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One of only few reports demonstrating the mutated p53 gainoffunction (GOF) activity resulting in a decrease of a malignant trait in human cancer revealed that expression of GOF mutant p53R248Q decreased the motility and invasiveness of the breast and lung cancer cells in a p53 transactivationdependent manner.
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Results show that uniform nuclear p53 expression was associated with invasion of breast cancer tumors.
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Among Mexican Breast cancer (BC) patients diagnosed at a young age, a high proportion with germline mutations in the TP53 gene has been identified. All patients with the TP53 mutations have a family history suggestive of Li-Fraumeni Syndrome. All patients with TP53 mutations have high-grade and HER2-positive tumors. None of these mutations or other pathological variants in TP53 are found in the healthy control group.
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It summarizes recent evidence linking the mevalonate pathway-mutant TP53 axis with cancer progression and further discuss the clinical relevance of this axis.
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This study is also the first to describe an IPM associated with TP53 mutations and can be used as a reference for understanding other cancers. Notably, the IPM provides an immunological perspective to elucidate the mechanisms that determine the clinical outcome of HCC.
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malignancy and biological behavior of ovarian carcinomas depend on interaction between p-p53(Ser20) and carcinoma stem cells biomarker expression
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This study performed extensive replica exchange with solute tempering simulations, in excess of 1.0 mus/replica, to generate disordered structural ensembles of p53-N-terminal transactivation domain (TAD) using six latest explicit solvent protein force fields. Such structural characterization is a key step toward establishing the sequence-disordered ensemble-function-disease relationship of p53.
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P53 aberrant overexpression is frequently observed in oral cavity squamous cell carcinoma tissues as a result of point mutation or deletion[review]
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Inactivation of HUWE1 in a human lung cancer cell line inhibited proliferation, colony-forming capacity, and tumorigenicity. Mechanistically, this phenotype was driven by increased p53, which was due to attenuated proteasomal degradation by HUWE1.
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The tumor suppressor p53 (p53) mutant lacking the disordered C-terminal (CT) domain abolished Intersegmental transfer (IST), whereas the mutant lacking the structured core domain maintained IST, indicating the importance of the CT domain.
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Nuclear resident HDAC4 induces senescence in human fibroblasts (BJ-TERT). HDAC4-induced senescence depends on TP53 activation.
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the findings from our own patient cohort confirm the importance of TP53 point mutations in a subpopulation of malignant peripheral nerve sheath tumors
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p53 expression evaluated by immunohistochemistry in bone marrow biopsy specimens at the time of AML diagnosis may indicate distinct clinical characteristics in patients with normal diploid cytogenetics and is a potentially valuable tool that can enhance risk-stratification.
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The Meg3-dependent association of PTBP3 with the promoters of p53 target genes suggests that Meg3 and PTBP3 restrain p53 activation. Our studies reveal a novel role of Meg3 and PTBP3 in regulating p53 signaling and endothelial function, which may serve as novel targets for therapies to restore endothelial homeostasis.
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The failure to observe stabilization of one of the mutants through the design of a second site suppressor mutation in an experimental study by our collaborators could either reflect upon the failure of the DBD (at least of this mutant) to recapitulate the complex behavior of full length p53 in the experimental construct or could result from the fact that any mutation at that conserved position is not tolerated
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Authors found that GTSE1 could regulate the p53 function to alter the cell cycle distribution dependent on the mutation state of p53. Results reveal that GTSE1 played a key role in the progression of breast cancer
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These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)
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Low expressions of TP53 is associated with non-small cell lung cancer.
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Mechanistic studies demonstrated that overexpression of Fn14 could reduce the formation of a Mdm2-p53-R248Q-Hsp90 complex by downregulating Hsp90 expression, indicating that degradation of p53-R248Q was accelerated via Mdm2-mediated ubiquitin-proteasomal pathway
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P53 level and transvaginal color Doppler ultrasound can provide certain valuable clinical information for the treatment and monitoring of cervical cancer.
