ANALYSIS OF MICROSATELLITE REPEATS IN PEDIATRIC BRAIN-TUMORS

Tumorigenesis has been shown to proceed through a series of genetic al terations involving protooncogenes and tumor suppressor genes. However , investigation of genomic instability of microsatellites has disclose d a new mechanism for human carcinogenesis, which is involved not only in hereditary nonpolyposis colon cancer (HNPCC) but also in a number of other malignancies. To determine whether microsatellite instability is involved in pediatric brain tumors, we screened 15 such tumors usi ng seven microsatellite marker loci on six chromosomes 4, 5, 9p, 9q, 1 1, 14, and 17. Using the polymerase chain reaction method, DNA samples from the tumors and from normal peripheral blood leukocytes from each patient were compared for the allelic pattern produced at each locus. Our preliminary results indicate loss of heterozygosity at the fatty acid binding protein (FABP) locus, located on chromosomal arm 4q28-q31 , the only trinucleotide repeat in the panel of markers used, for 3 of 15 cases, suggesting the presence of previously unidentified sequence s relevant to brain tumorigenesis at or in the vicinity of this locus. We did not observe any microsatellite instability in these samples, i ndicating that the mechanisms operating in HNPCC are not active in thi s subset of pediatric brain tumors.