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1. Maynard MA, Ohh M: Molecular targets from VHL studies into the oxygen-sensing pathway. Curr Cancer Drug Targets; 2005 Aug;5(5):345-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inheritance of a faulty von Hippel-Lindau (VHL) tumor suppressor gene is the cause of VHL disease, a rare multisystemic autosomal dominant disorder characterized by the development of hypervascular tumors in a number of organs, including the retina, brain, spine, pancreas, adrenal gland, and the kidney.
  • Recent discoveries have demonstrated that the VHL gene product pVHL serves as a substrate-recognition component of an E3 ubiquitin ligase complex that targets hypoxia-inducible factor (HIF) transcription factor for polyubiquitination and subsequent degradation.
  • Accordingly, tumor cells devoid of functional pVHL show an inappropriate accumulation of HIF, as well as downstream HIF-target genes, such as vascular endothelial growth factor (VEGF), a potent angiogenic factor.
  • Next generation anti-cancer drugs will undoubtedly emerge from our understanding of the molecular pathways governing normal cellular metabolism, growth and differentiation that have gone awry during neoplastic transformation, and studies in VHL disease will serve as one of the proving grounds for the efficacy of 'designer' anti-cancer drugs tailored against the VHL-HIF pathway.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA-Binding Proteins / metabolism. Nuclear Proteins / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / genetics. Ubiquitin-Protein Ligases / genetics. von Hippel-Lindau Disease / genetics
  • [MeSH-minor] Animals. Antigens, Neoplasm / metabolism. Basic Helix-Loop-Helix Transcription Factors. Carbonic Anhydrase Inhibitors / pharmacology. Carbonic Anhydrases / metabolism. Gene Expression Regulation. Humans. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Oxygen / metabolism. Vascular Endothelial Growth Factors / antagonists & inhibitors. Von Hippel-Lindau Tumor Suppressor Protein

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  • (PMID = 16101382.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Carbonic Anhydrase Inhibitors; 0 / DNA-Binding Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factors; 0 / endothelial PAS domain-containing protein 1; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen
  • [Number-of-references] 188
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2. van Rooijen E, Voest EE, Logister I, Bussmann J, Korving J, van Eeden FJ, Giles RH, Schulte-Merker S: von Hippel-Lindau tumor suppressor mutants faithfully model pathological hypoxia-driven angiogenesis and vascular retinopathies in zebrafish. Dis Model Mech; 2010 May-Jun;3(5-6):343-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] von Hippel-Lindau tumor suppressor mutants faithfully model pathological hypoxia-driven angiogenesis and vascular retinopathies in zebrafish.
  • Biallelic inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene predisposes human patients to the development of highly vascularized neoplasms in multiple organ systems.
  • The most severe neovascularization is observed in distinct areas that overlap with high vegfa mRNA expression, including the vhl mutant brain and eye.
  • Significantly, vessels in the brain and eye express cxcr4a, a marker gene expressed by tumor and vascular cells in VHL-associated hemangioblastomas and renal cell carcinomas.
  • Importantly, they will allow for a cost-effective, non-invasive and efficient way to screen for novel pharmacological agents and combinatorial treatments.
  • [MeSH-major] Anoxia / complications. Anoxia / pathology. Mutation / genetics. Retinal Neovascularization / complications. Retinal Neovascularization / pathology. Tumor Suppressor Proteins / metabolism. Zebrafish / metabolism. Zebrafish Proteins / metabolism
  • [MeSH-minor] Animals. Disease Models, Animal. Edema / complications. Edema / pathology. Humans. Macula Lutea / metabolism. Macula Lutea / pathology. Mutant Proteins / metabolism. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / metabolism. Retinal Detachment / complications. Retinal Detachment / pathology. Signal Transduction

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  • (PMID = 20335444.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C23207/A8066
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Tumor Suppressor Proteins; 0 / Vhl protein, zebrafish; 0 / Zebrafish Proteins; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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3. Thoren KL, Balingit AG, Billingsley J: Multiple pheochromocytomas in a patient with blurred vision. Clin Nucl Med; 2008 Sep;33(9):597-601
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multiple imaging was obtained because of concern for von Hippel-Lindau disease (VHL) after bilateral retinal angiomas were discovered on ophthalmologic consultation as a follow-up from the Emergency Department.
  • I-123 MIBG was performed before surgery to confirm that the lesions were indeed pheochromocytomas and also to rule out metastatic disease.
  • He was started on alpha- and beta-blocker medication for at least 3 weeks, followed by surgery.
  • DNA testing was performed and revealed mutations in the VHL gene previously reported to be associated with von Hippel-Lindau syndrome type II and genetic counseling was recommended.
  • He was presented in urology tumor board conference with recommendations for follow-up CT and laboratory tests after 3 months.
  • [MeSH-minor] 3-Iodobenzylguanidine. Adult. Brain / radiography. Humans. Magnetic Resonance Imaging. Male. Spine / radiography. Tomography, X-Ray Computed

