Thyroid Gland Carcinoma

P=N/A, N=300, Recruiting, Memorial Sloan Kettering Cancer Center | Not yet recruiting --> Recruiting

Our findings uncover a previously unrecognized link between mitochondrial metabolic reprogramming, immune evasion and LNM in PTC and establish MGST1 as a robust biomarker for metastatic risk stratification and a pivotal metabolic-immune regulator. Moreover, the target-specific activity of toxoflavin provides a rational therapeutic strategy for patients with high-risk PTC characterized by MGST1-driven mitochondrial reprogramming and immune evasion.

For cases lacking these specific markers, VEGFR-targeted multikinase inhibitors (e.g., lenvatinib) remains the standard of care for RAIR-DTC...The therapeutic paradigm in thyroid cancer is shifting from non-selective multikinase inhibition toward molecularly matched, combination-based, and adaptively sequenced strategies. Early and comprehensive genomic profiling-including fusion detection-is essential to optimize treatment selection, address resistance, and expand precision therapy options across disease subtypes.

XSLJZ inhibits thyroid cancer cell proliferation and induces cell death through multi-component, multi-target synergistic regulation of the AGE-RAGE→PI3K/Akt signaling pathway.

miR-335-5p inhibited the expression of nearly all analyzed genes in less-differentiated thyroid cell lines. Thus, miR-335-5p may be a viable therapeutic target to restore radioiodine avidity in BRAF-mutant metastatic thyroid cancer and enhance KI treatment redifferentiation.

This study identifies a malignant cell-intrinsic signature for predicting PTC prognosis. Validated by single-cell data, our findings suggest that targeting ion channels may represent a potential therapeutic strategy for modulating neuro-immune interactions in thyroid cancer, pending experimental validation.

In addition, ITM2A counteracted TGF-β-induced dedifferentiation and epithelial-mesenchymal transition, and enhanced antigen presentation as well as PD-L1-dependent T-cell responses. ITM2A maintained the differentiated state of THCA through metabolic reprogramming and shaped an immunologically favorable microenvironment, suggesting that it may serve as a potential biomarker for prognosis prediction and a therapeutic target for optimizing immunotherapy strategies.

METTL7B promotes glycolysis and malignant progression in PTC by stabilizing HIF-1α through USP28-mediated deubiquitination.

P1, N=16, Not yet recruiting, University of Pennsylvania

Although paclitaxel and lenvatinib have been used as drug treatments, combination therapy with dabrafenib and trametinib has recently been reported to be effective. Furthermore, lenvatinib, a molecularly targeted agent, shows limited efficacy against ATC and is associated with frequent adverse events. In contrast, combination therapy with dabrafenib and trametinib is considered an effective therapeutic option for patients with BRAF V600E mutation-positive ATC, when appropriate management and monitoring are implemented.

This study developed and validated an interpretable ML model capable of accurately predicting reoperation outcomes in patients with recurrent or persistent PTC. The model may assist clinicians in identifying high-risk individuals and tailoring personalized treatment strategies.

The expression of ITGA7 in TC tissues and cells was significantly lower than that in normal tissues and cells. ITGA7 inhibits TC progression by interacting with FN1 and suppressing PI3K/AKT signaling pathway activation.