ArticleProceedings of the National Academy of Sciences of the United States of America2014
Bap1 is essential for kidney function and cooperates with Vhl in renal tumorigenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 147 citations in OpenAlex.
- Somatic mutational landscape in von Hippel-Lindau familial hemangioblastoma.Molecular oncology · 2026Article
- BAP1 deficiency-induced SKA3 promotes clear cell renal cell carcinoma malignant progression by regulating chromosomal instability.Cell death & disease · 2026Article
- A single chromosome 3p break initiates clear cell renal cell carcinoma evolution.bioRxiv : the preprint server for biology · 2026Article
- Determinants of pancreatic tropism in metastatic renal cell carcinoma.JCI insight · 2026Article
- Distinct genomic, microenvironmental, and nephron signatures in VHL kidney cysts and tumors.Scientific reports · 2026Article
- Role of single-nucleotide polymorphism microarray in the classification of BAP1-inactivated melanocytic tumours.Histopathology · 2025Article
- Characterisation of an autochthonous mouse ccRCC model of immune checkpoint inhibitor therapy resistance.Scientific reports · 2025Article
- A Boolean network model of hypoxia, mechanosensing and TGF-β signaling captures the role of phenotypic plasticity and mutations in tumor metastasis.PLoS computational biology · 2025Article
- BAP1 complexes with YY1 and RBBP7 and its downstream targets in ccRCC cells.Open life sciences · 2025Article
- Lactylation in cancer: Mechanisms in tumour biology and therapeutic potentials.Clinical and translational medicine · 2024Review
- Toward a CRISPR-based mouse model ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Oncogenic Cell Tagging and Single-Cell Transcriptomics Reveal Cell Type-Specific and Time-Resolved Responses to Vhl Inactivation in the Kidney.Cancer research · 2024Article
- Downregulation of the kidney glucagon receptor, essential for renal function and systemic homeostasis, contributes to chronic kidney disease.Cell metabolism · 2024Article
- Potential Role of VHL, PTEN, and BAP1 Mutations in Renal Tumors.Journal of clinical medicine · 2023Article
- Novel genetically engineered mouse models for clear cell renal cell carcinoma.Scientific reports · 2023Article
- BAP1 as a guardian of genome stability: implications in human cancer.Experimental & molecular medicine · 2023Review
- The expanding role of BAP1 in clear cell renal cell carcinoma.Human pathology · 2023Review
- BAP1 is a novel regulator of HIF-1α.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A novel immune-related model to predict prognosis and responsiveness to checkpoint and angiogenesis blockade therapy in advanced renal cancer.Frontiers in oncology · 2023Article
- Treatment strategies for clear cell renal cell carcinoma: Past, present and future.Frontiers in oncology · 2023Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Why different species are predisposed to different tumor spectra is not well understood. In particular, whether the physical location of tumor suppressor genes relative to one another influences tumor predisposition is unknown. Renal cancer presents a unique opportunity to explore this question. Renal cell carcinoma (RCC) of clear-cell type (ccRCC), the most common type, begins with an intragenic mutation in the von Hippel-Lindau (VHL) gene and loss of 3p (where VHL is located). Chromosome 3p harbors several additional tumor suppressor genes, including BRCA1-associated protein-1 (BAP1). In the mouse, Vhl is on a different chromosome than Bap1. Thus, whereas loss of 3p in humans simultaneously deletes one copy of BAP1, loss of heterozygosity in the corresponding Vhl region in the mouse would not affect Bap1. To test the role of BAP1 in ccRCC development, we generated mice deficient for either Vhl or Vhl together with one allele of Bap1 in nephron progenitor cells. Six2-Cre;Vhl(F/F);Bap1(F/+) mice developed ccRCC, but Six2-Cre;Vhl(F/F) mice did not. Kidneys from Six2-Cre;Vhl(F/F);Bap1(F/+) mice resembled kidneys from humans with VHL syndrome, containing multiple lesions spanning from benign cysts to cystic and solid RCC. Although the tumors were small, they showed nuclear atypia and exhibited features of human ccRCC. These results provide an explanation for why VHL heterozygous humans, but not mice, develop ccRCC. They also explain why a mouse model of ccRCC has been lacking. More broadly, our data suggest that differences in tumor predisposition across species may be explained, at least in part, by differences in the location of two-hit tumor suppressor genes across the genome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.