We report the cytogenetic findings in two meningiomas from a child presenting with multiple meningiomas. In contrast to the chromosomal profile of adult meningiomas, both tumors studied revealed excess of chromosomes in addition to monosomy 22. This difference is remarkable considering several repor
Abnormalities of chromosome 22 in pediatric meningiomas
β Scribed by Dr. Jaclyn A. Biegelm; Beverly S. Emanuel; Annette H. Parmiter; Leslie N. Sutton; Lucy B. Rorke
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 542 KB
- Volume
- 9
- Category
- Article
- ISSN
- 1045-2257
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β¦ Synopsis
Abstract
Cytogenetic studies of eight meningiomas in young children or adolescents were performed. Two tumors exhibited normal karyotypes. Two tumors from patients with bilateral acoustic neurofibromatosis demonstrated monosomy 22 as the only abnormality. Four patients had more complicated karyotypes in which one or both of the chromosomes 22 were missing or structurally altered. The most common secondary changes in these four tumors involved monosomy or structural abnormalities of Chromosome 6. These findings confirm that the primary cytogenetic changes in meningioma are similar in children and adults. Molecular analyses of pediatric meningiomas with deletions or translocations of chromosome 22 will be useful for identifying the role of chromosome 22 tumor suppressor genes in this disease. Genes Chrorn Cancer 9:81β87 (1994). Β© 1994 WileyβLiss, Inc.
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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
We report on a patient with multiple congenital anomalies and ring chromosome 22 who died at age 16 years of bronchopneumonia. Autopsy documented multiple psammomatous meningiomas of the spinal dura and tentorium. n m o r tissue for cytogenetic analysis was not available. Although abnormalities of c
Cytogenetic and molecular genetic analyses have shown that a tumor-suppressor gene for human meningioma is located on the long arm of chromosome 22. Recently, somatic mutations of the NF2 gene have been identified in sporadic meningiomas. However, tumorigenesis of certain cases of meningioma cannot