Thyroid Gland Anaplastic Carcinoma

IBC induces apoptosis and pyroptosis, with caspase-dependent Poly ADP-ribose Polymerase (PARP) and Gasdermin E (GSDME) cleavage simultaneously. This study reveals a novel function of IBC in inducing pyroptosis in tumor cells, expands its known pharmacological spectrum and highlights its value as a therapeutic agent for ATC.

Combining ICIs with targeted therapies or adoptive cell therapies is being explored to overcome resistance and improve efficacy. However, challenges such as tumor heterogeneity and immune evasion mechanisms persist.

The patient was thereafter treated with a combination of pembrolizumab, nab-paclitaxel and carboplatin, resulting in a sustained near-complete response lasting over 30 months, accompanied by a manageable safety profile. The favorable response in this case suggests that further evaluation of this triplet regimen could be considered for anaplastic thyroid cancer, though this remains a speculative premise requiring validation. Further studies are also needed to clarify the underlying mechanisms of this combination and to identify predictive biomarkers for patient selection.

The study demonstrated that ketone body metabolite AcAc inhibits the proliferation, migration, and invasion of ATC cells and induces cell cycle arrest by inducing autophagy. Ketogenic diet provides a new strategy for the treatment of ATC.

BA inhibits ATC cell growth, an effect associated with the alteration of CLU-linked mitophagy and key signaling pathways. These findings highlight that CLU as a potential therapeutic target and suggested BA as a promising strategy for thyroid cancer intervention.

EZH2 is highly expressed in ATC, and its inhibitors EPZ6438 and GSK343 have anti-cancer potential. Two types of nanoparticles were successfully constructed with good sustained-release, targeting effects, and biosafety. They could improve the therapeutic efficacy and reduce toxic side effects, with GSK343-BSA@CS showing significant effects.

In vivo, MED reduced tumor growth in humanized NOG mice, decreased PD-L1 and AKT/NF-κB signaling, enhanced CD8+ T-cell activation (CD69, IFN-γ), indicating immune-dependent antitumor activity. MED suppresses thyroid cancer progression by inhibiting proliferation and immune evasion through the inactivation of AKT/NF-κB, supporting its potential as a therapeutic candidate.

P2, N=51, Active, not recruiting, National Cancer Center Hospital East | Trial primary completion date: Jun 2025 --> Sep 2025

P1, N=6, Recruiting, City of Hope Medical Center | Trial completion date: Feb 2026 --> Oct 2027 | Trial primary completion date: Feb 2026 --> Oct 2027

Lenvatinib therapy was initiated at the previous hospital, resulting in tumor shrinkage, and total thyroidectomy was performed 62 days after the initiation of treatment...We report a case of poorly differentiated thyroid carcinoma with an SMARCB1 mutation. The accumulation of similar cases and additional immunohistochemical evaluations of past specimens may contribute to the development of targeted therapeutic strategies.

Neoadjuvant therapy shows promise in improving resectability for unresectable and poorly differentiated thyroid cancers, with 51% of patients achieving R0 resection. Future studies should investigate optimal therapy selection, timing, dosing, and long-term outcomes, including disease-specific survival and patient-reported measures.

Interestingly, we showed for the first time, to our knowledge, a positive correlation between CHD4 and NOX4 protein expression in malignant thyroid tissues. The results of this study suggest that CHD4 could be used as a complementary molecular marker to improve the diagnosis and the management of PTCs-BRAFV600E .