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Gene Cluster and the D9S171 Locus1
Department of Pathology, Sahlgrenska Hospital, S-413 45 Gothenburg, Sweden [K. I., E. E. S., N. Y., V. P. C.]; Department of Neurosurgery, Tokyo Medical and Dental University, Tokyo 113, Japan [K. I.]; Department of Neurosurgery, Kanazawa University, Kanazawa 920, Japan [N. Y.]; Laboratory of Molecular Neuro-Oncology, Department of Neurosurgery, Emory University School of Medicine, Altanta, Georgia 30322 [C. D. J.]; and Ludwig Institute for Cancer Research, Stockholm Branch, and Department of Pathology, Karolinska Hospital, S-171 76 Stockholm, Sweden [V. P. C.]
Deletions of the 9p-localized type-I interferon (IFN) genes and adjacent loci often occur during the development of malignant glioma. We have applied restriction fragment length polymorphism and microsatellite analysis to 12 loci covering this region of 9p and 3 loci on 9q in 74 human glial tumor tissues to define and further localize the smallest region of hemizygous or homozygous deletion common to the tumors. Three regions of homozygous deletion were evident among the panel of tumors; only one of these, however, residing between D9S171 and the IFN
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gene cluster, was involved in multiple cases (13 glioblastomas). Hemizygous deletion of this same region was observed in an additional 27 tumors. In total these data indicate the frequent inactivation of a novel tumor suppressor gene residing adjacent to and centromeric of the type-I IFN genes in malignant gliomas.
1 This work was supported by grants from the Swedish Cancer Society, the National Cancer Institute (CA55728), the Arne and Ingabritt Ljungbergs Fund, the Jubillee Clinics Research Fund, and the Assar Gabrielssons Fund.
2 These authors contributed equally to this work.
3 To whom requests for reprints should be addressed, at Department of Pathology, Box 100, Karolinska Hospital, S-171 76 Stockholm, Sweden.
Received 4/ 1/94. Accepted 5/ 3/94.
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