By Francis Ali-Osman
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A mutant epidermal growth factor receptor common in human glioma confers enhanced tumorigenicity. Proc. Natl. Acad. Sci. USA 91:7727–7731. 55. Y. 1998. The molecular genetics of central nervous system tumors. Pathology 30:196–202. 56. , Lois A, et al. 1994. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature 368:753–756. 57. D. , et al. 1993. Oncoprotein MDM2 conceals the activation domain of tumor suppressor p53. Nature 362:857–860. 58. , et al. 1998. Gene amplification as a prognostic factor in primary brain tumors.
3 (70,79), allowing for candidate genes within this region to be examined for mutation. The incidence of 19q deletion is not significantly different between low- and high-grade oligodendrogliomas, suggesting that this alteration is an early event in the neoplastic development of these tumors (68). This finding contrasts with the 19q loss observed in astrocytic gliomas that is generally restricted to the high-grade cases (79). Deletion of chromosome 1p is another frequent event in oligodendrogliomas, occurring in 40– 90% of these tumors (2,68).
Et al. 1990. The GAP-related domain of the neurofibromatosis type 1 gene product interacts with ras p21. Cell 63:843–849. 50. , et al. 1997. P-TEN, the tumor suppressor from human chromosome 10q23, is a dualspecificity phosphatase. Proc. Natl. Acad. Sci. USA 94:9052–9057. 51. , et al. 1998. Drug resistance of human glioblastoma cells conferred by a tumorspecific mutant epidermal growth factor receptor through modulation of Bcl-XL and caspase-3-like proteases. Proc. Natl. Acad. Sci. USA 95:5724–5729.