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

Meningiomas are usually benign tumors; however, they can recur after surgic al resection and occasionally shaw histological progression to a higher mal ignancy grade. Five such rare cases of aggressively recurring meningiomas w ere present in our departmental cohort of 923 primary meningeal neoplasms o perated over a 17-year period. Four other aggressively recurring meningeal tumors with a very similar clinical and histomorphological appearance (thre e undifferentiated meningeal sarcomas, one hemangiopericytoma) were also in cluded in this study. We investigated whether disease progression can be tr aced by genetic alterations and whether a pattern of genetic alterations is specific for meningiomas. A total of 40 specimens from primary tumors and multiple recurrences of the nine patients were analyzed with 26 polymorphic allelic markers for deletions on 1p, Iq, 9q, 10q, 14q, and 22q. Loss of he terozygosity (LOH) at 22q was observed in all meningiomas cases at the earl iest time point analyzed. Allelic loss at 1p was seen in the original tumor in two cases and upon meningioma recurrence in two others. Deletion on 10q occurred during tumor progression in two cases, and on 9q and 14q in one c ase. While allelic loss at 22q appears to be an early event in aggressive m eningioma disease, there is a clear correlation of further deletions on chr omosome arms Ip, Sq, 10q, and 14q with histopathological and clinical progr ession, as shown in these intraindividual trackings. None of these genetic findings were present in the non-meningiomatous meningeal tumors, indicatin g that meningothelial cells have their own lineage-specific genetic pathway s towards clinical malignancy. (C) Elsevier Science Inc., 1999. All rights reserved.