ArticleBrain pathology (Zurich, Switzerland)2001
p73 is not mutated in meningiomas as determined with a functional yeast assay but p73 expression increases with tumor grade.
Article in Brain pathology (Zurich, Switzerland), 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 37 citations in OpenAlex.
- Insights into brain tumor diagnosis: exploringFrontiers in neurology · 2024Review
- Article
- Overexpression of CCDC69 activates p14Journal of ovarian research · 2019Article
- Molecular biology of unreresectable meningiomas: implications for new treatments and review of the literature.Skull base : official journal of North American Skull Base Society ... [et al.] · 2008Article
- Recurrent cytogenetic aberrations in histologically benign, invasive meningiomas of the sphenoid region.Journal of neuro-oncology · 2007Article
- Aberrant expression of DeltaNp73 in benign and malignant tumours of the prostate: correlation with Gleason score.Journal of clinical pathology · 2005Article
- Characterization of the p53 mutants ability to inhibit p73 beta transactivation using a yeast-based functional assay.Oncogene · 2003Article
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10 authors at 1 institution in 1 country.
Funding
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Abstract
The p53 gene is normally wild type in meningiomas. Since all three members of the p53 gene family recognize the same DNA sequence, tumors containing wild type p53 could decrease transactivation of p53 target genes by mutating either p63 or p73. In meningiomas the most likely target is p73, because loss of heterozygosity of the chromosomal band containing p73 is the commonest genetic lesion in these tumors. To screen p73 for mutations we have developed a functional assay which tests the ability of p73 to activate transcription from a p53-responsive promoter in yeast. The assay correctly identified p73 mutants with mutations equivalent to hotspot mutations in p53, demonstrating that the assay can detect transcriptionally inactive p73. No mutations in p73 were identified in meningiomas. p73 RNA level was higher in more advanced tumors, but there was no correlation between the expression level of p73 and p21, a known p53 target gene. The yeast assay was also used to measure the intrinsic sensitivity of the p73 protein to mutagenesis. Like p53, p73 is exceptionally easy to inactivate as a transcription factor by point mutation. Taken together, these results indicate that p53 and p73 serve very different functions in tumors.
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