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Use of Microsatellite Markers on Chromosome 22

Jesús Sainz, PhD; Michael E. Baser, PhD; Nicola K. Ragge, MD; R. A. Nelson, MD; Stefan-M. Pulst, MD

Arch Otolaryngol Head Neck Surg. 1993;119(12):1285-1288.

Abstract
Objective
Using highly informative microsatellite markers flanking the neurofibromatosis type 2 gene, we determined the frequency of chromosome 22 allele loss in vestibular schwannomas.

Design
Peripheral lymphocyte/vestibular schwannoma DNA pairs were analyzed with five different microsatellite markers on chromosome 22.

Patients
Samples were taken from 32 patients (17 females and 15 males). Twenty-seven tumors occurred sporadically, and five were from patients with neurofibromatosis type 2.

Results
Using the microsatellite markers D22S351, CRYB2, D22S268, D22S304, and interleukin type 2Rβ, we found loss of heterozygosity for at least two markers in 12 tumors. Ten tumors showed loss of heterozygosity for markers flanking the neurofibromatosis type 2 gene. Although microsatellite markers require little DNA for analysis and are highly informative, allele patterns may be difficult to interpret in some cases.

Conclusions
Loss of heterozygosity of chromosome 22 alleles was a frequent event in vestibular schwannomas. In 10 tumors, heterozygosity was lost for centromeric and telomeric markers indicating likely monosomy 22. However, 63% of tumors did not reveal a detectable chromosomal loss. Unless a second vestibular schwannoma locus exists, these tumors likely harbor point mutations in the neurofibromatosis type 2 gene or deletions below the level of resolution of the markers used in this study.

(Arch Otolaryngol Head Neck Surg. 1993;119:1285-1288)

Author Affiliations
From the Neurogenetics Laboratory, Division of Neurology, Cedars-Sinai Medical Center (Drs Sainz, Baser, Ragge, and Pulst); the House Ear Clinic and House Ear Institute (Dr Nelson); and the Children's Hospital, Los Angeles, Calif (Dr Ragge).

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