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Deletions on chromosome 22 in sporadic meningioma

✍ Scribed by Martin H. Ruttledge; Ya-Gang Xie; Fei-Yu Han; Myriam Peyrard; V. Peter Collins; Magnus Nordenskjöld; Jan P. Dumanski

Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
733 KB
Volume
10
Category
Article
ISSN
1045-2257

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✦ Synopsis

Meningiomas are the second most common group of primary central nervous system tumors in humans. Cytogenetic and molecular studies imply that genes involved in the primary development of meningioma reside on chromosome 22. The recently characterized neurofibromatosis type 2 gene (NFZ) has been shown to be mutated in two cases of sporadic meningiorna, suggesting that this is the chromosome 22 gene which is involved in tumorigenesis. We have investigated a series of 170 meningiomas by deletion mapping analysis with 43 markers from chromosome 22 to ascertain if NFZ is the only gene on this autosome that is inactivated. Half of the tumors showed results consistent with m o n m y for chromosome 22, whereas I3 cases showed terminal deletions of 22q, including the NFZ region. Homozygous (complete) deletions were detected in tumors from two patients. In one of them complete loss was found at the NFZ locus and cosmid contigs from the region were used to determine the extent of the deletions. The second tumor showed homozygous loss of two large genomic regions outride the NFZ region. These aberrations were confined to only one part of this large tumor, suggesting that they may be involved in the later stages of meningioma development. An additional four tumors had interstitial deletions on chromosome 22, in three of them without overlap with NFZ. Our results show that NFZ is completely inactivated in sporadic meningioma but do not rule out the possibility that additional chromosome 22 loci are important in tumorigenesis. Genes Chromosom Cancer IO:/2Z-130 (1994).

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