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[Cancer Research 51, 639-643, January 15, 1991]
© 1991 American Association for Cancer Research

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Loss of Heterozygosity on 6q, 16q, and 17p in Human Central Nervous System Primitive Neuroectodermal Tumors

Gregory A. Thomas1 and Corey Raffel2

The Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah 84132 [G. A. T.] and the Division of Neurosurgery, Childrens Hospital of Los Angeles and the Department of Neurosurgery, University of Southern California School of Medicine, Los Angeles, California 91011 [C. R.]

The loss of genetic material from specific chromosomal locations in a given tumor type has been taken for evidence of the importance of tumor suppressor genes at these loci in the genesis of the tumor. The primitive neuroectodermal tumor of the central nervous system has such a loss on 17p in one-third of tumors. In this report, a detailed analysis of 17p loss in 23 tumors has been performed using 10 probes mapping to this region. In addition, an analysis for allelic deletion on chromosomes 6q, 16q, and 22q has been performed. Six of the 23 tumors showed loss of markers on 17p, and the area of common loss spanned 17p11.2 to 17pter. Five of 23 tumors showed loss of markers on 6q, and 3 showed loss on 16q. No tumor lost markers on 22q. Only one tumor showed loss at more than one location. These data suggest that primitive neuroectodermal tumors either are a heterogeneous group of tumors with more than one mechanism leading to a tumor or that more than one recessive oncogene may play a role in the genesis of these tumors.

1 This work supported by American Cancer Society Clinical Oncology Career Development Award 89-189 (to G. A. T.).

2 To whom requests for reprints should be addressed, at 1300 N. Vermont Ave., Ste. 906, Los Angeles, CA 90027.

Received 6/21/90. Accepted 10/30/90.




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Copyright © 1991 by the American Association for Cancer Research.