Thyroid Gland Papillary Carcinoma

P=N/A, N=400, Not yet recruiting, Xijing Hospital

P=N/A, N=200, Completed, Minia University

POSTN expression is associated with tumor progression by regulating AKT/mTOR signaling, which further leads to apoptosis and autophagy. POSTN may also be considered a valuable target for therapeutic strategies in PTC.

The Bethesda system provides high diagnostic accuracy for definitive cytological categories in pediatric thyroid nodules. Even indeterminate categories carry elevated malignancy risk, supporting careful surgical consideration and the value of BRAF V600E testing for preoperative risk stratification.

CSDE1 promotes PTC progression through the Wnt/β-catenin pathway under the regulation of METTL3-mediated m⁶A modification, serving as a promising prognostic biomarker and therapeutic target.

Exploratory analysis in a limited TERT cohort (8 mutated vs 103 wild-type) identified prospective radiomics patterns associated with TERT promoter mutations, suggesting potential surrogate imaging biomarkers that warrant further investigation. Micro-CT radiomics shows promise as a complementary tool for diagnostic classification in thyroid cancer and offers a platform for quantitative 3D tissue characterization pending broader validation.

Co-expression network analysis highlighted disrupted transcriptional coordination in tumors. This work establishes a multidimensional epigenetic framework for PTC with combinatorial diagnostic signatures and condition-specific associations between DNA modifications and driver mutations (BRAF vs. RAS).

A combined model integrating US-FNAC and serum BRAF V600E testing improved diagnostic performance, with a sensitivity of 81.25%, specificity of 85.19%, and AUC of 0.873, significantly outperforming either method alone. These findings suggest that serum BRAF V600E detection is a useful complementary, minimally invasive approach for diagnosing PTC, particularly micro-PTC, and may improve early detection and risk stratification when combined with US-FNAC.

However, as an inhibitor of this pathway, LY2109761 could reverse the effects induced by GOLPH3 overexpression. Collectively, these findings establish GOLPH3 as a critical driver of PTC malignancy through TGF-β pathway activation, providing a mechanistic link between Golgi function and cancer signaling. This work not only advances our understanding of PTC pathogenesis but also identifies GOLPH3 as a potential therapeutic target for aggressive PTC, offering a paradigm for exploring Golgi-associated proteins in endocrine malignancies.

Through the Wnt5a/β-catenin signaling pathway, this axis may support epithelial-mesenchymal transition (EMT) and enhance cellular migration and invasion. Collectively, our findings elucidate the functional mechanism of the DLEU2-ELAVL1-RCC2 axis in PTC cells and provide a possible molecular target for treating PTC.

Furthermore, prospective studies are necessary to assess the practical utility of the CRG signature. The publisher apologizes for any inconvenience caused.