ArticleThe American journal of pathology2011
β-Catenin and K-RAS synergize to form primitive renal epithelial tumors with features of epithelial Wilms' tumors.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Hallmark discoveries in the biology of Wilms tumour.Nature reviews. Urology · 2024Review
- Article
- Non-coding RNAs in Wilms' tumor: biological function, mechanism, and clinical implications.Journal of molecular medicine (Berlin, Germany) · 2021Review
- The Vanderbilt O'Brien Kidney Center.American journal of physiology. Renal physiology · 2021Review
- Wilms tumor-suppressing peptide inhibits proliferation and induces apoptosis of Wilms tumor cells in vitro and in vivo.Journal of cancer research and clinical oncology · 2019Article
- FXR1 expression domain in Wilms tumor.Journal of pediatric surgery · 2019Article
- The genetic changes of Wilms tumour.Nature reviews. Nephrology · 2019Review
- Association ofAging · 2019Article
- Pharmacologic Inhibition of β-Catenin With Pyrvinium Inhibits Murine and Human Models of Wilms Tumor.Oncology research · 2017Article
- β-Catenin directs the transformation of testis Sertoli cells to ovarian granulosa-like cells by inducing Foxl2 expression.The Journal of biological chemistry · 2017Article
- Bilateral Wilms tumour: a review of clinical and molecular features.Expert reviews in molecular medicine · 2017Review
- Functional KRAS mutations and a potential role for PI3K/AKT activation in Wilms tumors.Molecular oncology · 2017Article
- K-Ras, H-Ras, N-Ras and B-Raf mutation and expression analysis in Wilms tumors: association with tumor growth.Medical oncology (Northwood, London, England) · 2017Article
- Multi-organ Mapping of Cancer Risk.Cell · 2016Article
- Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with β-Catenin Activation or Wt1 Ablation and Igf2 Upregulation.Neoplasia (New York, N.Y.) · 2016Article
- Senescence Process in Primary Wilms' Tumor Cell Culture Induced by p53 Independent p21 Expression.Journal of Cancer · 2016Article
- A Murine Model of K-RAS and β-Catenin Induced Renal Tumors Expresses High Levels of E2F1 and Resembles Human Wilms Tumor.The Journal of urology · 2015Article
- Genetic and chromosomal alterations in Kenyan Wilms Tumor.Genes, chromosomes & cancer · 2015Article
- Acute Inhibition of MEK Suppresses Congenital Melanocytic Nevus Syndrome in a Murine Model Driven by Activated NRAS and Wnt Signaling.The Journal of investigative dermatology · 2015Article
- Hyperglycemia in the absence of cilia accelerates cystogenesis and induces renal damage.American journal of physiology. Renal physiology · 2015Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Wilms' tumor (WT) is the most common childhood renal cancer. Although mutations in known tumor-associated genes (WT1, WTX, and CATNB) occur only in a third of tumors, many tumors show evidence of activated β-catenin-dependent Wnt signaling, but the molecular mechanism by which this occurs is unknown. A key obstacle to understanding the pathogenesis of WT is the paucity of mouse models that recapitulate its features in humans. Herein, we describe a transgenic mouse model of primitive renal epithelial neoplasms that have high penetrance and mimic the epithelial component of human WT. Introduction of a stabilizing β-catenin mutation restricted to the kidney is sufficient to induce primitive renal epithelial tumors; however, when compounded with activation of K-RAS, the mice develop large, bilateral, metastatic, multifocal primitive renal epithelial tumors that have the histologic and staining characteristics of the epithelial component of human WT. These highly malignant tumors have increased activation of the phosphatidylinositol 3-kinase-AKT and extracellular signal-regulated kinase pathways, increased expression of total and nuclear β-catenin, and increased downstream targets of this pathway, such as c-Myc and survivin. Thus, we developed a novel mouse model in which activated K-RAS synergizes with canonical Wnt/β-catenin signaling to form metastatic primitive renal epithelial tumors that mimic the epithelial component of human WT.
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