterns of beta-catenin expression were observed, with the proportion of cells showing enhanced expression decreasing with increasing lesion size. p53 status did not alter these patterns. We also show that beta-catenin dysregulation marks pancreatic abnormalities occurring in ApcMin+/- and (ApcMin+/-, p53-/-) mice. In these mice both adenomas and adenocarcinomas of the pancreas arose and were characterized by increased expression of beta-catenin. We have extended these analyses to intestinal lesions arising in mice mutant for the mismatch repair gene Msh2. In these mice, increased expression of beta-catenin was again observed. However, in contrast with ApcMin+/- mice, a subset of lesions retained normal expression. Taken together, these findings show that increased expression of beta-catenin is an efficient marker of early neoplastic change in both murine intestine and pancreas in Apc mutant mice. However, we also show that dysregulation of beta-catenin is not an obligate step in the development of intestinal lesions, and therefore that genetic events other than the loss of Apc function may initiate the transition from normal to neoplastic epithelium.
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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.