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JNCI Journal of the National Cancer Institute 2000 92(20):1688-1689; doi:10.1093/jnci/92.20.1688
© 2000 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 92, No. 20, 1688-1689, October 18, 2000
© 2000 Oxford University Press

BRIEF COMMUNICATION

Mutational Analysis of Endothelial Cells Derived From von Hippel–Lindau-Related Renal Cancer

Maartje Los, Olaf A. J. Kerckhaert, Richard Zewald, Hans Kristian Ploos van Amstel, Emile E. Voest

Affiliations of authors: M. Los, O. A. J. Kerckhaert, E. E. Voest (Laboratory of Medical Oncology, Division of Medical Oncology, Department of Internal Medicine), R. Zewald, H. K. Ploos van Amstel (Department of Medical Genetics), University Medical Center Utrecht, The Netherlands.

Correspondence to: Emile E. Voest, M.D., Laboratory of Medical Oncology, Division of Medical Oncology, Department of Internal Medicine, University Medical Center Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands (e-mail: e.e.voest@digd.azu.nl).

von Hippel–Lindau (VHL) disease is an autosomal dominant, inherited cancer syndrome that is characterized by extensively vascularized tumors, such as hemangioblastomas of the retina and central nervous system, renal cell carcinomas (RCCs), and pheochromocytomas (1). The VHL tumor suppressor gene was cloned in 1993 and is located at chromosome 3p25–3p26 (2). According to the two-hit hypothesis for tumor suppressor genes, inactivation of both alleles of the VHL gene leads to tumor formation. One copy of the VHL gene is mutated by inheritance, and the second hit causes inactivation of the remaining wild-type VHL gene (3).

Although the VHL protein is widely expressed in different . . . [Full Text of this Article]

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