Abstract

The earliest genetic alteration in human astrocytoma progression is mutation of the p53 tumour suppressor gene, while one of the earliest phenotypic changes is the stimulation of neovascularization. Here, we tested the role of p53 in the angiogenic process by introducing a tetracycline-regulated wild type p53 gene into null glioblastoma cells. The parental cells expressed strong angiogenic activity while upon induction of wild type, but not mutant, p53 expression, the cells secreted a factor able to neutralize the angiogenicity of the factors produced by the parental cells as well as of basic fibroblast growth factor.

Keywords

BiologyMutantAngiogenesisCancer researchNeovascularizationWild typeAstrocytomaGeneGene expressionMutationTumor suppressor genePhenotypeGlioblastomaMolecular biologyGeneticsCarcinogenesis

MeSH Terms

Angiogenesis InhibitorsAnimalsBrain NeoplasmsCell MovementCorneaDisease ProgressionEndotheliumVascularFemaleGene Expression RegulationNeoplasticGlioblastomaHumansNeoplasm ProteinsNeovascularizationPathologicProtein BiosynthesisProteinsRatsRatsInbred F344Tumor CellsCulturedTumor Suppressor Protein p53

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Publication Info

Year
1994
Type
article
Volume
8
Issue
2
Pages
171-176
Citations
310
Access
Closed

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Cite This

Erwin G. Van Meir, Peter J. Polverini, V R Chazin et al. (1994). Release of an inhibitor of angiogenesis upon induction of wild type p53 expression in glioblastoma cells. Nature Genetics , 8 (2) , 171-176. https://doi.org/10.1038/ng1094-171

Identifiers

DOI
10.1038/ng1094-171
PMID
7531056

Data Quality

Data completeness: 81%