PD-L1 expression

P2, N=65, Completed, University of Chicago | Active, not recruiting --> Completed

P2, N=50, Not yet recruiting, Fred Hutchinson Cancer Center

P2, N=35, Recruiting, Sun Yat-sen University | Not yet recruiting --> Recruiting | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Dec 2026 --> Jul 2027

FGFR4-high expression is associated with an immune-responsive phenotype in HCC and predicts inferior efficacy of lenvatinib plus PD-1 blockade.

These findings elucidate the synergistic mechanism between β-elemene and aPD-L1. Moreover, given the clinical availability of both agents, they provide a strong rationale for further clinical evaluation of this combination therapy.

In vivo xenograft experiments confirmed that DSTN knockdown significantly inhibited HNSCC tumor growth. In conclusion, this study demonstrates that DSTN is a key driver promoting the malignant progression of HNSCC; high DSTN expression indicates poor prognosis, while its downregulation exerts tumor-suppressive effects through multiple mechanisms, including inhibiting the secretion of MMPs, suppressing glucose metabolism, blocking the Wnt/β-catenin signaling pathway, and inducing disulfidptosis.

Future directions emphasize next-generation ICIs, optimized combination regimens, and AI-driven biomarker integration to achieve durable, personalized treatments. This review underscores the potential of immunotherapy to redefine TNBC management while highlighting the imperative for continued innovation to address unmet clinical needs.

These findings indicate that PD-L1+CTCs reflect tumor-driven immune suppression and may facilitate metastatic spread. Therefore, PD-L1+CTCs should be considered as promising prognostic biomarkers and may provide a rationale for early immunotherapy.

Immune analysis indicated an immune-hot phenotype, but nuclear PD-L1 positivity did not correlate with T-cell density. This study highlights the significance of PTEN loss and nuclear PD-L1 expression in basal subtype BCa, contributing to improved risk stratification and potential precision treatments in bladder cancer.

Crucially, to bridge the translational gap between computational inference and clinical reality, we emphasize the mandatory integration of orthogonal ex vivo validation (e.g., patient-derived organoids and microphysiological systems). Ultimately, by transforming static spatial snapshots into testable dynamic trajectories, this computation-experiment closed-loop aims to generate actionable insights and prioritize rational combination strategies safely under expert oversight.

The PI3K inhibitor LY294002 reversed these pro-tumor and immunosuppressive effects. High COQ10B expression is closely associated with ESCC progression and poor prognosis. These malignant biological behaviors and the associated immunosuppressive tumor microenvironment are potentially mediated via the activation of the PI3K/AKT/HIF-1A signaling pathway.

The patient subsequently received adjuvant treatment with immunotherapy (penpulimab) combined with chemotherapy, followed by penpulimab maintenance therapy, resulting in a progression-free survival of >44 months...Third, it explores the clinical implications of the KRAS mutation in this unique tumor subtype. The overarching goal of this exploration is to offer valuable clinical guidance for managing this rare and understudied subtype of lung cancer, particularly in the context of multimodal therapy involving immunotherapy.