The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumour and acts as a tumour suppressor
Author:
Affiliation:
1. School of Cellular and Molecular Medicine University of Bristol UK
2. Institute of Biomedical & Clinical Sciences University of Exeter Medical School UK
3. Cancer Section UCL Great Ormond Street Institute of Child Health London UK
Funder
CHILDREN with CANCER UK
Publisher
Wiley
Subject
Cancer Research,Genetics,Molecular Medicine,General Medicine,Oncology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/1878-0261.13101
Reference53 articles.
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3. Nephrogenic rests and the pathogenesis of Wilms tumor: Developmental and clinical considerations
4. Mutational activation of the beta‐catenin proto‐oncogene is a common event in the development of Wilms' tumors;Koesters R;Cancer Res,1999
5. Frequent association of beta‐catenin and WT1 mutations in Wilms tumors;Maiti S;Cancer Res,2000
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1. Characterization of alternative splicing in high-risk Wilms’ tumors;2023-11-02
2. Characterization of alternative mRNA splicing in cultured cell populations representing progressive stages of human fetal kidney development;Scientific Reports;2022-11-15
3. Underlying mechanisms of epithelial splicing regulatory proteins in cancer progression;Journal of Molecular Medicine;2022-09-27
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