Thyroid Gland Carcinoma

Verteporfin reversed these effects...MMRN1 acts as a tumor suppressor in TC by activating the Hippo pathway and modulating oxidative stress and ferroptosis. These findings highlight MMRN1 as a potential therapeutic target for TC treatment.

Platinum/PEM/Pembro may be a therapeutic option for TTF-1-negative non-sq NSCLC with good PS and adenocarcinoma histology, although careful management of irAE is required.

[68Ga]Ga-DOTA-FAPI-04 PET/CT showed higher diagnostic accuracy for the identification of recurrent MTC over standard [18F]F-FDG and [68Ga]Ga-DOTATATE PET/CT, with higher regional detection rates for liver and osteoblastic skeletal metastases. Furthermore, while the exploratory FAST score provides a framework for patient stratification and personalizing targeted theranostic strategies, it requires future validation through larger multicentre trials prior to clinical adoption.

These mechanisms collectively promote the thyroid carcinogenesis. Collectively, we have confirmed a novel mechanism by which the VPS53-EGFR axis drives thyroid carcinogenesis induced by LDR, and provided new insights into thyroid tumor biology.

We describe a patient with radioactive iodine-refractory, metastatic oncocytic thyroid carcinoma with an NBN gene (c.2166_2167delGCinsAT) pathogenic variant, who developed progressive disease despite receiving systemic therapy with lenvatinib and pembrolizumab. A mutual exclusivity analysis demonstrated a tendency for pathogenic variants in one MRN complex genes to co-occur with pathogenic variants in the other two MRN complex genes. In conclusion, the MRN complex pathogenic variants could be potentially oncogenic in TCs and may be linked to aggressive forms of TC.

It is characterized by nuclear and cytoplasmic beta catenin expression indicating activation of Wnt/beta-catenin signaling pathway. We present a case of cribriform morular thyroid carcinoma with nodal recurrence, initially misdiagnosed as tall cell PTC highlighting its diagnostic challenges and clinical relevance of accurate diagnosis.

Pin1 knockdown or treatment with the pharmacological Pin1 inhibitor KPT-6566 stabilizes NCOA4, enhances ferritinophagy, and triggers ferroptosis, markedly restraining ATC growth both in vitro and in vivo. These findings identify Pin1 as a previously unrecognized suppressor of ferroptosis through NCOA4-dependent ferritinophagy and support Pin1 inhibition as a potential therapeutic strategy for ATC.

P2, N=2175, Active, not recruiting, ECOG-ACRIN Cancer Research Group | Trial primary completion date: Oct 2026 --> Oct 2027

When cytologic-radiologic discordance persists, early consideration of core needle biopsy is warranted. Management requires a multidisciplinary approach, with surgical resection of isolated metastatic disease integrated within an individualized, sequential systemic therapy strategy.

This protocol offers a technically straightforward, cost-effective, and purely tumorous organoid platform for lung adenocarcinoma research. Its simplicity and reproducibility also make it suitable for undergraduate laboratory teaching, where it can help students acquire fundamental 3D tumor organoid culture techniques within a limited lab schedule.

Among the tested compounds, entrectinib exhibited consistently strong binding affinities across all variants (-9.7 to -10.7 kcal/mol), whereas reduced binding affinities were observed for several inhibitors against E734K, A756D, and R897G variants...Clinical databases reported that p.Met918Thr (pathogenic) and p.Arg897Gln (risk factor) emerged as significant variants linked to MEN2-related cancers and Hirschsprung disease. As a conclusion, this integrative in silico study identifies deleterious RET nsSNPs with potential structural, functional, and therapeutic significance providing mechanisms for precision oncology and future clinical investigation.