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Amplification at 12q13-14 in Human Malignant Gliomas Is Frequently Accompanied by Loss of Heterozygosity at Loci Proximal and Distal to the Amplification Site¹

Department of Pathology, Sahlgrenska Hospital, S-41345 Gothenburg, Sweden [G. R., J. R., K. I., V. P. C.]; Department of Neuropathology, Heinrich-Heine-University, D-40225 Düsseldorf, Germany [G. R., J. R.]; and Ludwig Institute for Cancer Research, Stochkolm Branch, and Institute of Oncology and Pathology, Division of Tumor Pathology, Karolinska Hospital, S-17176 Stockholm, Sweden [K. I., V. P. C.]

We have recently reported that a subset of human malignant gliomas shows amplification and overexpression of multiple genes from chromosomal segment 12q13-14, including CDK4, SAS, and MDM2. In the present study we have performed an allelotyping for 16 polymorphic loci spanning both arms of chromosome 12 in a series of 136 gliomas. Allelic deletions were found in 50% (7 of 14) of the malignant gliomas with 12q13-14 amplification and involved loci located on 12q proximal and distal to the amplification site. In contrast, the incidence of allelic loss on chromosome 12 was significantly lower in gliomas without 12q13-14 amplification [14% (11 of 79) in the WHO grade III and IV gliomas, 9% (4 of 43) in the WHO grade I and II gliomas]. The frequent association between 12q13-14 amplification and loss of alleles from 12q is in line with a model suggesting chromosome breakage and deletion as important events in the development of gene amplification.

¹ Supported by grants from the Swedish Cancer Fund, the Child Cancer Foundation of Sweden, the Inga-Britt and Arne Lundberg Foundation, the Assar Gabrielssons Fund, and the Stiftelsen Jubileumsklinikens Research Fund.

² Supported by a postdoctoral fellowship from the Deutsche Forschungsgemeinschaft.

³ To whom requests for reprints should be addressed, at Institute of Oncology and Pathology, Division of Tumor Pathology, Box 100, Karolinska Hospital, S-17176 Stockholm, Sweden.

Received 12/ 1/94. Accepted 1/ 6/95.

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