The immune mechanism of its occurrence is still unclear and needs to be further studied. Traditional glucocorticoid is still the first-line drug, but the new targeted drug Efgartigimod has less adverse reactions and faster onset of action, which may become a good choice, but needs to be verified by a larger sample.
Prognosis in TETs relies primarily on histology and staging, whereas molecular and immunological biomarkers represent emerging tools for risk stratification and treatment selection. Multiparametric models integrating clinical, pathological, and molecular data may pave the way for precision oncology in TETs.
Although gene amplification is rare, protein expression is more frequent, suggesting potential for targeted therapy. Detailed molecular profiling and innovative research methods are essential to further explore the therapeutic potential of HER2 in these rare cancers.
Recognition of this relationship is important for clinical management, long-term surveillance, and therapeutic decision-making in patients with thymoma. Future studies are warranted to further define the oncogenic consequences of thymic dysfunction and its implications for cancer development.
Novel therapeutic approaches are emerging, including PRMT5 inhibitors in MTAP-deficient tumors, TROP-2-directed antibody-drug conjugates (e.g., sacituzumab govitecan), and chimeric antigen receptor (CAR) T-cell therapies targeting mesothelin. Bispecific agents such as bintrafusp alfa and ivonescimab, which co-target various pathways, offer innovative strategies. Despite these advances, TC remains a challenging malignancy with no standardized treatment algorithm. Collaborative efforts across institutions will be essential to accelerate progress and improve outcomes in this rare disease.
Tumor microenvironment in high AKT2 expression patients demonstrated immunosuppressive characteristics such as reduced γδT cells aggregation and increased Tregs infiltration.
Subsequent next-generation sequencing of the lymph node metastasis revealed a novel heterozygous MUTYH frameshift mutation, c.848delT (p.M283Rfs*3), which was confirmed to be of germline origin by Sanger sequencing of the patient's normal thyroid tissue. This case expands the disease spectrum associated with heterozygous MUTYH carriers and enhances the understanding of the phenotypic heterogeneity of tumors in this population.
The levels of phosphorylated-mechanistic target of rapamycin complex 1 (p-mTORC1)/mTORC1, p-v-akt murine thymoma viral oncogene homolog 1 (AKT)/AKT, and p-phosphatidylinositol-3 kinase (PI3K)/PI3K were significantly downregulated following GPR176 knockdown. GPR176 is upregulated in OS and is associated with a poor prognosis. GPR176 suppresses mitophagy to promote OS progression by facilitating mTORC1 activity via the PI3K-AKT pathway.
Systemic therapy advances include KIT/PIK3CA-targeted agents (imatinib, everolimus) showing modest efficacy, while programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) inhibitors demonstrate 20-30% response rates in thymic carcinoma but are associated with a >50% risk of severe immune-related adverse events (irAEs). Platinum-based chemotherapy [cisplatin, doxorubicin, cyclophosphamide (CAP) regimen] remains standard for advanced disease...TETs management is evolving rapidly through technological and biological advances. Future progress hinges on: (I) validating artificial intelligence (AI)-driven imaging classifiers; (II) conducting randomized controlled trials (RCTs) comparing surgical approaches; (III) elucidating immunotherapy toxicity mechanisms; and (IV) developing predictive composite biomarkers integrating genomic, immunological, and clinical parameters to enable precision medicine while mitigating fatal toxicities.
Thymoma further increased the risk of both AAN-I-IFN production and severe disease. These findings suggest a crucial immunological mechanism that could guide risk stratification and targeted interventions for MG patients during viral infections, such as COVID-19.