Clinical trial · Observational
Drivers of Hypoxia-induced Angiogenesis in Tumor Development
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
The study aims to elucidate hypoxia-induced angiogenesis in tumor development using central nervous system (CNS) hemangioblastoma tumorgenesis as a model. In a pilot-project the investigators will identify genetic drivers of CNS hemangioblastoma progression and associated cyst development using whole genome sequencing and copy number profiling of tumor DNA paired with clinical information about each tumor's growth pattern. The investigators will look for recurrent mutations across tumors to identify common genetic mechanisms involved in early tumorigenesis.
Conditions
Conditions (1)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Von Hippel-Lindau Disease | — | UNRESOLVED | — |
Interventions
Interventions (1)
| Intervention | Type | Mapped drug | Match |
|---|---|---|---|
| Whole exome sequencing | Genetic | — | UNRESOLVED |
Design
Arms and outcomes
Arms (1)
- label
- 1
- description
- Individuals currently living, over the age of 18 years and known carriers of a pathogenic variant in the VHL gene.
- interventionNames
- Genetic: Whole exome sequencing
Primary outcomes (1)
- measure
- Somatic variants
- timeFrame
- July 2019-December 2019
- description
- somatic genetic variants
Eligibility
Eligibility (as posted)
- Sex
- All
- Minimum age
- 18 Years
Show eligibility criteria text
Inclusion Criteria: * Currently living, carrier of a pathogenic variant in the VHL gene, at least one surgically removed CNS hemangioblastoma that is accessible for the study. Exclusion Criteria: * Under the age of 18 years, deceased individuals
References
Publications (18)
- BACKGROUNDHanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7;100(1):57-70. doi: 10.1016/s0092-8674(00)81683-9. No abstract available. PMID 10647931
- BACKGROUNDMaher ER, Neumann HP, Richard S. von Hippel-Lindau disease: a clinical and scientific review. Eur J Hum Genet. 2011 Jun;19(6):617-23. doi: 10.1038/ejhg.2010.175. Epub 2011 Mar 9. PMID 21386872
- BACKGROUNDNordstrom-O'Brien M, van der Luijt RB, van Rooijen E, van den Ouweland AM, Majoor-Krakauer DF, Lolkema MP, van Brussel A, Voest EE, Giles RH. Genetic analysis of von Hippel-Lindau disease. Hum Mutat. 2010 May;31(5):521-37. doi: 10.1002/humu.21219. PMID 20151405
- BACKGROUNDAmmerman JM, Lonser RR, Dambrosia J, Butman JA, Oldfield EH. Integra Foundation Award: Long-term natural history of hemangioblastomas in Von Hippel-Lindau disease: implications for treatment. Clin Neurosurg. 2006;53:324-31. No abstract available. PMID 17380770
- BACKGROUNDWanebo JE, Lonser RR, Glenn GM, Oldfield EH. The natural history of hemangioblastomas of the central nervous system in patients with von Hippel-Lindau disease. J Neurosurg. 2003 Jan;98(1):82-94. doi: 10.3171/jns.2003.98.1.0082. PMID 12546356
- BACKGROUNDGlasker S, Klingler JH, Muller K, Wurtenberger C, Hader C, Zentner J, Neumann HP, Velthoven VV. Essentials and pitfalls in the treatment of CNS hemangioblastomas and von Hippel-Lindau disease. Cent Eur Neurosurg. 2010 May;71(2):80-7. doi: 10.1055/s-0029-1234040. Epub 2010 Mar 12. PMID 20229452
- BACKGROUNDVortmeyer AO, Falke EA, Glasker S, Li J, Oldfield EH. Nervous system involvement in von Hippel-Lindau disease: pathology and mechanisms. Acta Neuropathol. 2013 Mar;125(3):333-50. doi: 10.1007/s00401-013-1091-z. Epub 2013 Feb 12. PMID 23400300