NECTIN2 (Nectin Cell Adhesion Molecule 2)

We have shown how a single point mutation of an amino acid residue located in the centre of the F strand of TIGIT dictates its interaction affinity with its ligand. These findings can provide a framework for the development of small-sized non-antibody therapeutics specifically targeted towards nectin-4 overexpressing cancer cells with minimal off-target effects on healthy cells.

Moreover, targeted interventions against distinct immune escape pathways-such as the Ubiquitin-Conjugating Enzyme E2T (UBE2T)/Cell Division Cycle 42 (CDC42)/Cluster of Differentiation 276 (CD276) and C-C Motif Chemokine Ligand 2-C-C Motif Chemokine Receptor 2/C-C Motif Chemokine Receptor 4 (CCL2-CCR2/CCR4) axes-have shown promise in reshaping the immune microenvironment and enhancing the efficacy of conventional immunotherapy. Collectively, this perspective outlines evolving strategies in immune checkpoint modulation, cellular ecosystem reprogramming, and neuroimmune intervention, providing a forward-looking framework to enhance the efficacy of immunotherapy in BCBrM.

Integrating public bulk cohorts with exploratory single-cell multi-omics supports a model in which chemotherapy sensitivity in triple-negative breast cancer is linked to inflamed, antigen-presenting microenvironments and adaptable antitumor immunity, whereas resistance is associated with stromal and tumor dominance. These candidate biomarkers and pathways require validation in larger independent cohorts, and clinical translation is premature given the exploratory single-cell cohort.

Our findings identify TIGIT as a promising immunotherapeutic target in PDAC and suggest that dual checkpoint blockade (TIGIT/PD-1), alongside restoration of DNAM-1 signaling, may overcome immune suppression. These results provide mechanistic rationale to inform future clinical trials in PDAC.

Notably, spatial omics studies further revealed that, after NACT, a subset of CD8+ T cells can be confined within "myelonets" microdomains organized by myeloid cells, where interactions such as NECTIN2-TIGIT impose spatial restriction and induce functional exhaustion of T cells, thereby compromising their effective tumor killing. This review aims to systematically summarize the baseline characteristics and heterogeneity of lymphoid- and myeloid-derived TILs in ovarian cancer, elucidate the mechanisms underlying immune remodeling induced by NACT and their complex relationships with clinical outcomes, and further discuss combination therapeutic strategies and biomarker development based on dynamic TIL changes to enhance the clinical application of precision immunotherapy.

Collectively, our findings establish TSPAN6 as a migrasome-related regulator driving adverse immunotherapy outcomes and responses. Targeting TSPAN6, potentially with mitoxantrone, presents a potential strategy to enhance immunotherapy efficacy.

On der(19)t(14;19), chromosome 19 sequences centromeric to the breakpoints were fused to the germline IGHVs, or IGHV-D-J rearrangement sequences followed by the 5' Eµ enhancer and IGHM/IGHD constant genes. In the non-CLL BL patients, BCL3 was retained on der(19)t(14;19) and potentially affected by the translocated IGH.

Conclusion SLC1A5 serves as an independent prognostic biomarker in melanoma. Its overexpression may shape an immunesuppressive microenvironment by dysregulating immune molecules expression and cellular infiltration, ultimately facilitating immune escape and malignant progression.

Our findings suggest that TIGIT and CD96 could be markers of the clinical stage and treatment response of HNSCC. Therefore, administering anti-TIGIT and anti-CD96 after radiotherapy may provide a novel approach for incorporating immunoradiotherapy into HNSCC treatment.

These findings provide mechanistic insights into immune evasion and suggest NECTIN-TIGIT signaling as a potential biomarker and therapeutic target. Future wet-laboratory validation and clinical studies are needed to confirm the translational relevance of this axis in thyroid cancer management.

Through systematic analysis, we developed a 12 PR-mRNAs signature that effectively predicts clinical outcomes in TNBC patients. The newly established risk assessment model not only provides a reliable tool for prognostic evaluation but also reveals NECTIN2 as a clinically significant biomarker, with elevated expression correlating with poorer survival outcomes.

Similarly, NK cell recognition of targets expressing the nectin CD112, which also engages both DNAM-1 and TIGIT, resulted in modest loss of DNAM-1 expression and heightened IFN-γ responses. Together, these observations suggest that DNAM-1 recognition of its ligands is delicately poised such that low avidity receptor engagement augments NK cell activation, and in particular IFN-γ responses, while stronger engagement can result in the rapid downregulation of DNAM-1 without any significant enhancement of effector responses.