Genetic abnormalities in oligodendroglial and ependymal tumours

Abstract

Oligodendroglial and ependymal tumours are not the most common glial neoplasms; however, they are important subtypes of gliomas with different tumour biologies. Cytogenetic information has suggested that losses of chromosomes 1 p and 19 q are the most frequent genetic alterations in oligodendroglial tumours. Combined loss of these chromosomes has been associated with better chemotherapeutic response and prolonged overall survival. Loss of chromosome 22 is a well defined abnormality in ependymomas. In addition, deletion of chromosome 6 q may be another frequent chromosomic aberration in paediatric ependymomas.

Analysis of HIC‐1 methylation and transcription in human ependymomas

“…Ependymomas are gliomas that presumably originate from the ependymal lining of the ventricular system and from remnants of the central canal of the spinal cord 1. They occur predominantly in children and young adults but show a broad age distribution.…”

“…They occur predominantly in children and young adults but show a broad age distribution. In children, ependymomas constitute the third most common brain tumor, accounting for 6–12% of all pediatric CNS neoplasms 1. Based on their histopathologic features and location, they are classified as myxopapillary ependymoma (WHO grade I), subependymoma (WHO grade I), ependymoma (WHO grade II) and anaplastic ependymoma (WHO grade III).…”

Common Pediatric Central Nervous System Tumors: Histology and Molecular Biology

“…Spinal cord ependymoma is one of the well-known associated lesion of neurofibromatosis type 2. 2,[15][16][17][18][19] Age below 1 year, location in the posterior fossa, and incomplete tumor excision have been correlated with an unfavorable outcome. 20…”

The embryology and molecular-genetic mechanisms of brain tumor pathogenesis: literature review

“…Вивчаючи гене-тичні порушення як прогностичні чинники у пацієнтів за наявності астроцитоми, встановлено кореляцію між втратою супресорних функцій трьох генів ТР53, NF1 та РТЕN і агресивним фенотипом астроцитом, отже, поганим прогнозом [25,45,46]. В епендимомах часто ідентифікують втрату хро-мосоми 22 і делеції 6q [47][48][49].…”