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Evidence for a Tumor Suppressor Gene on Chromosome 19q Associated with Human Astrocytomas, Oligodendrogliomas, and Mixed Gliomas¹

Molecular Neuro-Oncology Laboratory and Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129 [A. v. D., D. N. L., B. R. S.]; Department of Pathology (Neuropathology), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 [D. N. L.]; Department of Neurosurgery, University of Zürich, Raemistrasse 100, CH-8091 Zürich, Switzerland [K. v. A.]; and Laboratory of Neuropathology, Department of Pathology, University of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland [I. P., O. D. W.]

Previous studies have shown frequent allelic losses of chromosomes 9p, 10, 17p, and 22q in glial tumors. Other researchers have briefly reported that glial tumors may also show allelic losses of chromosome 19, suggesting a putative tumor suppressor gene locus on this chromosome (D. T. Ransom et al., Proc. Am. Assoc. Cancer Res., 32: 302, 1991). To evaluate whether loss of chromosome 19 alleles is common in glial tumors of different types and grades, we performed Southern blot restriction fragment length polymorphism analysis for multiple chromosome 19 loci in 122 gliomas from 116 patients. Twenty-nine tumors had loss of constitutional heterozygosity of 19q, and four tumors had partial deletions of 19q. Allelic losses on 19q were restricted to grade III anaplastic astrocytomas (4/9) and grade IV glioblastomas (11/46), grade II oligodendrogliomas (2/5) and grade III anaplastic oligodendrogliomas (2/2), and grade II (5/8) and grade III (5/7) mixed oligoastrocytomas. These data demonstrate genetic similarities between astrocytomas, oligodendrogliomas, and mixed glial tumors and indicate the presence of a glial tumor suppressor gene on chromosome 19q.

¹ Funded by Grant CD455 from the American Cancer Society (B. R. S.) and a generous gift from the Preuss Foundation (B. R. S.).

² A.v.D. is a postdoctoral fellow supported by the Deutsche Forschungsgemeinschaft. To whom request for reprints should be addressed, at Molecular Neuro-Oncology Laboratory, Massachusetts General Hospital, Building 149, Floor 6W, Charlestown, MA 02129.

³ D.N.L. is a recipient of NIH Public Health Service Grant NRSA CA09144.

Received 5/20/92. Accepted 6/17/92.

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