Loss of genes on the long arm of chromosome 22 in human meningiomas.
It has been proposed that loss of genes at specific chromosomal loci leads to tumorigenesis in some human tumors. This type of oncogenesis was first demonstrated in retinoblastoma and Wilms' tumor. Recently, it has been reported that acoustic neuroma, ductal breast tumor, and renal cell carcinoma may be caused by the same mechanism. Cytogenetic studies demonstrated that some meningiomas have monosomy of chromosome 22. In addition, human meningiomas are often associated with bilateral acoustic neuroma in which specific loss of alleles on chromosome 22 has been demonstrated. Then, we compared constitutional and tumor genotypes from 14 cases of sporadic human meningiomas, using four polymorphic DNA probes on chromosome 22 (SIS, D22S1, D22S9, IGLC). Loss of constitutional heterozygosity was found in three of 11 informative cases. Two of the three meningiomas maintained constitutional heterozygosity at the IGLC locus and another one showed no loss of heterozygosity at IGLC or D22S9. These results suggest that loss of genes on chromosome 22 caused by either a partial deletion or a mitotic recombination at a locus distal to D22S9 plays an important role in tumorigenesis of the human meningioma.
D002872:Chromosome Deletion; D002892:Chromosomes, Human, Pair 22; D004262:DNA Restriction Enzymes; D005260:Female; D006580:Genetic Carrier Screening; D006801:Humans; D007962:Leukocytes / Q000166:cytology; D008297:Male; D008577:Meningeal Neoplasms / Q000235:genetics*; D008579:Meningioma / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
D004262:DNA Restriction Enzymes