Detection of chromosomal imbalances in spinal meningiomas by comparative genomic hybridization.

Creative Commons License

Arslantas A., Artan S., Oner U., Durmaz R., Muslumanoglu H., Atasoy M., ...Daha Fazla

Neurologia medico-chirurgica, cilt.43, sa.1, 2003 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 43 Sayı: 1
  • Basım Tarihi: 2003
  • Doi Numarası: 10.2176/nmc.43.12
  • Dergi Adı: Neurologia medico-chirurgica
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Anahtar Kelimeler: meningioma, comparative genomic hybridization, chromosome 22q, tumor suppressor gene, ANAPLASTIC MENINGIOMAS, TUMOR-SUPPRESSOR, HISTOPATHOLOGICAL FINDINGS, NEUROFIBROMATOSIS TYPE-2, GENE, DELETION, PROGRESSION, 1P, IDENTIFICATION, AMPLIFICATION
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

Little is known about genetic mutations during the malignant progression of spinal meningiomas. This study investigated genomic changes across the entire genome in spinal meningioma samples to determine possible mechanism(s) of tumorigenesis. Paraffin-embedded tissue sections of 16 spinal meningiomas were analyzed by the comparative genomic hybridization (CGH) technique. Lymphocytes of the patients were evaluated as controls. Genomic change was detected in 11 samples. Complete or partial loss of chromosome 22 was the most commonly seen abnormality in eight cases. Chromosome losses on 1p, 9p, and 10q and gains on 5p and 17q were the other abnormalities. These changes are all frequently seen in meningiomas, but are mostly specific to atypical and anaplastic meningiomas. However, in the present study, copy number changes on chromosomes 9p (3 samples), 17q (2 samples), and 1p (2 samples) were seen even in the benign tumors. Our results suggest that in addition to the neurofibromatosis type 2 tumor suppressor gene, other cancer-related genes located on 1p, 9p 10q, and 17q might be involved in the etiology of spinal meningiomas.