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Departments of Neurology (Drs. Liang and Greenberg), Neurosurgery (Dr. Ross), Pediatrics (Dr. Meltzer), Radiation Oncology (Drs. Meltzer and Trent), and Human Genetics (Dr. Trent), University of Michigan, Ann Arbor, MI.
Transfer of human chromosome 6 can suppress the malignant phenotype of melanoma. Because of the neural ectoderm origin of melanoma and since up to 30% of gliomas have abnormalities involving chromosome 6, we performed restriction fragment length polymorphism analysis to determine the importance of allelic loss on chromosome 6 in gliomas. DNA samples from tumor and white blood cells were obtained from patients with pathologically verified gliomas. Of the 20 paired samples, there were two gangliogliomas and one grade I, four grade II, two tumors labeled "low grade," two grade III, and nine grade IV astrocytomas. DNA was hybridized with polymorphic probes D6S29 (6p21), c-myb (6q23.3-24), SOD2 (6q25), D6S37 (6q26), and ESR (6q27). All grades of tumor revealed areas of genetic loss. Allelic imbalance (AI) was present in 11 of 47 (23%) of informative loci on 6q and four of seven (57%) on 6p. Loci at 6p21 and 6q26 were most often lost. In contrast, probes from three non-chromosome 6 loci demonstrated a combined total of 11% allelic loss. Genetic loss from chromosome 6 is a frequent event in glial neoplasms.
Address correspondence and reprint requests to Dr. Bertrand C. Liang, Building 49, Laboratory of Cancer Genetics, NIWNCHGR, 9000 Rockville Pike, Bethesda, MD 20892.
Supported in part by PHHS grant 1 P20NS31114-01 (B.C.L., D.A.R., H.S.G.) from the NINDS and CA-29476 (J.M.T.). B.C.L. is the Susan Jacobson Fellow of the American Brain Tumor Association.
Presented in part at the 45th annual meeting of the American Academy of Neurology, New York, Ny, April 1993.
Received June 22, 1993. Accepted for publication in final form September 9, 1993.
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