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DNA Hypermethylation Is Associated with 17p Allelic Loss in Neural Tumors¹

Oncology Center [M. M., B. D. N., S. B. B.], Department of Medicine [S. B. B.], and Human Genetics Program [M. M., S. B. B.] of the Johns Hopkins Medical Institutions, Baltimore, MD; The Ludwig Institute for Cancer Research [V. R. C.], Department of Medicine and Center for Molecular Genetics, University of California, San Diego, CA; and the Department of Pediatrics, Washington University, School of Medicine, and the Pediatric Oncology Group, St. Louis, MO [G. M. B.]

It has long been debated whether the accumulation of allelic losses in tumors involves the selection of cells which have stochastically lost chromosomal regions or whether there is, inherent to the neoplastic state, a process which predisposes to genetic instability. Changes in DNA methylation are commonly seen in human tumors and can alter chromosome structure. We now have examined specific types of primary neural tumors which allow us to determine relationships between abnormal DNA hypermethylation and allelic loss. In primary brain tumors which frequently lose chromosome 17p (30–50%) even in the earliest stages, we now show that 84% (21 of 25) exhibit hypermethylation at locus D17S5, on 17p. However, in primary neuroblastomas, a tumor type which does not lose chromosome 17p, no regional hypermethylation is observed. These data suggest that on chromosome 17p, regional D17S5 hypermethylation constitutes a molecular change which is associated with genetic instability.

¹ Supported by NIH Grant R01-CA43318.

² To whom requests for reprints should be addressed, at 424 N. Bond Street, Baltimore, MD 21231.

Received 3/25/93. Accepted 5/ 4/93.

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