Genomic Alterations in Low-Grade, Anaplastic Astrocytomas and Glioblastomas

Ali ARSLANTAS1, Sevilhan ARTAN2, Ülkü ÖNER3, M Hamza MÜSLÜMANOGLU2, Muhsin ÖZDEMIR2, Ramazan DURMAZ1, Didem ARSLANTAS4, Murat VURAL1, Erhan COSAN1, Metin Ant ATASOY1

1Department of Neurosurgery, Medical Faculty, Osmangazi University, Eskisehir, Turkey
2Department of Medical Genetics, Medical Faculty, Osmangazi University, Eskisehir, Turkey
3Department of Pathology, Medical Faculty, Osmangazi University, Eskisehir, Turkey
4Department of Public Health, Medical Faculty, Osmangazi University, Eskisehir, Turkey


To extend our understanding of potential stepwise genetic alterations that may underlie tumor progression from low-grade astrocytomas to glioblastomas, histopathologic and comparative genomic hybridization analyses were performed on tumor specimens from 68 primary lesions, including 40 glioblastomas, 10 anaplastic and 18 low-grade astrocytomas. The number of aberrations per case increased towards the higher grade tumors (grade II: 1.66±1.49; grade III: 2.80±1.68; grade IV: 3.02±1.07; F=6.955, p=0.002). A gain of 7/7q was common and the most frequently seen aberration in low-grade astrocytomas, whereas loss of 10q was the most frequently seen anomaly in anaplastic astrocytomas and glioblastomas. Chromosome 7p amplification was only detected in glioblastomas. Chromosome 10/10q deletion and combination of 1p, 19q and 17p deletions were specific to high-grade astrocytic tumors. Sequences of chromosome 7 and 10 seem to have pivotal roles in the biology of human gliomas. The genomic copy deletions of chromosomes 1p and 19q might provide an alternative mechanism in the genesis of astrocytomas. Pathology & Oncology Research, Vol 13, Nr 1, 39-46, 2007

Key words: anaplastic astrocytoma; comparative genomic hybridization; genomic imbalances; glioblastoma multiforme; low-grade astrocytoma

Received: Sep 7, 2006; accepted: Jan 30, 2007
Correspondence: Ali ARSLANTAS, , ,

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