ArticleNeoplasia (New York, N.Y.)2016
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.
Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Dose-Dependent and Non-Autonomous Signaling in CAKUT: A Lineage-Specific Framework from Conditional Knockout Studies.Biomolecules · 2026Review
- Cross-cancer transcriptomic analysis reveals conserved developmental, ferroptosis, and immune remodeling modules in Wilms tumor and oral cancer.Frontiers in genetics · 2026Article
- Expression of ENL YEATS domain tumor mutations in nephrogenic or stromal lineage impairs kidney development.Nature communications · 2025Article
- Single-cell multiomics reveals ENL mutation perturbs kidney developmental trajectory by rewiring gene regulatory landscape.Nature communications · 2024Article
- Hallmark discoveries in the biology of Wilms tumour.Nature reviews. Urology · 2024Review
- Altered binding affinity of SIX1-Q177R correlates with enhanced WNT5A and WNT pathway effector expression in Wilms tumor.Disease models & mechanisms · 2023Article
- Article
- Genetic changes associated with relapse in favorable histology Wilms tumor: A Children's Oncology Group AREN03B2 study.Cell reports. Medicine · 2022Article
- Article
- Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development.Genomics · 2022Article
- The tumor suppressor WT1 drives progenitor cell progression and epithelialization to prevent Wilms tumorigenesis in human kidney organoids.Stem cell reports · 2021Article
- Review
- Stromal β-catenin activation impacts nephron progenitor differentiation in the developing kidney and may contribute to Wilms tumor.Development (Cambridge, England) · 2020Article
- Choosing The Right Animal Model for Renal Cancer Research.Translational oncology · 2020Review
- Platforms of in vivo genome editing with inducible Cas9 for advanced cancer modeling.Cancer science · 2019Article
- Mutations in microRNA processing genes in Wilms tumors derepress theGenes & development · 2018Article
- Overgrowth syndromes and pediatric cancers: how many roads lead toGenes & development · 2018Article
- Loss ofGenes & development · 2018Article
- Haploinsufficiency for the Six2 gene increases nephron progenitor proliferation promoting branching and nephron number.Kidney international · 2018Article
- Wilms' Tumor Protein 1 and Enzymatic Oxidation of 5-Methylcytosine in Brain Tumors: Potential Perspectives.Frontiers in cell and developmental biology · 2018Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Wilms tumor, a common childhood tumor of the kidney, is thought to arise from undifferentiated renal mesenchyme. Variable tumor histology and the identification of tumor subsets displaying different gene expression profiles suggest that tumors may arise at different stages of mesenchyme differentiation and that this ontogenic variability impacts tumor pathology, biology, and clinical outcome. To test the tumorigenic potential of different cell types in the developing kidney, we used kidney progenitor-specific Cre recombinase alleles to introduce Wt1 and Ctnnb1 mutations, two alterations observed in Wilms tumor, into embryonic mouse kidney, with and without biallelic Igf2 expression, another alteration that is observed in a majority of tumors. Use of a Cre allele that targets nephron progenitors to introduce a Ctnnb1 mutation that stabilizes β-catenin resulted in the development of tumors with a predominant epithelial histology and a gene expression profile in which genes characteristic of early renal mesenchyme were not expressed. Nephron progenitors with Wt1 ablation and Igf2 biallelic expression were also tumorigenic but displayed a more triphasic histology and expressed early metanephric mesenchyme genes. In contrast, the targeting of these genetic alterations to stromal progenitors did not result in tumors. These data demonstrate that committed nephron progenitors can give rise to Wilms tumors and that committed stromal progenitors are less tumorigenic, suggesting that human Wilms tumors that display a predominantly stromal histology arise from mesenchyme before commitment to a stromal lineage.
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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.