Role of VHL gene mutation in human cancer.
By William Y. Kim, W. Kaelin. Journal of Clinical Oncology, 2004
983 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/e1db540ae326c6f62981024393609f0d83b45759
How researchers see this paper
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In Cancer Research
- David M. Sabatini
- J. Pouysségur
- N. Mazure
- Masayuki Yamamoto
- Eyal Gottlieb
- Frédéric Dayan
- C. Sawyers
- Ian Tomlinson
In Molecular Biology
- David M. Sabatini
- Masayuki Yamamoto
- K. I. Tong
- J. Pouysségur
- D. Guertin
- A. Kobayashi
- Moon-Il Kang
- N. Mazure
Citations in the corpus
- Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1 (2006, background): “It has been reported that I B and Hif1 , two prototype transcription factors important for the environmental response, are also degraded rapidly through the proteasomedependent protein degradation pathway exploiting Cul1- and Cul2-type E3 ligases, respectively (1, 20).”
- Defining the role of mTOR in cancer. (2007, background): “In cells exposed to hypoxia, levels of the HIF1α transcription factor increase and this facilitates expression of VEGF, a HIF1α target gene. mTORC1 regulates the translation and activity of HIF1α (Bernardi et al., 2006; Hudson et al., 2002), suggesting that the antiangiogenic properties of rapamycin”
- Cancer related mutations in NRF2 impair its recognition by Keap1-Cul3 E3 ligase and promote malignancy (2008, background): “The correlation of mutation in the ubiquitin-proteasome pathway with cancer growth has long been recognized (27, 28).”
- Loss of Keap1 function activates Nrf2 and provides advantages for lung cancer cell growth. (2008, neutral): “For instance, the transcription factors InB (11) and hypoxia-inducible factor-1a ( 12 ) use Cul1 and Cul2, respectively, to form specific E3 ligases.”
- Perturbations of the AKT signaling pathway in human cancer (2005, background): “…of the von-Hippel–Lindau tumor suppressor gene (VHL) causes hamartomatous tumors associated with the von-Hippel–Lindau syndrome, although somatic mutations of this gene have also been found in hemangioblastomas and clear-cell Oncogene renal carcinomas (reviewed in Kim and Kaelin, 2004).”
- Succinate dehydrogenase and fumarate hydratase: linking mitochondrial dysfunction and cancer (2006, background): “Generally, VHL disease is a cancer predisposition syndrome caused by the loss of function of pVHL (Kim and Kaelin, 2004).”
- Hypoxia-inducible factor determines sensitivity to inhibitors of mTOR in kidney cancer (2006, background): “The most common molecular abnormality in renal cell carcinoma is loss of VHL , which is found in about 50–70% of sporadic case”
- Mitochondrial tumour suppressors: a genetic and biochemical update (2005, background): “Germline mutations in these genes can lead to the development of phaeochromocytoma and clear-cell renal-cell carcinom”
- Hypoxia signalling in cancer and approaches to enforce tumour regression (2006, background): “From hypoxia to tumour invasion Hypoxia, or genetic alterations of the hypoxia signalling cascad”