@entity1653 is a common @entity5 of the meninges covering the central nervous system. Although generally a @entity5 , @entity1653 often recurs and is malignant in 5-10% of all cases. @entity393 loci, and specifically inactivation of the @entity13755 @entity5 suppressor gene, is considered one of several critical steps in the tumorigenesis of @entity1653 . However, cytogenetic and molecular investigations have failed to detect either aberrations of chromosome 22 or mutations in the @entity13755 gene in approximately 40% of all @entity5 , thus making it apparent that an alternative mechanism(s) is responsible for the development of a large fraction of @entity1653 . This subset of @entity1653 is not distinct with regard to clinical and histopathological features from @entity5 showing deletions on chromosome 22. It is, therefore, important to attempt the elucidation of molecular pathway(s) that may operate in the tumorigenesis of these @entity5 . We used comparative genomic hybridization (CGH) to identify regions of the genome other than chromosome 22, contributing to the development of @entity1653 . We analyzed 25 @entity5 that had undergone detailed LOH analysis on chromosome 22 and were shown to contain no detectable deletions. Two benign, malignancy grade I, @entity1653 showed concurrent deletion of 1p and 3p. These results suggest that loss of both 1p and 3p may contribute to @entity105 . This may represent genetic changes that are alternative to deletions on chromosome 22.

1p and 3p deletions in XXXX without detectable aberrations of chromosome 22 identified by comparative genomic hybridization.

@entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'benign tumor', 'tumors'] @entity1653 :: ('MESH:D008579', 'Disease') :: ['meningiomas', 'Meningioma', 'meningioma'] @entity393 :: ('MESH:D034381', 'Disease') :: ['Loss of chromosome 22'] @entity105 :: ('MESH:D063646', 'Disease') :: ['meningioma tumorigenesis'] @entity13755 :: ('4771', 'Gene') :: ['NF2']
@entity1653 :: (MESH:D008579,Disease) :: ['meningiomas']
