Open AccessHomozygous Deletions of the CDKN2C /p 18 INK4C Gene on the Short Arm of Chromosome 1 in Anaplastic Oligodendrogliomas
Author(s) -
Pohl Ute,
Cairncross J. Gregory,
Louis David N.
Publication year - 1999
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.1999.tb00545.x
Subject(s) - gene , cdkn2a , biology , oligodendroglioma , chromosome , point mutation , genetics , microbiology and biotechnology , cancer research , mutation , glioma , astrocytoma
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.