TAP1 (Transporter 1)

In contrast, HEXIM1+CAF-C1 may act as an independent risk factor for poor prognosis in CRC. Our findings enhance understanding of immune escape mechanisms in CRC, show how novel subtypes affect prognosis, and offer insights for new diagnostic and treatment strategies.

Co-culture showed effective spheroid infiltration, cytotoxicity, and structural disruption, with infiltrating CAR T cells displaying higher CD4+ fraction, activation, exhaustion, effector/terminal differentiation, and IFN-γ/TNF-α production. This 3D platform recapitulates critical TME constraints and provides a cost-effective, feasible preclinical tool to assess CAR T therapies beyond conventional 2D assays.

These findings highlight SUMOylation as a critical regulator of the adaptive anti-tumor immune response. We propose SUMOylation inhibition as a strategy to enhance immunogenic peptide presentation, thereby improving the efficacy of cancer immunotherapies.

In the IMvigor210 cohort, this signature identified tumors with higher PD-L1 blockade response (55.6% vs. 32.8%, p = 0.034) and improved survival trends in the TMB-high subset. The proposed 20-gene signature quantitatively captures immune heterogeneity in dMMR/MSI-H tumors and serves as a practical, interpretable biomarker to identify true ICI responders and guide precision immunotherapy.

The structure also reveals how TAP's amino-terminal transmembrane domains scaffold the MHC I chaperone tapasin. These findings elucidate the mechanism of US6-mediated immune evasion and highlight potential targets for therapeutic modulation of immune presentation in infection and cancer.

We also found that CPSF1 amplification can impact 3'UTR length regardless of MYC status. Our study highlights the importance of CPSF1 as a promising prognostic factor in cancer and as a therapeutic intervention target to study in the future.

This study demonstrates that peptide-trained T cells can upregulate NLRC5 and MHC-I expressions on tumour cells, thereby restoring antigen presentation and enhancing tumour immunogenicity. These findings underscore the therapeutic potential of cancer vaccines in treating APM-downregulated NPC.

As EZH2 is highly expressed in numerous precancers, PPT@GSK126 has broad application prospects for reducing these tumor burdens. Schematic images presenting the mechanism of action regarding EZH2 in promoting MT of OLK into HNSCC via inhibiting MHC-I associated APM (left panel) and the proposed therapeutic strategy for preventing OLK carcinogenesis (right panel).

This study is the first to identify TP53 mutation as a biomarker of resistance to ICI-based therapy in ICC, and to uncover its immune-evasive phenotype using spatial profiling. These findings provide mechanistic insight into immune evasion and support the development of TP53-guided immunotherapeutic strategies in ICC.

Our results show that LC priming of T cells is enhanced following treatment with Ctrl-LEVs whereas LEVs from HPV16 E6/E7 expressing cells suppress LC function. Functional impairment of LC priming of T cells by E6/E7-LEVs released in the epithelium may contribute to viral persistence in HPV16-infected skin.

Their involvement in BCR and PI3K-AKT pathways underscores novel vulnerabilities for overcoming refractory disease. Our findings provide a foundation for developing strategies to improve outcomes in high-risk DLBCL patients with hypoxic microenvironments.