Homozygous Deletions of theCDKN2C/p 18INK4CGene on the Short Arm of Chromosome 1 in Anaplastic Oligodendrogliomas
| Autor: | David N. Louis, Cairncross Jg, Ute Pohl |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Oligodendroglioma
Biology Polymerase Chain Reaction Pathology and Forensic Medicine Dosage Compensation Genetic Homologous chromosome medicine Humans Coding region Genes Tumor Suppressor Allele neoplasms Gene Anaplasia Regulation of gene expression Genetics Brain Neoplasms Genes p16 General Neuroscience Point mutation Homozygote Chromosome medicine.disease nervous system diseases Chromosomes Human Pair 1 Cancer research Neurology (clinical) Gene Deletion Research Article |
| Zdroj: | Brain Pathol |
| ISSN: | 1015-6305 |
| Popis: | Allelic deletions of the short arm of chromosome 1 are common in oligodendrogliomas and have been correlated with chemosensitivity and better prognosis in patients with high‐grade oligodendrogliomas. In these tumors, 1p loss is also inversely related to deletions of the CDKN2A gene on 9p, which encodes the key cell cycle regulatory molecule p16(INK4A). Because the CDKN2C gene, which encodes the homologous p18(INK4C) cell cycle regulatory protein, maps to chromosomal band 1p32, CDKN2C is an attractive candidate for the oligodendroglioma suppressor gene on chromosome 1. To evaluate this possibility, we studied 39 high‐grade oligodendrogliomas for homozygous deletions and point mutations of the CDKN2C gene, as well as for allelic loss of 1p. Although no mutations were detected in the CDKN2C coding region, two tumors had homozygous deletions that involved CDKN2C. Interestingly, these cases did not have CDKN2A gene deletions. Coupled with the recent report of rare point mutations of CDKN2C in oligodendrogliomas, these findings suggest that CDKN2C inactivation may be oncogenic in a small percentage of human oligodendrogliomas. |
| Databáze: | OpenAIRE |
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