Loss of heterozygosity on chromosome 10, 13q(Rb), 17p, and p53 gene mutations in human brain gliomas.
Using the methods of restriction fragment length polymorphism (RFLP) and single strand conformation polymorphism (SSCP) analyses, we have examined 33 cases of human gliomas with various malignant grades to detect the deletions of putative tumor suppressor gene loci, chromosome 10, 13q(retinoblastoma gene, Rb), 17p, and p53 mutation. We observed loss of heterozygosity (LOH) at loci on chromosome 10 (36%), 13q(Rb) (54%), and 17p(50%) in malignant gliomas. There, however was no allelic loss on chromosome 10 and 17p in low-grade gliomas. Rb gene deletions were seen in low-grade gliomas, including oligodendroglioma and ependymoma. This finding suggests that Rb inactivation may be an early genetic event in the development and progression of gliomas. We correlated the results of LOH on chromosome 17p and p53 mutation. Among the 8 cases which showed LOH on chromosome 17p, only three cases (38%) revealed p53 mutations. Low incidence of p53 mutations in cases with chromosome 17p deletions suggests that some other tumor suppressor genes may be located on chromosome 17p.
Lee
S H
SH
Department of Neurosurgery, Korea Cancer Center Hospital, Seoul.
Kim
J H
JH
Rhee
C H
CH
Kang
Y S
YS
Lee
J H
JH
Hong
S I
SI
Choi
K S
KS
D001254:Astrocytoma / Q000235:genetics / Q000473:pathology; D001483:Base Sequence; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology; D002879:Chromosomes, Human, Pair 10; D002882:Chromosomes, Human, Pair 13; D002886:Chromosomes, Human, Pair 17; D017353:Gene Deletion; D016161:Genes, Retinoblastoma; D016158:Genes, p53; D005910:Glioma / Q000235:genetics* / Q000473:pathology; D006579:Heterozygote; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation; D009837:Oligodendroglioma / Q000235:genetics / Q000473:pathology; D012150:Polymorphism, Restriction Fragment Length; D018807:Polymorphism, Single-Stranded Conformational