PD-L1 (Programmed death ligand 1)

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

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

P1, N=18, Recruiting, Thomas Jefferson University | Not yet recruiting --> Recruiting | Trial completion date: Jan 2027 --> Apr 2028 | Trial primary completion date: Jan 2027 --> Oct 2027

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

Systemic bevacizumab remains the most mature systemic option with consistent real-world evidence and published dosing guidance. HPV-specific immunotherapy has recently transformed adult RRP management with an FDA-approved, short-course treatment option; ongoing studies will clarify optimal sequencing with bevacizumab and the role of checkpoint inhibition.

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

Ficerafusp alfa plus pembrolizumab demonstrated favorable safety and tolerability with promising antitumor activity in the first-line treatment of R/M HNSCC, particularly in those with HPV-negative tumors.

nCIT establishes a new standard of care for resectable non-small cell lung cancer, offering improved pathological and survival outcomes while preserving surgical safety. Future research should focus on unresolved issues such as patient selection, biomarker integration and the role of adjuvant immunotherapy to refine personalized treatment strategies.

Conversely, EBV-negative tumors retain ICOSL/SOCS1 expression, but exhibit minimal T cell infiltration, partly due to high SOCS1 expression, preventing immune-mediated clearance. Overall, our data indicate that SOCS1 expression, regulated by EBV-induced miR-155, along with ICOSL status determines whether tumors attract T cells and whether those T cells can effectively eradicate cancer cells.

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.

In vitro and in vivo experiments demonstrate that, when combined with immune checkpoint blockade (ICB) therapy, HCFCMP not only significantly inhibits primary tumor growth but also effectively suppresses distant tumor progression. This substantially improves the immunotherapeutic response rate and provides a promising strategy for addressing tumor metastasis and recurrence.

Plasma PA can function as a biomarker to evaluate the efficacy of ICIs in gastrointestinal cancers. Overall, our results identify the DGKα/PA axis as a metabolic driver of immune evasion and CTLs exclusion, representing a promising target to enhance ICIs' efficacy in gastrointestinal cancer treatments.