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and Interferon ß-1 Gene Deletions in Human Glial Tumors
Department of Neurosurgery, Henry Ford Hospital, Detroit, Michigan 48202 [C. D. J., J. H.]; Departments of Neurosurgery [E. C.] and Clinical Genetics [M. N.], Karolinska Hospital, Stockholm, Sweden; Ludwig Institute for Cancer Research, Montreal, Canada [W. K. C.]; and Ludwig Institute for Cancer Research, Stockholm, Sweden [V. P. C.]
We have applied restriction fragment length polymorphism analysis to a 30-member panel of primary glioma DNAs, which had been previously examined for loss of genetic information (C. D. James, E. Carlbom, J. P. Dumanski, M. Hansen, M. Nordenskjold, V. P. Collins, and W. K. Cavenee, Cancer Res., 48:55465551, 1988), to determine the frequency and sublocalization of loss of genetic information from chromosome 9. We have also utilized scanning densitometry for dosage determination of the 9p-localized interferon
and interferon ß-1 genes among these same tumors. Our results reveal the following: (a) for those cases in which loss has occurred, the region of common loss lies on the short (p) arm of the chromosome; (b) loss of genetic information from the short arm of chromosome 9 occurs frequently in glial tumors of intermediate (anaplastic, grade III) and high (glioblastoma, grade IV) histological malignancy (10 of 20 cases) but not in tumors of low (grade II) histological malignancy (0 of 10 cases); (c) tumors with 9p deletions are hemi- or nullizygous for interferon ß-1 and the interferon
gene cluster; (d) cases of interferon nullizygosity occur exclusively among tumors of highest histological malignancy (glioblastoma). These data, especially the determination of a region of nullizygosity, suggest proximity to or residence within a gene(s) whose function(s) is (are) critical to the suppression of the malignant evolution of glial tumors.
1 Current address: Department of Pediatrics, Emory University SOM, 2040 Ridgewood Drive N.E., Atlanta, GA 30322.
Received 10/29/90. Accepted 1/ 8/91.
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