162

AP1B1

ADTB1|AP105A|BAM22|CLAPB2;adaptor-related protein complex 1, beta 1 subunit;AP1B1;adaptor-related protein complex 1, beta 1 subunit

AP-1 complex subunit beta-1|Golgi adaptor HA1/AP1 adaptin beta subunit|adapter-related protein complex 1 subunit beta-1|adaptor protein complex AP-1 subunit beta-1|beta-1-adaptin|beta-adaptin 1|beta-prime-adaptin|beta1-adaptin|clathrin assembly protein co

22q12|22q12.2

protein-coding

In this article the authors provide a brief description of the current understanding of meningioma genetics. Chromosome 22 abnormalities, especially inthe Neurofibromatosis Type 2 (NF2) gene, have been associated with meningioma development. Loss of heterozygosity of chromosome 22 occurs in approximately 60%of meningiomas; however, loss of NF2 gene function occurs in only one third of these lesions. This discrepancy supports the theory that a second tumor suppressor gene exists on chromosome 22, and the authors introduce several possible gene candidates, including BAM22, LARGE, INI1, and MN1 genes. Deletionsof 1p have also been shown to correlate with meningioma progression. The geneticsimilarities and differences among sporadic, NF2-associated, pediatric, and radiation-induced meningiomas are discussed, with the observation that the nonsporadic meningiomas have a higher incidence of multiple chromosomal abnormalities at presentation. Ultimately, a better understanding of the molecular pathways of meningioma tumorigenesis will lead to new, successful treatments.