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Surgical Neurology Branch, National Institute of Neurological Disorder and Stroke, NIH, Bethesda, Maryland 20892 [A. S., B. I., E. H. O., I. U. A.], and Department of Neurosurgery, University of Tennessee, Memphis, Tennessee 38119 [W. C. C., J. T. R.]
1 To whom requests for reprints should be addressed, at Surgical Neurology Branch, Building 10/5D37, National Institute of Neurological Disorder and Stroke, NIH, Bethesda, MD 20892.
Molecular analysis of malignant astrocytomas demonstrated three distinct groups of tumors with chromosome 17p abnormalities, which include (a) deletion of the p53 locus (17p13.1) and mutations in the remaining allele, (b) deletion of the p53 locus but no detectable mutations in the remaining allele, and (c) deletions not including the p53 locus but mutations in one of the alleles. Furthermore, deletion mapping analysis demonstrated allelic loss of genes distal to D17S28/D17S5 markers (17p13.3) in group C tumors. The loss of heterozygosity of genes on chromosome 17 without detectable mutation (group B) or deletion (group C) in the p53 gene implies the presence of a second tumor suppressor gene in the telomeric region of 17p, the homozygous functional inactivation of which may play a role, either alone or in conjunction with p53, in the initiation and/or progression of astrocytic neoplasms.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 9/29/92. Accepted 10/23/92.
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