Transcriptomic analyses of combination-treated tumors showed suppression of Wnt/β-catenin- and TGF-β-pathway-associated signatures alongside activation of immune-stimulatory responses. These results position SMYD2 as a dual regulator of tumor growth and immune suppression, and as a promising target to overcome ICI resistance in HCC.

The time-dependent ROC AUC at both the level of IL-1ra and frequency of CD8(+)CD45RO(+)CD27(+)CD127(+) T cells significantly predict OS (p = 0.0193 and p = 0.0442). These preliminary findings indicated that localized non-ablative irradiation against metastatic lymph node has a potential to enhance the clinical efficacy of anti-PD-1 immunotherapy in patients with m-GC, and IL-1ra level and frequency of CD8(+)CD45RO(+)CD27(+)CD127(+) T cells in peripheral blood before treatment may be candidate biomarkers to predict clinical efficacy of Nivo-lRT_mLN.

We present a comprehensive transcriptomics analysis of metastatic and primary tumor biopsies from MSS mCRC patients treated with botensilimab (BOT; Fc-enhanced anti-CTLA-4) ± balstilimab (BAL; anti-PD-1). This study identified distinct tumor microenvironment states that align along an immunophenotype axis marked by CD74, interferon-γ, and APOBEC3 expression identified previously for primary CRC. Our findings provide novel insights into molecular correlates of immunotherapy response in MSS mCRC, potentially informing future therapeutic strategies to expand ICI efficacy to historically unresponsive tumors.

Importantly, combined CTLA-4 and PD-1 blockade reactivated anti-tumor T cell features in non-responders in vitro, highlighting CTLA-4 as a potential driver of resistance. Together, these findings support personalized immunotherapy strategies guided by systemic immune biomarkers in advanced NSCLC.

A composite score integrating 8q24 status, tumor mutational burden, and PD-L1 expression effectively identified non-responders. Prognosis-driven and cell-line screening revealed 8q24-specific therapeutic vulnerabilities, providing a framework for targeted combination strategies in this genomically defined patient subset.

The successful development of immunotherapeutics for GBM requires generating a robust antitumor immune response while overcoming T-cell anergy and tolerance. The immune system has various checkpoint pathways; thus, targeting multiple checkpoints simultaneously will have potential survival benefits.

Immunotherapy is a cornerstone in advanced EC management, guided by molecular classification. Key challenges include limited efficacy in pMMR tumors, lack of robust predictive biomarkers, and uncertainty in treatment sequencing. Future strategies should focus on biomarker-driven approaches and rational combinations.

Studies have shown that treatments targeting specific targets can inhibit tumor progression and prolong patient survival to a certain extent, but the efficacy has individual differences and is still limited. Therefore, future research still needs to further explore the molecular mechanism of DSRCT and discover more accurate and effective therapeutic targets.

We further identified a spatially organized immune triad composed of CD8⁺ TR, CD4⁺ TR, and type-3 dendritic cells (DC3) that is exclusive to responding tumors. These findings define coordinated cellular interactions within the tumor microenvironment that underpin successful immunotherapy and provide a framework for spatial biomarkers of response.

This "Neutrophil-Tumor" cascade delivered heterobifunctional immunomodulation drugs with spatial and temporal precision, offering a translatable solution to the toxicity-efficacy dilemma that currently constrains STING-based cancer therapy.

This trimodal cell death triggers immunogenic cell death (ICD) and DAMPs release. In vivo, TEP NPs reprogram the tumor microenvironment by recruiting immune effectors, establishing a closed-loop of tumor killing and immune activation.

This GLCD strategy effectively suppressed tumor growth on both unilateral and bilateral subcutaneous 4T1 breast tumor models by simultaneously impairing glycolysis and oxidative phosphorylation, enhancing antigen presentation, and promoting the infiltration of antitumor T cells. This study highlights the potent combination of glucose/lactate metabolic intervention with immunotherapy for improved antitumor treatment.