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People with Li-Fraumeni Syndrome have a mutation in one copy of their TP53 genes, with more than 90% lifetime risk to develop cancer.
A set of 16 specific primer pairs covering all the exons and flanking regions of TP53 and flanked by universal sequences CS1 and CS2 was designed (see Table 1 in the Data Supplement that accompanies the online version of this article at http://www.clinchem.org/content/vol63/ issue3).
Patients 40 years old and older whose MDS didn't carry TP53 mutations with mutations in RAS pathway genes or the JAK2 gene tended to have a shorter survival than those without RAS or JAK2 mutations.
Proteomics analysis revealed a myriad of differentially expressed proteins and several signaling pathways strongly linked to JDF12-induced apoptosis, including EGFR and TP53 pathways (Figure 7).
Mutations represent the most frequent form of TP53 inactivation in CLL and are frequently (70% of the cases) accompanied by the loss of the second allele (17p13 deletion).
Our institution performed a standard molecular sequencing panel of 47 genes on this tumor, which revealed a TP53 c.817C>T (p.R273C) gene mutation.
In contrast, expression of the tumor suppressor protein (Tp53) was not detected by immunohistochemistry in less than half of tumor specimens.
Conclusions: Dioscin inhibited tumor growth via inducing apoptosis, which was accompanied by altered expression of apoptotic pathway proteins, such as TP53, BAX, BCL2 and CASP3.
The TP53 gene product is a nuclear phosphoprotein that is expressed at low levels in most normal tissues and plays a key role in the control of cell cycle progression, genome stability and apoptosis.
Methods: Binding capacity of mutated TP53 in MDA-MB-468 breast cancer cell line to BRCA1 and RAD51 proteins in comparison to WT TP53 in MCF7 cell line was studied by Immunoprecipitation.
The polymorphism on codon 72 (Arg72Pro) of TP53 tumor suppressor gene has been extensively investigated regarding association with a wide range of cancers worldwide.
Almost all tumors (96%) were characterized by mutations of the gene encoding TP53 in addition to statistically recurrent mutations in nine other loci, including NF1, BRCA1, BRCA2, RBI, and CDK12, although these were of low prevalence.
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- TPA-Induced Sequence 7