CD8 (cluster of differentiation 8)

SBRT can inhibit tumor growth, modulate LAG-3 expression, promote T cell infiltration and cytokine secretion in HCC. The Cqy-12-Cy5 can dynamically monitor the modulation of LAG-3 by SBRT, providing a strategy for guiding the timing of combination therapy and promoting synergistic immunotherapeutic efficacy.

NIR theranostics represent a new arena for precision oncology. Future directions involve biocompatible, degradable/activatable NIR-II probes and multimodal systems complemented by AI-guided imaging for clinical translation and personalized cancer therapy.

NEDD4L is downregulated in CRC and associated with the dysregulation of the TME. NEDD4L overexpression could inhibit CRC metastasis and immune evasion by repressing STAT3 signaling, suggesting that it is a potential target for improving CRC treatment efficacy.

Our findings identify the Nrf2-Gpx2 axis as a master regulator of immunogenicity in ESCC. Targeting this axis represents a promising strategy to convert "cold" tumors into "hot" environments, thereby improving the efficacy of radiotherapy and immunotherapy.

Circulating CD28-KLRG1+ CD8+ T cells are valuable and convenient biomarkers for first-line chemoimmunotherapy in advanced NSCLC and provide insight into how late-differentiated or senescent T cells engage in the antitumor immunity when immunotherapy is added to conventional therapies.

These findings suggest that pregabalin increases the proliferative ability of pancreatic cancer cells in vitro without promoting tumor growth in vivo. Additionally, it induces an alteration with an increase in tumor-infiltrating lymphocytes and dendritic cells, along with a decrease in M2-like tumor-associated macrophages and cancer-associated fibroblasts in vivo.

In vivo experiments showed that BASP1 knockdown markedly inhibited tumor growth in mouse models bearing 4T1 tumors, accompanied by decreased MDSCs infiltration and increased Granzyme B + CD8 + T cell accumulation in tumor tissues. Collectively, BASP1 may serve as a potential prognostic biomarker and a therapeutic target for BC intervention, functioning both as a pro-tumorigenic gene and as an immunomodulatory molecule that shapes an immunosuppressive microenvironment.

PTPN1 may inhibit T cell proliferation via the JAK2-STAT5 axis while simultaneously advancing liver cancer progression by activating the PI3K-AKT pathway in cancer cells. These findings suggest that PTPN1 could serve as a promising target for immunotherapy in liver cancer.

We provide a quantitative framework showing that ≥77 genes and ≥3-mm tissue diameter regions preserve predictive spatial signal at scalable throughput. The registration details of the trial are EudraCT 2017-002246-68.

LVSI+ EECs exhibited marked epithelial reprogramming, transitioning from differentiated ciliated epithelium to hyperproliferative and metabolically remodelled phenotypes, and contained TC4, a metastatic epithelial subset characterized by hypoxia, partial epithelial-mesenchymal transition, immunosuppression, and progesterone resistance...Using spatial multiplex immunofluorescence, we confirmed hypoxic tumour epithelial cells at the invasive front coexisting with an immunosuppressive microenvironment, and revealed spatial colocalization of PD-L1+ tumour cells, PD-L1+ macrophages, and PD-1+ T cells within LVSI thrombi. Our comprehensive study provides deeper insights into LVSI as an actively coordinated multicellular process, potentially improving LVSI risk prediction, supporting treatment decision-making, and informing new therapies targeting the tumour microenvironment.

Importantly, combining EFHD2 knockdown with immune checkpoint blockade synergistically enhanced radiosensitivity and restored antitumor T cell responses. Collectively, these findings demonstrate that EFHD2 drives lactate-mediated immunosuppression and DNA repair to promote radioresistance in CRC, suggesting that targeting the EFHD2 axis may restore antitumor immunity and improve therapeutic outcomes.

The RNA-seq results demonstrated that CTLA-4 was upregulated in the distant tumor on 9 days after complete radiofrequency ablation. Anti-tumor immune response initially associated with radiofrequency ablation was relatively transient, while an immunosuppressive microenvironment was formed in the distant tumor in 9 days. Anti-CTLA-4 therapy after complete ablation significantly delayed distant tumor growth and promoted an anti-tumor immune microenvironment.