ReviewCancer genetics2015
The roles of chromatin-remodelers and epigenetic modifiers in kidney cancer.
Review in Cancer genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Emerging roles for the epigenetic modifiers PBRM1 SETD2 and BAP1 in clear cell renal cell carcinoma pathogenesis and prognosis beyond VHL.Discover oncology · 2026Review
- The SLC1A1/EAAT3 dicarboxylic amino acid transporter is an epigenetically dysregulated nutrient carrier that sustains oncogenic metabolic programs.Nature communications · 2025Article
- Exploration of a prognostic signature for mitochondria-related genes and the therapeutic prospects of vorinostat in clear cell renal cell carcinoma.Translational andrology and urology · 2025Article
- AURKB promotes immunogenicity and immune infiltration in clear cell renal cell carcinoma.Discover oncology · 2024Article
- Rare germline heterozygous missense variants in BRCA1-associated protein 1, BAP1, cause a syndromic neurodevelopmental disorder.American journal of human genetics · 2022Article
- Review
- Single nucleotide variants of succinate dehydrogenase A gene in renal cell carcinoma.Cancer science · 2021Article
- Modeling Neoplastic Growth in Renal Cell Carcinoma and Polycystic Kidney Disease.International journal of molecular sciences · 2021Review
- Epigenome screening highlights that JMJD6 confers an epigenetic vulnerability and mediates sunitinib sensitivity in renal cell carcinoma.Clinical and translational medicine · 2021Article
- Identification of a novel immune-related microRNA prognostic model in clear cell renal cell carcinoma.Translational andrology and urology · 2021Article
- Background, applications and challenges of radiogenomics in genitourinary tumor.American journal of cancer research · 2021Review
- Kidney cancer PDOXs reveal patient-specific pro-malignant effects of antiangiogenics and its molecular traits.EMBO molecular medicine · 2020Article
- Article
- Distinct genomic subclasses of high-grade/progressive meningiomas: NF2-associated, NF2-exclusive, and NF2-agnostic.Acta neuropathologica communications · 2020Article
- Histone 3 lysine-27 demethylase KDM6A coordinates with KMT2B to play an oncogenic role in NSCLC by regulating H3K4me3.Oncogene · 2020Article
- Review
- Identification and validation of novel metastasis-related signatures of clear cell renal cell carcinoma using gene expression databases.American journal of translational research · 2020Article
- The Role of Serine Peptidase Inhibitor Kazal Type 13 (SPINK13) as a Clinicopathological and Prognostic Biomarker in Patients with Clear Cell Renal Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Article
- Second line therapy with axitinib after only prior sunitinib in metastatic renal cell cancer: Italian multicenter real world SAX study final results.Journal of translational medicine · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is the major subtype of kidney cancer that is characterized by frequent inactivation of the von Hippel-Lindau (VHL) gene in 80-90% of the tumors. Recent reports using massive parallel sequencing technologies have discovered additional cancer driver genes. PBRM1 was found to be mutated in about 40% of ccRCC tumors, whereas BAP1 and SETD2 were each mutated in about 10-15% of ccRCC tumors. JARID1C and UTX, two histone H3 demethylases, were also found to harbor mutations in ccRCC, albeit at lower rates. ccRCC tumors display a high degree of intra-tumoral heterogeneity, with some mutations present in all cancer cells (ubiquitous), whereas others are subclonal. The VHL mutations were always ubiquitous in the tumors; PBRM1 mutations were also ubiquitous but to a lesser extent. On the contrary, mutations in BAP1, SETD2, JARID1C, and UTX were all subclonal, meaning that they were present in a subset of cancer cells in a tumor. The prognostic value of PBRM1 mutations in ccRCC is still controversial, whereas BAP1 mutations were tightly linked to worse clinical outcomes in multiple studies. The molecular functions of these newly identified cancer driver genes are discussed, and they were known readers, writers, or erasers of histone marks on histone H2 and H3 tails that are very close to each other, suggesting that these factors might functionally interact and affect common pathways. The studies on these newly identified tumor suppressors will shed light on ccRCC tumorigenesis and development, and will likely lead to development of novel therapeutic interventions for ccRCC patients.
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