AI Article Synopsis
- Most low-grade oral epithelial dysplasia often stays the same or gets better, but a small percentage (4-11%) can develop into oral squamous cell carcinoma (OSCC) within a few years.
- Research was conducted on nucleostemin (NS) and phospho-STAT3 (p-STAT3) expression in rodent and human samples, finding that both markers increased in lesions compared to normal tissue, suggesting their involvement in cancer progression.
- In human studies, higher levels of NS and more intense p-STAT3 expression were linked to high-grade dysplasia and OSCC, with significant findings indicating that elevated NS signals in low-grade dysplasia can predict progression to OSCC within a short timeframe.
Article Abstract
Most low-grade oral epithelial dysplasia remains static or regress, but a significant minority of them (4-11%) advances to oral squamous cell carcinoma (OSCC) within a few years. To monitor the progression of epithelial dysplasia for early cancer detection, we investigated the expression profiles of nucleostemin (NS) and phospho-STAT3 (p-STAT3) in rodent and human samples of dysplasia and OSCCs. In a 4NQO-induced rat oral carcinogenesis model, the number and distribution of NS and p-STAT3-positive cells increased in hyperplastic, dysplastic, and neoplastic lesions compared to normal epithelium. In human samples, the NS signal significantly increased in high-grade dysplasia and poorly differentiated OSCC, whereas p-STAT3 was more ubiquitously expressed than NS and showed increased intensity in high-grade dysplasia and both well and poorly differentiated OSCC. Analyses of human dysplastic samples with longitudinally followed outcomes revealed that cells with prominent nucleolar NS signals were more abundant in low-grade dysplasia that advanced to OSCC in 2 or 3 years than those remaining static for 7-14 years. These results suggest that NS upregulation and STAT3 activation are early events in the progression of low-grade dysplasia to OSCC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8605099 | PMC |
| http://dx.doi.org/10.1016/j.neo.2021.11.001 | DOI Listing |
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