ArticleMedicine2020
Comprehensive analysis of mutations of renal cell carcinoma in an autosomal dominant polycystic kidney disease patient.
Article in Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Pellino1-mTOR/S6K1 signaling axis is a key pathogenesis for the development of polycystic kidney disease.Cell death & disease · 2026Article
- Autosomal Dominant Polycystic Kidney Disease-Related Multifocal Renal Cell Carcinoma: A Narrative Iconographic Review.International journal of molecular sciences · 2025Review
- NS398 as a potential drug for autosomal-dominant polycystic kidney disease: Analysis using bioinformatics, and zebrafish and mouse models.Journal of cellular and molecular medicine · 2021Article
- Modeling Neoplastic Growth in Renal Cell Carcinoma and Polycystic Kidney Disease.International journal of molecular sciences · 2021Review
- Autosomal Dominant Polycystic Kidney Disease Patients Requiring Nephrectomy: Characteristics and Surgical Considerations.ANZ journal of surgeryArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC) is known to be more prevalent in autosomal dominant polycystic kidney disease (ADPKD) patients than in the general population. However, little is known about genetic alterations or changes in signaling pathways in RCC in patients with ADPKD.In the current report, whole-exome and transcriptome sequencing was performed for paired samples of tumor tissue, cyst tissue, and peripheral blood (triple set) from a patient diagnosed with ADPKD and RCC.A 68-year-old man with ADPKD underwent left partial nephrectomy and was diagnosed with RCC. DNA and RNA were extracted from the triple set of the patient. A nonsense mutation in PKD2 (p.Arg742X), which is well known as a pathogenic variant in ADPKD, was identified in the paired triple set. In the tumor sample, a somatic missense mutation of VHL (p.S65L) was found, which is known as a pathogenic mutation in Von Hippel-Lindau syndrome and RCC. Furthermore, loss of chromosome 3p, where VHL is located, was detected. Upregulated VEGFA was found in the analysis of RCC mRNA, which might be caused by the loss of VHL and accelerate angiogenesis in RCC.Proliferation was also expected to be activated by the MAPK signaling pathway, including NRAS and MAPK1 expression.
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Registered trials
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