The tumor suppressor protein p53 (TP53) gene is associated with various types of cancer; however, little is known about TP53 expression in patients with childhood acute lymphoblastic leukemia (ALL). The aim of the present study was to investigate the prognostic value of TP53 expression in childhood ALL. To achieve this, TP53 mRNA levels of 146 children with ALL and 23 child donors with idiopathic thrombocytopenic purpura were determined by reverse transcription-quantitative PCR. Relapse-free survival (RFS) and overall survival (OS) were analyzed using the Kaplan-Meier method. The results demonstrated that TP53 mRNA level in patients with ALL was higher compared with that in the ITP donors (P=0.019). Patients with highly-expressed TP53 exhibited lower percentages of peripheral blood blast, higher platelet counts and inferior complete remission rates compared with patients with low expression of TP53. Survival analyses revealed that high TP53 expression was associated with poor OS and RFS in childhood ALL (P=0.018 and P=0.028, respectively) and was an independent prognostic factor in multivariate analysis for poor RFS (P<0.001) and OS (P<0.001). In conclusion, high TP53 expression is associated with poor outcomes and may be used as a molecular prognostic marker to be incorporated into an improved risk classification system for childhood ALL.
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http://dx.doi.org/10.3892/ol.2019.11064 | DOI Listing |
Cells
February 2025
Istituto di Genetica Molecolare Luigi Luca Cavalli-Sforza, Consiglio Nazionale delle Ricerche (IGM-CNR), 20133 Pavia, Italy.
Epidemiological studies have revealed significant sex differences in the incidence of tumors unrelated to reproductive functions, with females demonstrating a lesser risk and a better response to therapy than males. However, the reasons for these disparities are still unknown and cancer therapies are generally sex-unbiased. The tumor-suppressor protein p53 is a transcription factor that can activate the expression of multiple target genes mainly involved in the maintenance of genome stability and tumor prevention.
View Article and Find Full Text PDFFront Pharmacol
February 2025
Department of General Internal Medicine, Tianjin Hospital, Tianjin, China.
Background: is expressed in various tumors and leukemia cell lines. This study aims to explore the effect of in lung adenocarcinoma (LUAD).
Methods: The data on LUAD patients were collected from the Cancer Genome Atlas and Gene Expression Omnibus database.
FEBS J
March 2025
Cell and Tumor Biology Group, Teni Lab, Cancer Research Institute, Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre (TMC), Navi Mumbai, India.
Mutations in the TP53 gene may lead to the loss of its tumor suppressor function and the acquisition of oncogenic properties. The enhanced stability of mutant p53 (mutp53) is one of the pivotal factors for its oncogenic functions, rendering proteins implicated in mutp53 stabilization as promising targets for therapeutic intervention. Although deubiquitinases (DUBs) are commonly deregulated in various cancers, their specific impact on mutp53 stabilization remains largely unexplored.
View Article and Find Full Text PDFJ Appl Toxicol
March 2025
Department of Molecular Biology and Genetics, Science Faculty, Atatürk University, Erzurum, Türkiye.
Detailed studies on the embryotoxic and teratogenic effects of synthetic cannabinoids known to be abused are very limited. The present study aimed to evalutate the possible embryotoxic, teratogenic, behavioral, and molecular effects of 4F-MDMB-BUTICA, a new generation synthetic cannabinoid, using zebrafish embryos. The zebrafish embryos were exposed to the cannabinoid at 0.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
The tumor suppressor p53 can trigger tumor resistance to chemotherapy by facilitating DNA damage repair and maintaining genomic integrity. Here, we report that a p53-induced circular RNA circASCC3 promotes chemotherapeutic resistance by resolving R-loops. Our results reveal that p53 directly activates the transcription of , the host gene of circASCC3.
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