Micro-RNAs signatures in papillary thyroid carcinoma.

p.aythelady61 shared this article with you from Inoreader Micro-RNAs signatures in papillary thyroid carcinoma. Via Head and Neck Related Articles Micro-RNAs signatures in papillary thyroid carcinoma. J BUON. 2020 Sep-Oct;25(5):2144-2146 Authors: Mastronikolis N, Tsiambas E, Roukas D, Fotiades P, Chrysovergis A, Papanikolaou V, Kyrodimos E, Mastronikoli S, Niotis A, Ragos V Abstract Among biomarkers that should be useful for a molecular discrimination of patients regarding treatment strategies and prognosis in solid malignancies, novel micro-RNAs (miRs) are under investigation. Quite recently, miRs are considered very promising and significant genetic markers for categorizing patients by their molecular characteristics, as well as extending their complicated genetic signatures. miRs are short, non-coding RNAs consisting of 20-25 nucleotides located at intra- or inter-gene regions. Functional miRs mediate a positive regulation of posttranscriptional gene silencing. Their deregulation in cancer cells due to genetic (e.g., mutations, translocations), epigenetic (e.g., DNA hyper-methylation of tumor suppressor genes, extensive genomic DNA hypo-methylation, aberrant histone modification patterns) and transcriptional alterations lead to a loss of miRs-mediated repression of target mRNA. Interestingly, a biphasic role of miRs in cancers of different histogeneti c origin has been confirmed. In some of them, their upregulation is correlated with an increased oncogenic activity, whereas in others, the same miR type acts as a suppressor agent. Thyroid carcinoma comprises different histological subtypes, such as papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), anaplastic thyroid cancer (ATC), and medullary thyroid carcinoma. In the current molecular review, we explored the role of a specific fraction of miRs in PTC subtype by categorizing them according to their up- or down-regulation status. PMID: 33277828 [PubMed - as supplied by publisher] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.