ArticleOncotarget2016
Chromosomal anomalies at 1q, 3, 16q, and mutations of SIX1 and DROSHA genes underlie Wilms tumor recurrences.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Systematic Review: Prognostic Molecular Biomarkers in Wilms Tumors.JCO precision oncology · 2026Pooled it
- Developmental reprogramming underlies chemotherapy resistance in favorable-histology Wilms tumor.Cell reports · 2026Article
- Gene Expression Analysis of (Paired) Primary and Relapsed Wilms Tumor Samples to Unravel the Underlying Factors Driving Tumor Recurrence.Cancer medicine · 2025Article
- Article
- Hallmark discoveries in the biology of Wilms tumour.Nature reviews. Urology · 2024Review
- Essential role of the amino-terminal region of Drosha for the Microprocessor function.iScience · 2023Article
- Gene expression-based dissection of inter-histotypes, intra-histotype and intra-tumor heterogeneity in pediatric tumors.Scientific reports · 2022Article
- Genetic changes associated with relapse in favorable histology Wilms tumor: A Children's Oncology Group AREN03B2 study.Cell reports. Medicine · 2022Article
- Finding the way to Wilms tumor by comparing the primary and relapse tumor samples.Cell reports. Medicine · 2022Article
- Analysis of the mutational status of SIX1/2 and microRNA processing genes in paired primary and relapsed Wilms tumors and association with relapse.Cancer gene therapy · 2021Article
- Review
- DROSHA is recruited to DNA damage sites by the MRN complex to promote non-homologous end joining.Journal of cell science · 2021Article
- Forty-five patient-derived xenografts capture the clinical and biological heterogeneity of Wilms tumor.Nature communications · 2019Article
- Deregulation of Drosha in the pathogenesis of hereditary hemorrhagic telangiectasia.Current opinion in hematology · 2019Review
- miR-140-5p alleviates the aggressive progression of Wilms' tumor through directly targetingCancer management and research · 2019Article
- Genetic and epigenetic analyses guided by high resolution whole-genome SNP array reveals a possible role ofOncotarget · 2018Article
- MiR-1180-5p regulates apoptosis of Wilms' tumor by targetingOncoTargets and therapy · 2018Article
- Associations betweenOncotarget · 2017Article
- Combining miRNA and mRNA Expression Profiles in Wilms Tumor Subtypes.International journal of molecular sciences · 2016Article
- Genomic imbalances pinpoint potential oncogenes and tumor suppressors in Wilms tumors.Molecular cytogenetics · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately half of children suffering from recurrent Wilms tumor (WT) develop resistance to salvage therapies. Hence the importance to disclose events driving tumor progression/recurrence. Future therapeutic trials, conducted in the setting of relapsing patients, will need to prioritize targets present in the recurrent lesions. Different studies identified primary tumor-specific signatures associated with poor prognosis. However, given the difficulty in recruiting specimens from recurrent WTs, little work has been done to compare the molecular profile of paired primary/recurrent diseases. We studied the genomic profile of a cohort of eight pairs of primary/recurrent WTs through whole-genome SNP arrays, and investigated known WT-associated genes, including SIX1, SIX2 and micro RNA processor genes, whose mutations have been recently proposed as associated with worse outcome. Through this approach, we sought to uncover anomalies characterizing tumor recurrence, either acquired de novo or already present in the primary disease, and to investigate whether they overlapped with known molecular prognostic signatures. Among the aberrations that we disclosed as potentially acquired de novo in recurrences, some had been already recognized in primary tumors as associated with a higher risk of relapse. These included allelic imbalances of chromosome 1q and of chromosome 3, and CN losses on chromosome 16q. In addition, we found that SIX1 and DROSHA mutations can be heterogeneous events (both spatially and temporally) within primary tumors, and that their co-occurrence might be positively selected in the progression to recurrent disease. Overall, these results provide new insights into genomic and genetic events underlying WT progression/recurrence.
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