ArticleMolecular oncology2017
Functional KRAS mutations and a potential role for PI3K/AKT activation in Wilms tumors.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Bioinformatics and computational exploration of novel inhibitors targeting KRAS G12C mutant protein in lung adenocarcinoma.Discover oncology · 2026Article
- Clinical benefit of additional whole-exome sequencing over panel sequencing in an all-comer real-world molecular tumor board.ESMO open · 2025Article
- Mechanistic study of CTHRC1 in promoting Wilms' tumor progression by regulating M2-type tumor-associated macrophages polarization.Journal of translational medicine · 2025Article
- PRC1 as an independent adverse prognostic factor in Wilms tumor via integrated bioinformatics and experimental validation.Scientific reports · 2025Article
- The Role of Circular RNA in the Pathogenesis of Chemotherapy-Induced Cardiotoxicity in Cancer Patients: Focus on the Pathogenesis and Future Perspective.Cardiovascular toxicology · 2024Review
- Nephroblastoma-specific dysregulated gene SNHG15 with prognostic significance: scRNA-Seq with bulk RNA-Seq data and experimental validation.Discover oncology · 2024Article
- Karanjin, A Promising Bioactive Compound Possessing Anti-cancer Activity against Experimental Model of Non-small Cell Lung Cancer Cells.Anti-cancer agents in medicinal chemistry · 2024Article
- Article
- Lymphatic disorders caused by mosaic, activating KRAS variants respond to MEK inhibition.JCI insight · 2023Article
- Article
- Digitoxin Affects Metabolism, ROS Production and Proliferation in Pancreatic Cancer Cells Differently Depending on the Cell Phenotype.International journal of molecular sciences · 2022Article
- Differential expression analysis of genes and long non-coding RNAs associated with KRAS mutation in colorectal cancer cells.Scientific reports · 2022Article
- Non-coding RNAs in Wilms' tumor: biological function, mechanism, and clinical implications.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Research advances in the targeted therapy and immunotherapy of Wilms tumor: a narrative review.Translational cancer research · 2021Review
- KRAS, YWHAE, SP1 and MSRA as biomarkers in endometrial cancer.Translational cancer research · 2021Article
- Identification of key genes and microRNAs involved in kidney Wilms tumor by integrated bioinformatics analysis.Experimental and therapeutic medicine · 2019Article
- Overcoming acquired resistance of gefitinib in lung cancer cells without T790M by AZD9291 or Twist1 knockdown in vitro and in vivo.Archives of toxicology · 2019Article
- The genetic changes of Wilms tumour.Nature reviews. Nephrology · 2019Review
- Corrigendum to: Functional KRAS mutations and a potential role for PI3K/AKT activation in Wilms tumors.Molecular oncology · 2019Article
- Association ofAging · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Wilms tumor (WT) is the most common renal neoplasm of childhood and affects 1 in 10 000 children aged less than 15 years. These embryonal tumors are thought to arise from primitive nephrogenic rests that derive from the metanephric mesenchyme during kidney development and are characterized partly by increased Wnt/β-catenin signaling. We previously showed that coordinate activation of Ras and β-catenin accelerates the growth and metastatic progression of a murine WT model. Here, we show that activating KRAS mutations can be found in human WT. In addition, high levels of phosphorylated AKT are present in the majority of WT. We further show in a mouse model and in renal epithelial cells that Ras cooperates with β-catenin to drive metastatic disease progression and promotes in vitro tumor cell growth, migration, and colony formation in soft agar. Cellular transformation and metastatic disease progression of WT cells are in part dependent on PI3K/AKT activation and are inhibited via pharmacological inhibition of this pathway. Our studies suggest both KRAS mutations and AKT activation are present in WT and may represent novel therapeutic targets for this disease.
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