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Pathways may identify targets for treating poorly differentiated, anaplastic thyroid cancer
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Molecular pathways may represent a novel target for poorly differentiated and anaplastic thyroid carcinomas, according to data published in The Journal of Clinical Endocrinology and Metabolism.
Researchers in Portugal profiled the anaplastic thyroid carcinoma (ATC) gene expression and analyzed the mutational status of N–, H–, andK–RAS; BRAF; TP53; CTNNB1; and PIK3CA genes in a series of 26 ATC tumors, and 22 poorly differentiated thyroid carcinoma (PDTC) tumors, according to data.
In the ATC tumors, researchers looked for pathogenic alterations in genes involved in the most deregulated cellular processes, including the mutated regions.
They also conducted analyses of genes for cell adhesion (AXIN1), proliferation (PTEN), and splice sites of five cyclin-dependent kinase inhibitors (CDKI)-encoding genes: CDKN1A (p21CIP1); CDKN1B (p27KIP1); CDKN2A (p14ARF, p16INK4A); CDKN2B (p15INK4B); CDKN2C (p18INK4C), according to researchers.
Data indicate that ATC tumors were characterized by the under-expression of epithelial components, upregulation of mesenchymal markers and genes from TGF-beta pathway. Researchers also identified the overexpression of cell cycle-related genes.
Further mutational analyses demonstrated that most mutations were present in TP53 (42% of ATC; 27% of PDTC) or RAS (31% of ATC; 18% of PDTC); and TP53 and RAS alterations indicated mutual exclusivity (P=.0354).
PIK3CA, PTEN and CDKI mutations were identified in 14% to 20% of PDTC tumors, and in 10% to 14% of ATC tumors, according to data. However, mutations BRAF, CTNNB1 and AXIN1 were rarely identified.
The identification of the roles of these pathways may allow future therapeutic targets for the treatment of ATC and PDTC, researchers wrote.
Disclosure: The researchers report no relevant financial disclosures.
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