PCNA and p53 protein expression were detected by immunohistochemical technique in 39 oral premalignant and malignant lesion;which included 11 oral mucosal leukoplakia(LK),9 oral lichen planus (LP),7 in situ carcinomas(ISC) and 12 squamous cell carcinomas(SCC);in order to investigate the significance of PCNA and p53 Protein overexpression in predicting malignant transformation.The results showed that the gradual strong expression of PCNA and mutated p53 protein positive signal from premalignant to malignant lesions.The remarkable correlation were found on PCNA expression between LK and ISC; on p53 protein expression between SCC I grade and SCC II grade and on PCNA and p53 protein expression between premalignant and malignant lesions.The results imply that expression of PCNA and mutated p53 protein may be as indicators for potential malignant development in benign lesions of oral mucosa premalignant.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
TP53 germline testing and hereditary cancer: how somatic events and clinical criteria affect variant detection rate.
Genome Med
January 2025
Hereditary Cancer Group, Oncobell Program, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Av. Gran Via 199-203, L'Hospitalet del Llobregat, 08908, Spain.
Background: Germline heterozygous pathogenic variants (PVs) in TP53 cause Li-Fraumeni syndrome (LFS), a condition associated with increased risk of multiple tumor types. As the associated cancer risks were refined over time, clinical criteria also evolved to optimize diagnostic yield. The implementation of multi-gene panel germline testing in different clinical settings has led to the identification of TP53 PV carriers outside the classic LFS-associated cancer phenotypes, leading to a broader cancer phenotypic redefinition and to the renaming of the condition as "heritable TP53-related cancer syndrome" (hTP53rc).
View Article and Find Full Text PDFPLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.
Commun Biol
January 2025
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro.
View Article and Find Full Text PDFDNA replication stress underpins the vulnerability to oxidative phosphorylation inhibition in colorectal cancer.
Cell Death Dis
January 2025
Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Mitochondrial oxidative phosphorylation (OXPHOS) is a therapeutic vulnerability in glycolysis-deficient cancers. Here we show that inhibiting OXPHOS similarly suppresses the proliferation and tumorigenicity of glycolytically competent colorectal cancer (CRC) cells in vitro and in patient-derived CRC xenografts. While the increased glycolytic activity rapidly replenished the ATP pool, it did not restore the reduced production of aspartate upon OXPHOS inhibition.
View Article and Find Full Text PDFPKCα regulates the secretion of PDL1-carrying small extracellular vesicles in a p53-dependent manner.
Cell Death Dis
January 2025
School of Pharmacy, Faculty of Medicine & State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Small extracellular vesicles (sEVs), carrying PD-L1, have been implicated in immune evasion and tumor progression. However, understanding how PD-L1 sEVs are secreted still needs to be improved. We found that the secretion dynamics of PD-L1 sEVs is similar to that of other sEVs.
View Article and Find Full Text PDFOrphan nuclear receptor NR2E3 is a new molecular vulnerability in solid tumors by activating p53.
Cell Death Dis
January 2025
Center for Precision Medicine Research, Marshfield Clinic Research Institute, Marshfield Clinic Health System, Marshfield, WI, USA.
The orphan nuclear receptor NR2E3 has emerged as a potential tumor suppressor, yet its precise mechanisms in tumorigenesis require further investigation. Here, we demonstrate that the full-length protein isoform of NR2E3 instead of its short isoform activates wild-type p53 and is capable of rescuing certain p53 mutations in various cancer cell lines. Importantly, we observe a higher frequency of NR2E3 mutations in three solid tumors compared to the reference population, highlighting its potential significance in tumorigenesis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!