Furthermore, the OST inhibitor NGI-1 and NGI-1-loaded nanoparticles exerted potent antitumor effects and further augmented the efficacy of lenvatinib and immunotherapy. These findings highlight DDOST as a promising therapeutic target to improve treatment outcomes in HCC.

In conclusion, the study demonstrates that ATEZO/BEV significantly improves OS compared to LEN in patients with unresectable HCC, despite similar PFS, ORR, and DCR. Both treatments have comparable safety profiles.

In vitro pharmacological inhibition of FGFR2 with a selective inhibitor Futibatinib further demonstrated that it inhibited DLBCL cell growth, cell proliferation, induced cell cycle arrest, promoted cell apoptosis. Further in vivo study found that combination of Futibatinib with chemotherapy displayed better anti-tumor activity relative to single drug therapy in DLBCL treatment.Collectively, our data highlight the importance of considering the GALNT3-FGFR2-MAPK signaling axis as an attractive therapeutic target for lymphomagenesis.

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.

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.

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.

Pooled positive selection screens identified 474 activating and 738 mutations mediating resistance to the FGFR inhibitors pemigatinib and futibatinib, together revealing 301 druggable FGFR mutations analogous to a strong PS3/BS3 evidence level. The functional screens identified 97% of acquired resistance mutations in clinical trials. Our comprehensive catalog of every druggable mutation in the FGFR kinase domains is readily available for clinical decision support.