PD-L1 (Programmed death ligand 1)

Elevated plasma FNG levels predict poor prognosis and reduced ICI efficacy in ESCC. They may be potential biomarkers for first-line ICI-based therapy and correlate with TAN infiltration. Further validation and mechanistic investigations are warranted.

Structural characterization identified nine high-impact nsSNPs (ΔΔG <  - 1.7 kcal/mol), particularly in TLR3 (L104N, L381P, L77P) and CD274 (W57S, C155S, G159D, Y112N), indicating potential disruption of receptor stability, immune checkpoint interactions, and inflammasome regulation. This integrative multi-omics and structural pharmacogenomics framework reveals a robust four-gene signature (CASP1, TLR3, PYCARD, CD274) that links necroptosis, ferroptosis, and immune modulation in BRCA, providing promising avenues for precision oncology and therapeutic target development.

Neoadjuvant treatment recruited macrophages and T-cells in the TME, but interestingly, an increased macrophage count upon final histology was related to poor response to treatment. The present study provides valuable insight to the TME composition of esophageal cancer and its modification after NAT, however, further studies are needed to assess the exact functional role of TME elements, and their impact on clinical outcomes.

The prospective study suggests that BACE plus tislelizumab offer promising efficacy and acceptable safety in advanced NSCLC, supporting further randomized trials.

Human T lymphocytes were engineered with a lentiviral vector to express anti-FRα-CAR5, which incorporates a fourth-generation CAR backbone (CD28, 4-1BB, CD27, and CD3 zeta) augmented by a secreted anti-PD-L1 scFv derived from atezolizumab...This fifth-generation CAR offers a promising strategy to enhance CAR T cell therapy efficacy in PD-L1-mediated immunosuppressive TMEs. These findings suggest that anti-FRα-CAR5 T cells therapy warrants further preclinical validation as a potential treatment strategy for NSCLC patients.

Nevertheless, ADCC boosted the capacity of cDC1 and DC2 to prime naïve T cell responses but not of DC3. Thus, our data suggests that the therapy with bispecific antibodies targeting NK cells may have the potential to facilitate adaptive antitumor immune responses via activation of cDC1 and DC2.

Proteomic profiling of the TME further elucidates the heterogeneity of immunotherapy responses, offering insights for precision strategies in ESCC neoadjuvant therapy. Trial registration This study was prospectively registered in the Chinese Clinical Trial Registry (ChiCTR2000041081).

A deep learning model based on iodine map has been proven to be a valuable, reliable, and interpretable tool for non-invasive prediction of PD-L1 expression in GC.

In TFE3-rearranged RCC, the fusion gene might influence morphology or PD-L1 expression, thereby be likely to affect the efficacy of immunotherapy. Assessment of a combination of histological morphology, immunophenotype, and genetic alterations can facilitate precise pathological diagnosis of RCC, supporting personalized targeted therapy and prognosis assessment.

P2, N=25, Not yet recruiting, Zheng Min

Taken together, we demonstrate a direct role of EVs in subverting the immune microenvironment and altering macrophage plasticity in a manner conducive to both tumor growth and proliferation. As such, a targeted delivery of microRNA inhibitors as drugs for altering macrophage plasticity may likely achieve better therapeutic response in pancreatic tumors.

CA-induced immune pharmacodynamic effects in peripheral blood and in the tumor microenvironment without preferential Treg cell activation in patients with metastatic/unresectable CEA+ solid tumors.