Allelic losses at 1p, 9q, 10q, 14q, and 22q in the progression of aggressive meningiomas and undifferentiated XXXX .

@entity1 @entity66 @entity5 @entity2698 @entity693 @entity1653 @entity3554
@entity1653 are usually benign @entity5 ; however, they can recur after surgical resection and occasionally show histological progression to a higher malignancy grade. Five such rare cases of aggressively recurring @entity1653 were present in our departmental cohort of 923 primary @entity3554 operated over a 17-year period. Four other aggressively recurring @entity3554 with a very similar clinical and histomorphological appearance (three undifferentiated @entity693 , one @entity2698 ) was also included in this study. We investigated whether disease progression can be traced by genetic alterations and whether a pattern of genetic alterations is specific for @entity1653 . A total of 40 specimens from @entity5 and multiple recurrences of the nine @entity1 were analyzed with 26 polymorphic allelic markers for deletions on 1p, 1q, 9q, 10q, 14q, and 22q. Loss of heterozygosity (LOH) at 22q was observed in all @entity1653 cases at the earliest time point analyzed. Allelic loss at 1p was seen in the original @entity5 in two cases and upon @entity1653 recurrence in two others. Deletion on 10q occurred during @entity5 progression in two cases, and on 9q and 14q in one case. While allelic loss at 22q appears to be an early event in aggressive @entity66 , there is a clear correlation of further deletions on chromosome arms 1p, 9q, 10q, and 14q with histopathological and clinical progression, as shown in these intraindividual trackings. None of these genetic findings were present in the non-meningiomatous @entity3554 , indicating that meningothelial cells have their own lineage-specific genetic pathways towards clinical malignancy.
