J Korean Neurol Assoc.  1994 Mar;12(1):110-119.

Cytogenetic Characteristics and Related Genes in Human Meningiomas

Affiliations
  • 1Department of Neurology, College of Medicine, Yeungnam University, Korea.
  • 2Department of Neurology, College of Medicine, Keimyung University, Korea.
  • 3Department of Anatomy, College of Medicine, Keimyung University, Korea.

Abstract

Cytogenetic techniques were used to detect specific chromosomal losses and / or stuctural changes in 6 meningioma cell population of 11meningioma patients. Polymorphic DNA markers were uti.lized to investigate the loss of constitutional heterozygosity on chromosomes 8. 17 and 22 in 9 meningioma cell population of 1l meningioma patients. As a result, 5 cases(M-2.4,5.9, and 10) represented 45. XX. -22 or 45, XY.-22 as stem line. In addition to chromosome 22, other chromosomes were lost randomly. In one case(M-3) normal karyotypic pattern was oberved. The 9q+ structural change was also noted in case M-2. This structural change was thought to be the chromosomal involvement secondary to the loss of chromosome 22 in meningioma. Retentions of constitutional heterozygosity on chromosomes 8 and 17 were found in all cases. Loss of constitutional hererozygosity on chromosome 22 were found at Hind m RFLP of v-sis in cases M-1 and M-7. EcoRI RFLP of v-sis in case M-1. Bgl II RFLP of v-sis case M-1. Xba I RFLP of v-sis in cases M-6. M-9 and M-11. And EcoRI RFLP of bcr in all cases. Rearrangement of chromosome 22 in case M-1 was detected on the Xba I RFLP of v-sis as extra band(3.14kb). The reduction to hemizygosity on chromosome 22 was one important step in tumorigenesis of meningioma. Monosomy 22 might operate at the primary level of tumor initiation. Random losses of other chromosomes or structural changes as 9q+ were postula!ed to be related to tumor development.


MeSH Terms

Carcinogenesis
Chromosomes, Human, Pair 22
Cytogenetic Analysis
Cytogenetics*
Genetic Markers
Humans*
Meningioma*
Monosomy
Polymorphism, Restriction Fragment Length
Genetic Markers
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