P3, N=480, Active, not recruiting, Merck Sharp & Dohme LLC | Trial primary completion date: Jun 2028 --> Aug 2025 | Trial completion date: Dec 2029 --> Mar 2026

P1/2, N=144, Recruiting, Tongji Hospital

Further, we performed a post-hoc exploratory analysis and developed an XGBoost model (scPro-X) using scRNA-seq data from pre-treatment tumor samples to predict 12-week ORR identified CD4_Tfh_CXCL13 and CD8_Tex_CTLA4 as potential biomarkers predictive of response. These findings demonstrate that IBI318 plus lenvatinib exhibit promising clinical activity and a manageable safety profile in patients with advanced NSCLC.

Following confirmation of multiple lung metastases, the patient was treated with doxorubicin monotherapy. Subsequent next-generation sequencing (NGS) revealed a RET fusion, leading to the diagnosis of an RET-rearranged spindle cell neoplasm. This case highlights the importance of genomic testing for certain spindle cell sarcomas and the potential benefit of RET-specific inhibitors against RET-altered sarcomas.

Silencing CLEC4G could reverse the effect of LiCl on PLC/PRF/5-R. CLEC4G modulates the PD-1 expression of HCC cells through the Wnt/β-catenin pathway, thereby reversing the resistance to Lenva.

Emerging evidence from clinical trials supports the efficacy of RET inhibitors in RET-altered PDAC. Broader integration of genomic testing in PDAC may uncover new therapeutic opportunities and improve patient outcomes.

Advancements in single-cell analysis and spatial transcriptomics are anticipated to unveil actionable molecular patterns and support the development of individualized strategies to interrupt immune evasion and therapeutic resistance in EC. These advances offer promise for personalized immunotherapy approaches that could significantly improve outcomes in endometrial cancer patients.

Notably, patients harboring TP53 alterations derived clinical benefit from adjuvant lenvatinib following curative surgery. In conclusion, TDS enables effective identification of MRD-associated genomic alterations and stratifies HCC patients who may benefit from adjuvant lenvatinib, providing a molecular basis for personalized postoperative management.

Sintilimab plus lenvatinib showed heterogeneous efficacy in HCC. High LINC01554 expression, elevated CD4+ Tcm cells, and solitary tumors may serve as predictive biomarkers for prolonged disease control.

Moreover, knocking down SOX4 could reverse the NOVA1 overexpression-mediated desensitization of HCC cells to Lenvatinib-induced cell apoptosis. In summary, this investigation indicates the essential role of NOVA1 self-renew of CSCs and tumorigenesis in the liver, suggesting it as an optimal HCC therapeutic target.

Tumor volume, apoptosis, KI67, YBX1, and JAK2/STAT3 phosphorylation levels were reduced in tumor tissue after RIOK1 knockdown and increased after further YBX1 overexpression. Overall, RIOK1 activates the JAK2/STAT3 pathway by promoting YBX1 phosphorylation, leading to HCC progression and lenvatinib resistance.

P1/2, N=30, Completed, National Taiwan University Hospital | Active, not recruiting --> Completed | Trial completion date: Dec 2024 --> Oct 2025