Thyroid Gland Anaplastic Carcinoma

Under specific circumstances, CNB can provide an effective diagnostic approach for thyroid tumors. Moreover, in this case, we identified a novel TP53 intronic mutation that may drive the development of thyroid PRMS.

Our two DUXAP10-CRISPRi cell lines significantly reduced the rapid growth and metastatic behaviors characteristic of ATC, affecting proliferation, viability, clonogenicity, apoptosis, invasion, migration, tumorigenesis, and metastasis. Thus, DUXAP10 is a proposed prognostic marker and therapeutic target for ATC disease propagation and progression.

Our findings suggest a possible association between PTX3 and aggressive TC, particularly ATC. Further studies are needed to validate these findings and elucidate the cellular origin and functional role of PTX3.

Selective BRAF and MEK inhibitors-including vemurafenib, dabrafenib, and selumetinib-have demonstrated efficacy in advanced thyroid cancers. The combination of dabrafenib and trametinib is FDA-approved for BRAF V600E-mutant anaplastic thyroid carcinoma (ATC) based on its significant survival benefits...Additionally, redifferentiation strategies using MAPK inhibitors to restore RAI avidity have shown promise, particularly in selected patients. These advances highlight the need to contextualize BRAF mutation status within a broader molecular and clinical framework to guide personalized, effective treatment strategies.

The patient was initially diagnosed with T4bN1bM1 and experienced disease progression following surgery and lenvatinib treatment. This possibility is supported by reliable evidence for the use of BRAF plus MEK inhibitor for brain metastasis from BRAF-mutated malignant melanoma. We conclude that encorafenib plus binimetinib treatment for brain metastasis from BRAF-mutated thyroid cancer is a safe and effective treatment choice.

Emerging data also indicate that reverse transcriptase inhibitors (e.g., lamivudine, nevirapine) can partially suppress retroelement activity, induce transcriptional reprogramming and restore radioiodine uptake in refractory thyroid tumors, highlighting a potential therapeutic vulnerability. By integrating cancer epigenetics and mobilome biology, this review reframes thyroid tumor evolution as a process shaped not only by genetic alterations but also by retroelement-mediated disruption of genome regulation. Retroelements may serve as biomarkers of aggressive transformation and as actionable targets in translational oncology.

Preclinical studies show that pharmacological inducers, including vitamin C, tenacissoside H, neferine, curcumin, and shikonin, as well as targeted agents such as dabrafenib and anlotinib, can trigger or synergize with ferroptosis. Although systemic toxicity and resistance remain obstacles, biomarker-driven selection and drug repurposing offer promise. Ferroptosis represents a mechanistically distinct and clinically exploitable pathway for ATC.

PD-L1 expression defines a biologically and clinically relevant subset of ATCs with distinct immune features and therapeutic vulnerabilities. Standardizing PD-L1 testing and integrating it with molecular and microenvironmental biomarkers will be essential to refine patient selection for immunotherapy and combination strategies, improving outcomes.

In thyroid tissue, genes related to immune response and metabolic processes, are regulated by TFs in an age- and sex-biased manner. These age- and sex-specific gene regulatory variations may contribute to the variation in risk of thyroid conditions with age and an overall higher risk of diseases in females compared to males, thus emphasizing the need for tailored screening and prevention strategies.

Contemporary thyroid cancer BrM outcomes are dependent on primary malignancy histology and may benefit from further molecular profiling.

WTAP regulated the m6A modification and mRNA stability of PRMT1. The WTAP/PRMT1 signaling axis modulated cuproptosis, thereby influencing ATC progression. These findings highlighted the potential of targeting the WTAP/PRMT1 pathway as a therapeutic strategy for ATC.

Collectively, these findings identify Nrf2 as a pivotal driver of ATC anoikis resistance and metastatic competence through regulation of the BCL-2/SLC7A11 axis. Targeting the Nrf2-dependent survival pathway may thus offer a promising therapeutic strategy for this otherwise refractory malignancy.