DELETIONS ON CHROMOSOME-22 IN SPORADIC MENINGIOMA

Meningiomas are the second most common group of primary central nervou s system tumors in humans. Cytogenetic and molecular studies imply tha t genes involved in the primary development of meningioma reside on ch romosome 22. The recently characterized neurofibromatosis type 2 gene (NF2) has been shown to be mutated in two cases of sporadic meningioma , suggesting that this is the chromosome 22 gene which is involved in tumorigenesis. We have investigated a series of 170 meningiomas by del etion mapping analysis with 43 markers from chromosome 22 to ascertain if NF2 is the only gene on this autosome that is inactivated. Half of the tumors showed results consistent with monosomy for chromosome 22, whereas 13 cases showed terminal deletions of 22q, including the NF2 region. Homozygous (complete) deletions were detected in tumors from t wo patients. In one of them complete loss was found at the NF2 locus a nd cosmid contigs from the region were used to determine the extent of the deletions. The second tumor showed homozygous loss of two large g enomic regions outside the NF2 region. These aberrations were confined to only one part of this large tumor, suggesting that they may be inv olved in the later stages of meningioma development. An additional fou r tumors had interstitial deletions on chromosome 22, in three of them without overlap with NF2. Our results show that NF2 is completely ina ctivated in sporadic meningioma but do not rule our the possibility th at additional chromosome 22 loci are important in tumorigenesis. (C) 1 994 Wiley-Liss, Inc.