Differentiated Thyroid Carcinoma

Our study is the pioneering research to provide new insights into the diagnosis, prognosis, and treatment of PTC through the analysis of OSGs, presenting potential clinical implications. Furthermore, this research reveals the molecular functions associated with resveratrol and its pharmacological targets regulating OS in PTC for the first time.

This study proposes a pre-RAIT serum protein (PSP) panel comprising FASLG, CXCL12, and HGF for risk stratification, with higher scores indicating a poorer prognosis, although this requires validation in larger cohorts. It underscores the importance of dynamic immune monitoring and proposes a novel, noninvasive strategy that leverages the role of systemic immunity for clinical patient stratification and outcome prediction.

In our small case series, no association was demonstrated between simultaneous MTC/PTC and age, CEA, calcitonin levels, gender, or number of operations. This entity likely represents a primary tumor with an incidental pathologic finding of a second malignancy.

The combination of high SUVmax, CT-detected calcification, and high thyroglobulin levels strongly suggests follicular carcinoma and may warrant resection.

Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.

P=N/A, N=876, Recruiting, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University | Not yet recruiting --> Recruiting

This study comprehensively mapped PRGs in PTC, established a validated risk model, and provided insights into immune-microenvironment interactions and therapeutic targets, advancing precision oncology for PTC.

Rescue experiments and immunofluorescence confirmed UBE2T promotes oncogenesis by destabilizing SOCS2, thereby relieving its inhibition of STAT3 phosphorylation. These findings establish UBE2T as a novel regulator of PTC progression through SOCS2/JAK-STAT3 axis manipulation, providing potential therapeutic targets to mitigate metastasis and recurrence in aggressive thyroid carcinomas.

BRAF inhibitors yielded only transient responses, and outcomes were poor. These cases underscore the diagnostic and therapeutic value of multigene testing in SCC, highlighting the need to integrate detailed clinical history into precision oncology strategies.

Our findings highlight the NR2F2-BGN axis as a critical regulator of PTC progression. Targeting this axis offers a promising therapeutic strategy for PTC treatment and immune microenvironment modulation.

Both the de novo synthesis and exogenous uptake of FAs are important for PTC cell proliferation. The combined inhibition of LPL and FASN inhibitors shows promise for PTC treatment.

The presence of infiltrative tumor margin, plump pink cells, and myxoid desmoplasia, may serve as active markers associated with the normalized BRAF V600E mutation. These findings suggest that the mutation acts as a driver in both early and late stages of PTC development. Furthermore, a direct relationship between tumor size and clonality underscores the role of BRAF V600E mutation in tumor progression and morphological evolution.