Detection of p16, RB, CDK4, and p53 gene deletion and amplification by fluorescence in situ hybridization in 96 gliomas.

作者: Arie Perry , Kari Anderl , Tom J. Borell , David W. Kimmel , Chiao H. Wang

DOI: 10.1093/AJCP/112.6.801

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摘要: Inactivation of the p53 gene is a common early event astrocytoma tumorigenesis. Alternatively, since p16, retinoblastoma (RB), and CDK4 genes have been implicated in malignant progression, detection losses or amplifications these gliomas could be diagnostically, prognostically, therapeutically important. We obtained smear preparations from 96 diffuse 10 nonneoplastic specimens. Dual-color fluorescence situ hybridizations using paired probes for CEN9/pl6, CEN8/RB, CEN17/p53, CEN12/CDK4 were performed revealed expected frequencies abnormalities, exceptfor losses, which low (7%). The latter supports concept thatp53 inactivation usually occurs by mitotic recombination. Detected abnormalities pl6/RB/CDK4 pathway highly associated with astrocytic differentiation univariately decreased patient survival. However, only age histologic classification retained statistical significance on multivariate analysis. conclude that gliomas, are markers phenotype. Thus, their hybridization may diagnostic cases equivocal morphologic features. Although our numbers small, we find no additional prognostic to genetic once age, grade, oligodendroglial histology taken into account.

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