The von Hippel-Lindau Tumor Suppressor Protein and Clear Cell Renal Carcinoma
Open accessAbstract
Germ line VHL tumor suppressor gene loss-of-function mutations cause von Hippel-Lindau disease, which is associated with an increased risk of central nervous system hemangioblastomas, clear cell renal carcinomas, and pheochromocytomas. Somatic VHL mutations are also common in sporadic clear cell renal carcinomas. The VHL gene product, pVHL, is part of a ubiquitin ligase complex that targets the α-subunits of the heterodimeric transcription factor hypoxia-inducible factor (HIF) for polyubiquitylation, and hence, proteasomal degradation, when oxygen is available. pVHL-defective clear cell renal carcinomas overproduce a variety of mRNAs that are under the control of HIF, including the mRNAs that encode vascular endothelial growth factor, platelet-derived growth factor B, and transforming growth factor α. In preclinical models, down-regulation of HIF-α, especially HIF-2α, is both necessary and sufficient for renal tumor suppression by pVHL. These observations are probably relevant to the demonstrated clinical activity of vascular endothelial growth factor antagonists in clear cell renal carcinoma and form a foundation for the testing of additional agents that inhibit HIF, or HIF-responsive gene products, in this disease.
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VHL tumor suppressor inactivation, causing pseudo-hypoxic stabilization of HIF-1α and HIF-2α, is an initiating event in hereditary and sporadic ccRCC.
“Inactivation of the VHL tumor suppressor gene, which results in pseudo-hypoxic stabilization of both HIF-1α and HIF-2α, is an initiating genetic event for both hereditary (VHL disease) and sporadic ccRCCs [16].”
From Revisiting the HIF switch in the tumor and its immune microenvironment. (2022) · cites this paper as [16]
The Abstract says VHL inactivation is important in hereditary and sporadic clear cell renal carcinoma and that HIF-α accumulates when pVHL is absent (page not supplied). But the Open Discussion says VHL loss appears early in VHL disease while its timing in sporadic carcinoma cannot be proved. The paper also says VHL-defective renal carcinomas may produce HIF-2α alone, so stabilization of both isoforms is not universal. (LLM, conf=0.89)
Experimental — accuracy not yet measured75% of sporadic clear cell RCCs are VHL-deficient.
“Although mTOR and the overall process of HIF-1α protein synthesis are limited under normoxia, it was found that 75% of sporadic clear cell RCCs are VHL-deficient, thus, in this case HIF-1α translation can proceed smoothly serving as a target for mTOR inhibitors intervention58.”
From HIF-1α pathway: role, regulation and intervention for cancer therapy (2015) · cites this paper as [58]
The passage labeled Abstract (page not available) says that 40%–80% of sporadic clear cell renal carcinomas are linked to biallelic VHL inactivation. That supports VHL deficiency as common, but it does not establish the specific figure of 75%. (LLM, conf=0.88)
Experimental — accuracy not yet measured
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- Authors
- Kaelin, W. G.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Kaelin, William G.
- ORCID
- Kaelin, William G.
- Venue
- Clinical Cancer Research
- Published
- 2007-01-15
- Volume
- 13
- Issue
- 2
- Pages
- 680s-684s
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2131473358
- Semantic Scholar
- b1ecaaf13be1baca02f75edb325c7d80e991f9a6
- Cited by
- 336
- References
- 80
- Citations by year
- 2026: 13 · 2025: 13 · 2024: 6 · 2023: 9 · 2022: 11 · 2021: 11 · 2020: 9 · 2019: 9 · 2018: 14 · 2017: 13 · 2016: 14 · 2015: 14 · 2014: 18 · 2013: 18 · 2012: 28
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal cell carcinoma treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- von Hippel-Lindau protein, VHL tumor suppressor, clear cell renal cell carcinoma, hypoxia-inducible factor, HIF-2α, HIF-1α, ubiquitin ligase, vascular endothelial growth factor, platelet-derived growth factor B, transforming growth factor-alpha, VEGF inhibitors, von Hippel-Lindau disease
- MeSH terms
- Carcinoma, Renal Cell, Genotype, Humans, Kidney Neoplasms, Mutation, RNA, Messenger, Transcription Factors, Signal Transduction, Gene Expression Regulation, Neoplastic, Dimerization, Vascular Endothelial Growth Factor A, Von Hippel-Lindau Tumor Suppressor Protein
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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