Loss of heterozygosity and the origin of meningioma

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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 dosis 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.