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.

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

In conclusion, our study demonstrated that EVs containing HSP90α, derived from lenvatinib-resistant liver cancer cells, can promote EMT and drug resistance in HCC cells by stimulating CXCL8 secretion from macrophages. This finding may provide new insights and strategies to overcome lenvatinib resistance in the future.

These findings suggest that tinengotinib might have activity in patients with cholangiocarcinoma with FGFR2 fusions that progressed following FGFR inhibitor therapy. Anti-tumour activity was also observed in patients with other FGFR alterations. The data from this phase 2 study supported the initiation of a phase 3 registration trial.

The patient was initially diagnosed with T4bN1bM1 and experienced disease progression following surgery and lenvatinib treatment. This possibility is supported by reliable evidence for the use of BRAF plus MEK inhibitor for brain metastasis from BRAF-mutated malignant melanoma. We conclude that encorafenib plus binimetinib treatment for brain metastasis from BRAF-mutated thyroid cancer is a safe and effective treatment choice.

P2, N=408, Completed, Merck Sharp & Dohme LLC | Active, not recruiting --> Completed

P2, N=29, Not yet recruiting, Tianjin Medical University Cancer Institute and Hospital

P2, N=160, Completed, Merck Sharp & Dohme LLC | Active, not recruiting --> Completed