Loss of heterozygosity and the origin of meningioma

Abstract

In some human tumors, loss of particular genes manifested indirectly by loss of heterozygosity for specific RFLPs seems to uncover either heterozygous deletions leading to a gene doses effect or homozygous deletions due to a silent allele at the corresponding locus, both causing the loss of regulatory functions (antioncogenes, suppressor genes). Meningioma, a benign human tumor derived from the coverings of brain and spinal cord, is associated with complete loss, rarely deletion, of one chromosome 22. About 60% of meningiomas exhibit monosomy 22 in all or part of cells; however, about 40% display a normal karyotype. Comparison of constitutional and tumor genomes from 12 patients showed loss of heterozygosity on 22 in three cases, suggesting the involvement of events at the DNA level.