Glial Tumors in the MNU Rat Model: Induction of Pure and Mixed Gliomas that Do Not Require Typical Missense Mutations of p53
| Autor: | Elisabeth J. Rushing, S C Schold, K J Land, Mark L. Watson, Demetrius M. Kokkinakis |
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| Rok vydání: | 1998 |
| Předmět: |
Male
Mixed Glioma Pathology medicine.medical_specialty Mutation Missense medicine.disease_cause Pathology and Forensic Medicine Rats Sprague-Dawley Cellular and Molecular Neuroscience Glioma medicine Animals neoplasms biology Glial fibrillary acidic protein Astrocytoma Methylnitrosourea Exons General Medicine medicine.disease Rats nervous system diseases Oligodendroglia Genes ras Neurology Astrocytes Carcinogens Synaptophysin biology.protein Immunohistochemistry Neurology (clinical) Oligodendroglioma Tumor Suppressor Protein p53 Carcinogenesis |
| Zdroj: | Journal of Neuropathology and Experimental Neurology. 57:1053-1060 |
| ISSN: | 0022-3069 |
| Popis: | Gliomas were induced in adult male Sprague-Dawley rats by continuous exposure to 100 ppm of N-nitrosmethy-lurea (MNU) in drinking water. Latency periods for such tumors were 20 and SO weeks following completion of exposure intervals of 20, 15, and 10 weeks, respectively. Based on histomorphology and the pattern of GFAP immunoreactivity, a large percentage of MNU-induced tumors (>40%) were anaplastic mixed gliomas, having both neoplastic astrocytic and oligoden-droglial components. Typical oligodendrogliomas and astrocytomas also occurred less frequently. Unlike the majority of tumors induced by ethylnitrosourea (ENU), MNU yielded glial tumors that did not express synaptophysin. Anaplastic mixed gliomas and glioblastoma multiforme (GBMs) had no missense p53 mutations in the commonly mutated exons 4 through 8 and did not overexpress wild-type p53, suggesting that MNU-induced oncogenesis in rat brain tumors may not require inactivation/alteration of the p53 tumor suppressor gene. The K-ras gene was also analyzed and found to have no activating mutations in brain tumors. This model is suitable for studying genetic events leading to the majority of gliomas that apparently express functional p53. |
| Databáze: | OpenAIRE |
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