PD-L1 expression

P2, N=120, Not yet recruiting, Gilead Sciences

P1/2, N=151, Recruiting, Takeda | Not yet recruiting --> Recruiting

P1, N=6, Suspended, UNC Lineberger Comprehensive Cancer Center | Not yet recruiting --> Suspended | Trial primary completion date: Jun 2026 --> Jun 2027

The proposed model achieved an AUC of 0.735 and an accuracy of 0.724, outperforming traditional supervised pretraining (AUC 0.695) and single-task MAE (AUC 0.712). These results demonstrate that combining self-supervised learning, multi-task learning, and GAN-based augmentation enables a reproducible and standardized model-based prediction of clinically reported PD-L1 status from CT images, providing a non-invasive complementary tool for treatment decision-making.

Methods Male BALB/c mice were randomly divided into 6 groups: normal group, model group, Euphorbia helioscopia water extract low-, medium-, and high-dose groups (0.9, 1.8, 3.6 g/kg), and aspirin group (20 mg/kg)...The protein expression levels of programmed death ligand 1 (PD-L1), cluster of differentiation 47 (CD47), phosphorylated nuclear factor κB p65 subunit (p-NF-κB p65), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) were decreased. Conclusion The aqueous extract of Euphorbia helioscopia L. can effectively inhibit LPS/NNK-induced formation of lung adenoma nodules by improving the immune environment, and its mechanism may involve regulating the activation of NF-κB and STAT3.

Our findings establish SENP3 as a novel posttranslational regulator of PD-L1 that promotes immune evasion in HCC through direct deSUMOylation and stabilization of PD-L1 protein. Therapeutic targeting of SENP3 may overcome resistance to immune checkpoint inhibitors in HCC by restoring antitumor immunity.

These strategies underscore the transformative potential of peptide therapeutics to harness the immune system and reshape TME, offering a promising avenue for more effective and durable TNBC treatment. SIGNIFICANCE STATEMENT: With growing interest in peptides as tumor microenvironment modulator, this review provides an in-depth analysis of interactions and crosstalk between immune and tumor cells and explores therapeutic potential of peptides in modulating immune cell signaling pathways, with ultimate impact as anticancer agents for triple-negative breast cancer.

Neutralization of mouse or human HE4 with monoclonal antibodies reduced myeloid PD-L1 expression, restored CD8+ T cell activity, and suppressed tumor growth in syngeneic and humanized models, while inducing fewer irAEs than PD-1 blockade. Clinically, high HE4 expression predicts poor prognosis but correlates with improved response to PD-1 inhibitors in lung adenocarcinoma, highlighting HE4 as both a therapeutic target and predictive biomarker.

P2, N=284, Active, not recruiting, National Cancer Center, Korea | Trial completion date: Jan 2027 --> Dec 2027 | Trial primary completion date: Jan 2024 --> Dec 2026

P1, N=8, Terminated, Pfizer | Active, not recruiting --> Terminated; The trial was terminated for strategic business reasons; the decision was not based on any safety and/or efficacy concerns

P4, N=35, The first affiliated hospital of anhui medical university; The first affiliated hospital of anhui medical university

P2, N=44, Shandong First Medical University and Shandong Academy of Medical Sciences (Shandong Cancer Hospital ＆Institute); Shandong First Medical University