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  • (PMID = 18716506.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 35MRW7B4AD / 3-Iodobenzylguanidine
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4. Reyns N, Assaker R, Louis E, Lejeune JP: Leptomeningeal hemangioblastomatosis in a case of von Hippel-Lindau disease: case report. Neurosurgery; 2003 May;52(5):1212-5; discussion 1215-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leptomeningeal hemangioblastomatosis in a case of von Hippel-Lindau disease: case report.
  • OBJECTIVE AND IMPORTANCE: We report a unique case of extended leptomeningeal hemangioblastomatosis in a patient presenting with clinical von Hippel-Lindau disease.
  • Magnetic resonance imaging of the brain and spine showed evidence of leptomeningeal contrast enhancement around the brainstem, spinal cord, and cauda equina and enlarged tortuous vessels around the mesencephalon.
  • It is assumed that the tumor arose in the pia mater and that its direction of growth was purely extramedullary, invading all subarachnoid spaces.
  • Nevertheless, the short life expectancy of our patient is usual in von Hippel-Lindau disease.
  • This case report illustrates the crucial challenge to develop a specific drug therapy related to angiogenesis in von Hippel-Lindau disease.
  • [MeSH-major] Hemangioblastoma / etiology. Hemangioblastoma / pathology. Meningeal Neoplasms / etiology. Meningeal Neoplasms / pathology. von Hippel-Lindau Disease / complications. von Hippel-Lindau Disease / pathology

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  • (PMID = 12699568.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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5. Harris AL: von Hippel-Lindau syndrome: target for anti-vascular endothelial growth factor (VEGF) receptor therapy. Oncologist; 2000;5 Suppl 1:32-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] von Hippel-Lindau syndrome: target for anti-vascular endothelial growth factor (VEGF) receptor therapy.
  • von Hippel-Lindau (VHL) syndrome is a familial cancer syndrome caused by germline mutations in the VHL tumor suppressor gene.
  • This increase in angiogenesis under normoxic conditions in key target organs such as the brain, kidney, and eye leads to high morbidity and reduced life expectancy.
  • Drugs designed to block the VEGF signaling pathway may prevent the long-term complications of the disease.
  • [MeSH-major] Endothelial Growth Factors / antagonists & inhibitors. Lymphokines / antagonists & inhibitors. Protein Isoforms / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Growth Factor / antagonists & inhibitors. Receptors, Mitogen / antagonists & inhibitors. von Hippel-Lindau Disease / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Enzyme Inhibitors / therapeutic use. Genes, Tumor Suppressor / genetics. Germ-Line Mutation / genetics. Humans. Indoles / therapeutic use. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / physiopathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrroles / therapeutic use. Receptors, Vascular Endothelial Growth Factor. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 10804089.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endothelial Growth Factors; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / Lymphokines; 0 / Protein Isoforms; 0 / Pyrroles; 0 / Receptors, Growth Factor; 0 / Receptors, Mitogen; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 71IA9S35AJ / Semaxinib; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 45
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6. Chavez JC, LaManna JC: Activation of hypoxia-inducible factor-1 in the rat cerebral cortex after transient global ischemia: potential role of insulin-like growth factor-1. J Neurosci; 2002 Oct 15;22(20):8922-31
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  • A logical explanation for HIF-1alpha accumulation might be that the brain remained hypoxic for prolonged periods after resuscitation.
  • By using the hypoxic marker 2-(2-nitroimidazole-1[H]-y1)-N-(2,2,3,3,3-pentafluoropropyl)-acetamide (EF5), we showed that the brain is hypoxic during the first hours of recovery from cardiac arrest, but the tissue is no longer hypoxic at 2 d.
  • In addition, we showed that IGF-1 was able to induce HIF-1alpha in pheochromocytoma cells and cultured neurons as well as in the brain of rats that received intracerebroventricular and systemic IGF-1 infusion.
  • [MeSH-major] Cerebral Cortex / metabolism. DNA-Binding Proteins / metabolism. Etanidazole / analogs & derivatives. Insulin-Like Growth Factor I / metabolism. Ischemic Attack, Transient / metabolism. Nuclear Proteins / metabolism. Proteasome Endopeptidase Complex. Transcription Factors. Tumor Suppressor Proteins. Ubiquitin-Protein Ligases
  • [MeSH-minor] Animals. Cardiopulmonary Resuscitation. Disease Models, Animal. Heart Arrest, Induced. Hydrocarbons, Fluorinated. Hypoxia, Brain / metabolism. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Immunohistochemistry. Ligases / metabolism. Male. Neurons / drug effects. Neurons / metabolism. PC12 Cells. Peptide Hydrolases / metabolism. Rats. Rats, Wistar. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, IGF Type 1 / biosynthesis. Up-Regulation. Von Hippel-Lindau Tumor Suppressor Protein

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  • (PMID = 12388599.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS-37111; United States / NINDS NIH HHS / NS / NS-38632
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)acetamide; 0 / DNA-Binding Proteins; 0 / Hif1a protein, rat; 0 / Hydrocarbons, Fluorinated; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 30DKA3Q1HL / Etanidazole; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.4.- / Peptide Hydrolases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease; EC 6.- / Ligases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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