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Proliferation of blood vessels in various chemically-induced animal tumors is independent of von Hippel-Lindau gene mutations

  1. Author:
    Shiao, Y. H.
    Diwan, B. A.
    Calvert, R. J.
    Perantoni, A. O.
    Waalkes, M. P.
    Zbar, B.
    Lerman, M. I.
    Rice, J. M.
    1. Year of Conference: 1997
  2. Conference Name: Annual Meeting of the American Association for Cancer Research
    1. 38
    2. Pages: A363
  4. Type of Work: Meeting Abstract
  1. Abstract:

    von Hippel-Lindau (VHL) gene function has been associated with down-regulation of vascular endothelial growth factor. Also, frequent germline VHL mutations in human VHL disease, which is characterized by development of certain vascular tumors including retinal angiomatosis and hemangioblastoma in the central nervous system, suggests a regulatory function of VHL in angiogenesis. To explore a possible role of VHL in tumor angiogenesis, we examined the VHL gene sequence in chemically-induced rat tumors of non-vascular origin, but with marked proliferation of blood vessels. PCR-SSCP using intron-derived primers was performed to analyze VHL mutations in DNA from 13 gliomas with vascular hyperplasia, 3 oligodendrogliomas, and 18 pheochromocytomas. No VHL gene mutations were detected. Levels of VHL protein expression in these tumors are being assessed to test for inactivation of VHL by other mechanisms, eg, down-regulation of VHL by loss of heterozygosity or hypermethylation of the VHL promoter.

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