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Section of Molecular Carcinogenesis, Department of Pathology [L. H., J. G., N. H.] and Division of Pediatric Neurosurgery [D. P.], Children's Hospital of Los Angeles Research Institute, Los Angeles, California 90027; Department of Neurosurgery, Mayo Clinic, Rochester, Minnesota 55905 [C. R.]; Center for Medical Genetics, University of Chicago, Chicago, Illinois 60637 [D. H. L.]; and National Cancer Center Research Institute, Tokyo, Japan [A. T.]
Loss of heterozygosity on chromosome 17p13.3 is frequently observed in solid tumors, and the presence of a tumor suppressor gene has been predicted in this region of chromosome 17. We have analyzed a primitive neuroectodermal tumor sample exhibiting loss of heterozygosity at the D17S34 locus, a commonly used telomeric marker on the short arm of chromosome 17. The remaining allele showed a rearrangement. Cosmids spanning the D17S34 locus and probes from that region were used to demonstrate a 9-kb deletion within the D17S34 locus and were found to contain evolutionary, conserved sequences. Genetic alterations in this region may also affect expression of immediately adjacent genes, such as ABR, and could be a common mechanism in the causation of primitive neuroectodermal tumors.
1 This work was supported in part by funds provided by the Breast Cancer Fund of California through the Breast Cancer Research Program of the University of California Grant 1RB-0001 (to J. G.) and by Public Health Service Grant CA47456 (to J. G.).
2 To whom requests for reprints should be addressed, at Section of Molecular Carcinogenesis, Department of Pathology, Ms#103, Children's Hospital of Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027. Phone: (213) 669-4595; Fax: (213) 666-0489.
Received 9/16/96. Accepted 11/18/96.
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