21 August 1997, Volume 15, Issue 8, Pages 997 – 1000

Short Report

New deletion in low-grade oligodendroglioma at the glioblastoma suppressor locus on chromosome 10q25-26 Daniel Maier1, Domenico Comparone1, Elisabeth Taylor1, Zuwen Zhang1, Otmar Gratzl1, Erwin G Van Meir2, Rodney J Scott1 & Adrian Merlo1,3 1Molecular Neuro-Oncology, Departments of Research and Neurosurgery, University Hospital, Schanzenstr.46, CH-4031 Basel, Switzerland     2Laboratory of Tumor Biology and Genetics, CHUV, Department of Neurosurgery, University Hospital, CH-1011 Lausanne, Switzerland     3Author for correspondence

Keywords

oligodendroglioma;   glioblastoma suppressor gene;   deletion mapping;   chromosome 10q25-26

Abstract

Loss of heterozygosity on chromosome 10 is considered to be associated with the progression of glioblastomas. Two closely related regions have recently been proposed to contain the glioblastoma suppressor locus on chromosome 10q25-26; a 1 cM region between the polymorphic (CA)n-repeat markers D10S587 and D10S216, and an area of 5 cM between the markers D10S221 and D10S209. To confirm and further delineate this region, we analyzed 51 glioblastomas and 11 intermediate and low-grade gliomas for loss of heterozygosity on chromosome 10. 47/62 mostly malignant gliomas displayed complete loss of chromosome 10 and nine tumors were unaltered, whereas four glioblastomas and two low-grade oligodendrogliomas had partial loss on distal 10q. With these six tumors, we constructed a deletion map with increased marker density at 10q25-26 which shows two centromeric breakpoints at the markers D10S587 and D10S216, thus only confirming the distal, but not the proximal candidate glioblastoma suppressor locus. Two out of four low-grade oligodendrogliomas displayed partial deletions on 10q25-26. This suggests that deletion on chromosome 10 is not merely a late event in the progression of glioblastomas, but could play a role earlier in the development of gliomas.

Received 6 February, 97; Revised 10 April, 97; Accepted 18 April, 97

^© Macmillan Publishers Ltd 1997