ArticleOncogene2013
Molecular basis for the tissue specificity of β-catenin oncogenesis.
Article in Oncogene, 2013. 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.
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
12 citing papers in PubMed, 19 citations in OpenAlex.
- The adrenal gland and primary aldosteronism: anatomy, steroidogenesis, regulation, and genetic insights.Frontiers in endocrinology · 2025Review
- Non-target genetic manipulation induces rhabdomyosarcoma inTranslational cancer research · 2020Article
- An immunohistochemical approach to detect oncogenic CTNNB1 mutations in primary neoplastic tissues.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Wnt-signaling enhances neural crest migration of melanoma cells and induces an invasive phenotype.Molecular cancer · 2018Article
- The role of Wnt/β-catenin signaling pathway in melanoma epithelial-to-mesenchymal-like switching: evidences from patients-derived cell lines.Oncotarget · 2016Article
- MUC4 is negatively regulated through the Wnt/β-catenin pathway via the Notch effector Hath1 in colorectal cancer.Genes & cancer · 2016Article
- Molecular etiology of an indolent lymphoproliferative disorder determined by whole-genome sequencing.Cold Spring Harbor molecular case studies · 2016Article
- The expression of tumour suppressors and proto-oncogenes in tissues susceptible to their hereditary cancers.British journal of cancer · 2015Article
- A critical role for the regulated wnt-myc pathway in naive T cell survival.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- From inception to output, Tcf1 and Lef1 safeguard development of T cells and innate immune cells.Immunologic research · 2014Review
- The nuclear effector of Wnt-signaling, Tcf1, functions as a T-cell-specific tumor suppressor for development of lymphomas.PLoS biology · 2012Article
- CTNNB1 Knockdown Inhibits Cell Proliferation and Aldosterone Secretion Through Inhibiting Wnt/β-Catenin Signaling in H295R Cells.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Wnt-β-catenin-T-cell factor signaling is causally linked to c-myc-dependent tumorigenesis in mouse and human colon epithelial cells. By contrast, β-catenin is not similarly associated with oncogenic transformation of other tissues, including T cells. The molecular basis for tissue specificity of β-catenin-dependent oncogenesis is unknown. Here, we demonstrate that adenomatous polyposis coli mutant APC(Min/+) mice, which have increased expression of β-catenin in all tissues, develop severe intestinal neoplasia, but fail to develop thymic lymphoma. Whereas β-catenin-dependent signals elicit a proliferative response from intestinal cells, thymocytes experience oncogene-induced senescence (OIS), growth arrest and apoptosis. We demonstrate that the differential cellular response of thymocytes and intestinal epithelial cells is a direct consequence of the gene expression elicited by β-catenin expression in each tissue. We find that whereas intestinal cells induce genes that promote proliferation thymocytes induce expression of genes associated with OIS, growth arrest and p53-dependent apoptosis. We correlate gene expression pattern with the role β-catenin plays in the development of each tissue and suggest that susceptibility of transformation by β-catenin is intimately related to its function during development. We propose that when oncogenes are used as signaling molecules, safety nets in the form of OIS, growth arrest and apoptosis prevent accidental transformation.
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.