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Current challenges and the diagnostic pitfalls in the grading… IDENTICAL

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645057/
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IDENTICAL MINOR CHANGES PARAPHRASED

Ninety percent of oral malignancies are oral squamous cell carcinomas (OSCC). OSCC describes the
malignant alteration in the squamous epithelium lining the oral cavity. Over the years, there has been
advancement in the diagnosis and management of OSCC, but, the 5-year survival rate stays roughly 62%.
World health organization (WHO) in 2017 defined OPMDs as †̃clinical manifestations that raise the
possibility of oral cancer, whether they occur in clinically normal mucosa or in a precursor lesion that can
be identified clinically. OPMDs include leukoplakia, erythroplakia, erythroleukoplakia, oral submucous
fibrosis (OSMF), palatal changes associated with reverse smoking, and less commonly, oral lichen planus
(OLP).
The effects of miRNA-184 on malignant progression are controversial, whether it acts as a tumor promoter
or suppressor. This incoherency might be due to the 'imperfect complementarity' of miRNA interactions
with target genes.
Cell migration, proliferation, and cell apoptosis have been shown to be reduced in the transfected miRNA-
184-mimicked cells. Our findings are consistent with those of Santhi et al., who showed that miRNA-184
had a down-regulated expression during oral cancer progression (from tumor to leukoplakia to cancer
tissues) and in oral surgical margins (from tumor to surgical margin to extra tissues). A study by Wong et
al. showed that OSCC cells expressed 59-fold more miRNA-184 than normal cells. It has been
hypothesised that the oncogene miRNA-184 induces proliferation and may inhibit apoptosis by targeting
the c-Myc antigen. It was also concluded that inhibition of miRNA-184 in tongue SCC cell lines could
reduce cell proliferation rate. Yu et al., however, proposed a different interpretation for the effects on
epithelial cell and cancer cell line epithelial cells (including Cal27 (aggressive cell line)) mediated by AKT
signaling. The inhibition of this pathway, which is associated with an increase in cell death and apoptosis,
was demonstrated by ectopic expression.