ArticleNeoplasia (New York, N.Y.)2019
Combined Genetic and Chromosomal Characterization of Wilms Tumors Identifies Chromosome 12 Gain as a Potential New Marker Predicting a Favorable Outcome.
Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Systematic Review: Prognostic Molecular Biomarkers in Wilms Tumors.JCO precision oncology · 2026Pooled it
- Tumor-Associated Macrophage Polarization in Wilms' Tumor After Neoadjuvant Chemotherapy.Cancers · 2026Article
- Analysis of prognostic factors and development of a predictive model following radical nephrectomy for Wilms tumor in children.Oncology letters · 2025Article
- Integration of single-nuclei and spatial transcriptomics to decipher tumor phenotype predictive of relapse-free survival in Wilms tumor.Frontiers in immunology · 2025Article
- DROSHA Regulates Mesenchymal Gene Expression in Wilms Tumor.Molecular cancer research : MCR · 2024Article
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Molecular Characterization Reveals Subclasses of 1q Gain in Intermediate Risk Wilms Tumors.Cancers · 2022Article
- A novel tumor doubling time-related immune gene signature for prognosis prediction in hepatocellular carcinoma.Cancer cell international · 2021Article
- Review
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Authors and funding
12 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To identify prognostic factors, array CGH (aCGH) patterns and mutations in WT1 and 9 other genes were analyzed in 128 unilateral Wilms tumors (WTs). Twenty patients had no aCGH aberrations, and 31 had WT1 alterations [silent and WT1 types: relapse-free survival (RFS), 95% and 83%, respectively]. Seventy-seven patients had aCGH changes without WT1 alterations (nonsilent/non-WT1 type) and were subtyped into those with or without +12, 11q-, 16q-, or HACE1 loss. RFS was better for those with than those without +12 (P = .010) and worse for those with than those without 11q-, 16q-, or HACE1 loss (P = .001, .025, or 1.2E-04, respectively). Silent and WT1 type and 8 subtype tumors were integrated and classified into 3 risk groups: low risk for the silent type and +12 subgroup; high risk for the no +12 plus 11q-, 16q-, or HACE1 loss subgroup; intermediate risk for the WT1 type and no +12 plus no 11q-, 16q-, or HACE1 loss subgroup. Among the 27 WTs examined, the expression of 146 genes on chromosome 12 was stronger in +12 tumors than in no +12 tumors, while that of 10 genes on 16q was weaker in 16q- tumors than in no 16q- tumors. Overexpression in 75 out of 146 upregulated genes and underexpression in 7 out of 10 downregulated genes correlated with better and worse overall survival, respectively, based on the public database. +12 was identified as a potential new marker predicting a favorable outcome, and chromosome abnormalities may be related to altered gene expression associated with these abnormalities.
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