TMB-L

Functionally, PGAP3 silencing significantly impaired proliferation, clonogenic growth, and migration in vitro. Our findings identify PGAP3 as a tumor-intrinsic gene associated with metabolic reprogramming and a CTL/CD8+-low immune contexture in PCa, supporting PGAP3 as a potential marker of the immune-cold tumor microenvironment and motivate future mechanistic studies in immunocompetent systems.

A conservative re-excision was performed, and a PET/CT scan showed no evidence of dissemination. With 16 months of follow-up available, longer-term monitoring will be required to determine the clinical behavior and biologic potential of this tumor.

This is the largest NSCLC dataset analyzed for biomarker distribution across histologies, age, sex and genetic ancestry. This dataset confirms sufficient enough biomarker prevalence across many histological subtypes of NSCLC, providing reassurance that all NSCLC cases should be considered for biomarker workup.

We discussed major OV platforms with respect to payload capacity, expression control, manufacturability, and clinical track records, including lessons learned from approved or late-stage OVs such as talimogene laherparepvec (T-VEC) and teserpaturev/G47Δ. Finally, we propose a pragmatic clinical workflow for rapid personalization to maximize therapeutic index. Tightly integrating neoantigen science with immunovirotherapy, including recent 2025 preclinical advances like oncolytic adenovirus neoantigen delivery sensitizing low-TMB tumors to PD-1 blockade, could enable next-generation personalized cancer vaccines capable of converting "cold" tumors into responsive, systemically controlled disease.

Our findings demonstrate that MTAP deletion is an infrequent but genomically coherent event in solid tumors, characterized by a canonical 9p21 co-deletion pattern. This real-world analysis underscores the importance of comprehensive genomic profiling to identify patients who may benefit from emerging MTAP-directed therapies.

Published cases suggest that IN-TSCT may exhibit aggressive clinical behavior, including metastatic spread in a subset of patients; however, the total number of reported cases remains very limited, and the true metastatic risk and prognostic spectrum have not yet been clearly defined. This review synthesizes the available literature to provide a comprehensive clinicopathologic and molecular overview of this emerging tumor entity.

This work establishes cuproptosis induction via NP@Fla-Cu as a transformative strategy against UM, effectively addressing challenges in tumor selectivity and off-target toxicity. The dual functionality of flavopiridol as a copper ionophore and mitophagy activator provides a promising combinatorial approach to overcome therapy resistance in immunosuppressive malignancies.

The presence of MS appeared to correlate with worse clinical outcomes, as 67% of patients with MS died, compared to none without. Our findings expand the recognized molecular diversity of MBNs and provide insights into their biological behaviors, underscoring the clinical significance of identifying potential prognostic factors.

Variants were significantly enriched in genes associated with GABAergic and serotonergic neuronal cell types, as well as in pathways regulating cell cycle and neurogenesis. These findings suggest that, in addition to VHL loss, dysregulation of neuronal differentiation programs and cell cycle control may play important roles in hemangioblastoma tumorigenesis.

To our knowledge, this represents only the third reported malignant hepatic glomus tumor with molecular confirmation of CARMN::NOTCH2 fusion. This tumor highlights the diagnostic challenges posed by hepatic glomus tumors, underscores the importance of integrating molecular studies into unusual hepatic neoplasms, and expands the clinicopathologic and molecular spectrum of this exceedingly rare entity.

Mutational signature analysis showed enrichment of apolipoprotein B mRNA editing enzyme catalytic subunit-associated signatures. This study suggests novel perspectives on the mechanisms of OMT tumor development and malignant transformation.

This review aims to discuss the progress and pitfalls of various immunotherapy approaches for thyroid cancer, including ICI therapies, adoptive cell therapies (CAR-T cell, TCR-T cell, and TIL therapy), oncolytic virotherapy, and macrophage/myeloid-modulating immunotherapies. A deeper understanding of subtype-specific immunobiology and precise tailoring of immunotherapeutic interventions may ultimately enable more effective and durable clinical responses for patients with advanced thyroid cancer.