Radiation-Induced Meningioma: A Distinct Molecular Genetic Pattern?

摘要: Radiation-induced meningiomas arise after low-dose irradiation treatment of certain medical conditions and are recognized as clinically separate from sporadic meningioma. These tumors often aggressive or malignant, they likely to be multiple, have a high recurrence rate following compared with meningiomas. To understand the molecular mechanism by which radiation-induced meningioma (RIM) arise, we genetic changes in 7 RIM 8 (SM) samples. The presence mutations 17 exons neurofibromatosis type 2 (NF2) gene, has been shown inactivated meningiomas, was analyzed SM using single-strand conformation polymorphism (SSCP) DNA sequencing. In contrast SM, showed NF2 50% specimens, no were found RIM. addition, Western blot analysis schwannomin/merlin protein, gene product, demonstrated protein levels comparable normal brain 4/4 tumor samples analyzed. Loss heterozygosity (LOH) genomic regions, reported for also all cases 22 polymorphic markers. Allele losses on chromosomes 1p (4/7), 9p (2/7), 19q 22q 18q (1/7). From these observations conclude that unlike inactivation chromosome deletions far less frequent RIM, their role development low dose is significant. Other chromosomal lesions, especially loss 1p, possibly induced irradiation, may more important tumors.