PD-L1 expression

Therapeutically, combined treatment with the BRD4 inhibitor JQ1 or the first bromodomain (BD1) selective inhibitor MS402 and an anti-GM-CSF antibody markedly suppressed TNBC progression and converted the tumor immune microenvironment from "cold" to "hot". In conclusion, our study reveals a previously unrecognized metabolic-epigenetic mechanism through which BRD4 drives GM-CSF-dependent TAMs activation and immune evasion in TNBC. Targeting BRD4 in combination with GM-CSF blockade represents a promising therapeutic strategy to overcome immune resistance in this aggressive breast cancer subtype.

Metformin pretreatment significantly enhanced PBMC-mediated cytotoxicity against tumor cells and patient-derived organoids in ex vivo co-culture systems. Our findings establish the SLC5A11-AMPK-PD-L1 axis as a novel mechanism linking metformin to tumor immunity, providing a molecular rationale for combining metformin with checkpoint inhibitors in cancer immunotherapy.

TTF-1 negativity identifies a subset of LUAD with worse outcomes to immunotherapy, chemo-immunotherapy, and KRASG12C inhibitors.

The DUO-E pMMR subpopulation was highly heterogeneous with frequent overlap of biomarkers and histology. Consistent with the primary analysis, durvalumab plus olaparib improved the PFS benefit observed with durvalumab versus control across a range of biomarker and histological subgroups.

The CT-based Hybrid RFE-CatBoost model enables accurate, reproducible prediction of PD-L1 expression in NSCLC, providing a promising noninvasive tool.

A moderate positive correlation was observed between PD-L1 expression and FDG uptake (R2 = 0.36) and a weaker correlation with FAPI uptake (R2 = 0.19). This Multi-parametric imaging can enhance immunohistochemistry, aiding in patient stratification for immunotherapy and overcoming the limitations of single-site biopsies.

To our knowledge, these are the first reported 5-year results of a PD-1 inhibitor plus chemotherapy in gastroesophageal adenocarcinoma. Nivolumab plus chemotherapy continued to demonstrate long-term survival benefit and acceptable safety after 5 years of follow-up, reinforcing its use as a standard first-line treatment for PD-L1 positive patients.

RNF26 is a pivotal molecular node linking the inflammatory microenvironment to immune suppression in HCC. By ubiquitinating and degrading GRP78 to instigate ER stress, it dually regulates antigen presentation and immune checkpoint expression. Targeting the RNF26-GRP78 axis represents a promising novel strategy for reversing HCC immune resistance and enhancing the efficacy of immunotherapy.

P1/2, N=74, Active, not recruiting, Servier Bio-Innovation LLC | Recruiting --> Active, not recruiting | N=176 --> 74

P2, N=54, Recruiting, Shanghai Pulmonary Hospital, Shanghai, China

P1, N=15, Recruiting, Emory University | Trial completion date: Jan 2027 --> Jan 2028 | Trial primary completion date: Jan 2026 --> Jan 2027

TME as defined by CD8 and TP53 mutational status may have predictive value for success of ICI therapy for patients with NSCLC with EGFR mutations.