Endolymphatic Sac Tumors in a Population of Patients With Von Hippel-Lindau Disease:The Natural History and Pathobiology, and a Prospective Non-Randomized Clinical Trial of Hearing Preservation Surgery in Patients With Early Stage Endolymphatic Sac Tumors
Completed
Conditions studied: Deafness, Kidney Diseases, Kidney Neoplasms, Neoplasms, Retinal Diseases
In brief
The von Hippel Lindau (VHL) gene has recently been identified as the genetic defect resulting in a syndrome of multiple neoplasias. Patients with VHL disease develop retinal angiomata, renal cysts and/or carcinomas, CNS hemangioblastomas as well as pancreatic cysts and pheochromocytomas. Investigators have shown the gene to be a tumor suppressor type proto-oncogene located at chromosomal locus 3p26. The gene includes three exons whose gene product targets a cellular transcription factor Elongin SIII. Binding of the VHL proteins to two subunits of this elongation factor inhibits transcription and may play a crucial role in the clinical development of the von Hippel Lindau phenotype.
Key facts
- Study ID
- NCT00001668
- Run by
- National Institute of Neurological Disorders and Stroke (NINDS)
- People needed
- 75
- Starts
- 1997-04-01
- Expected to finish
- 2000-04-01
- Last updated by the study team
- 2008-03-04
Who can join
Age: any. Sex: any. Healthy volunteers: not accepted.
Where it is running
- National Institute of Neurological Disorders and Stroke (NINDS) — Bethesda, Maryland, United States
Full record on ClinicalTrials.gov
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