An allelotype study of primary and corresponding recurrent glioblastoma multiforme.
- Author:
Jie HU
1
;
Cheng-chuan JIANG
;
Ho-Keung NG
;
Jesse C S PANG
;
Carol Y K TONG
;
Shang-qun CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Alleles; Chromosome Mapping; methods; Chromosomes, Human, Pair 1; genetics; Chromosomes, Human, Pair 10; genetics; Chromosomes, Human, Pair 19; genetics; Chromosomes, Human, Pair 20; genetics; Chromosomes, Human, Pair 21; genetics; Chromosomes, Human, Pair 7; genetics; Chromosomes, Human, Pair 9; genetics; DNA; genetics; Female; Glioblastoma; genetics; pathology; surgery; Humans; Loss of Heterozygosity; Microsatellite Repeats; Neoplasm Recurrence, Local
- From: Chinese Journal of Medical Genetics 2003;20(1):56-58
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate molecular genetic alterations associated with primary and corresponding recurrent glioblastoma multiforme(GBM) and to identify which chromosomal regions of the whole genome may be involved in the recurrence of primary GBM.
METHODSA high-resolution allelotyping study of one patient's primary GBM and corresponding recurrent GBM was performed by PCR-based loss of heterozygosity(LOH) analysis with the use of 382 fluorescent dye-labeled polymorphic microsatellite markers covering all 22 autosomes. The mean genetic distance between two flanking markers is 10 cM.
RESULTSLOH at locus D9S157 on 9p21 and at loci D10S537, D10S185, D10S192, D10S597, D10S587, D10S217 on 10q21.3-26.3 was observed in the primary GBM. As for corresponding recurrent tumor, LOH was observed not only in expanded regions on 9p21 and 10q21.3-26.3 but also on multiple other chromosomal arms, including 1q, 7p,7q, 21q, 20p, 20q, 10p, 19p, 19q.
CONCLUSIONChromosome 9p and 10q may be involved in the development of this GBM. Although histopathological diagnoses of the primary and corresponding recurrent tumor are identical, the recurrence of GBM is characterized by an increased involvement of molecular genetic abnormalities and may be accompanied by inactivation of more tumor suppressor genes.