作者: EG Meir Van , T Kikuchi , M Tada , H Li , AC Diserens
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摘要: Chromosome 17p has been shown to be an early and frequent target for loss of heterozygosity through mitotic recombination in astrocytomas. These losses are frequently accompanied by point mutations the p53 gene remaining allele, resulting wild type function. However, a fraction astrocytomas retain constitutional do not have mutations; some these lose activity binding protein product amplified mdm2 genes. To test whether biological function is necessary step astrocytoma progression we analyzed expression 13 glioma cell lines. All lines expressed 2.8-kilobase transcript showed various amounts immunoprecipitation, except line LN-Z308 which had only small truncated mRNA no expression. was functionally or mutant transfected them with plasmid construct harboring chloramphenicol acetyltransferase (CAT) reporter under control transcriptional elements that induced but p53. Four were Sequencing two confirmed genotype. results show inactivation obligatory glioblastoma genesis. This suggests either pathways (p53 dependent independent) may lead tumor group classified histologically as cases bypassed due presence downstream effector