MET (MET proto-oncogene, receptor tyrosine kinase)

P2, N=60, Active, not recruiting, Duke University | Trial completion date: Mar 2026 --> Nov 2026

The clinical future lies in interception: leveraging liquid biopsies for early detection, targeting both tumor-intrinsic vulnerabilities and permissive metastatic niches and adapting therapy dynamically to anticipate resistance. Understanding this genomic odyssey is essential for transforming mCRC into a controllable chronic condition.

P1, N=158, Active, not recruiting, Janssen Research & Development, LLC | Trial completion date: Dec 2026 --> Apr 2027

Here, we report circular, dual-targeting multivalent aptamer-drug hybrids (Dualo-mvApDHsD/S) that codeliver doxorubicin (Dox) and STING agonist (diABZI) for synergistic chemo-immunotherapy...Notably, Dualo-mvApDHsD/S synergize with PD-1 blockade to achieve durable tumor eradication and long-term protection. These findings establish multivalent aptamer-drug hybrids as a versatile platform for multitarget, multipayload precision therapeutics and highlight their potential for next-generation TDC design.

The study underscores the importance of integrating NGS-based molecular testing with PD-L1 evaluation for personalised management of NSCLC. Distinct patterns of PD-L1 expression across molecular subtypes, particularly lower in EGFR-mutated tumours and higher in KRAS-mutated tumours, underscore the need for tailored therapeutic strategies and informed sequencing of targeted therapies and immunotherapies.

Using FMI data, clinicians were able to direct patients toward clinical trials and to modify SOC clinical management for several NSCLC patients. These results demonstrate the benefit of FMI genomic profiling in identifying actionable driver mutations that would otherwise be missed by SOC methodology. The findings suggest that CGP is a promising and robust tool for improving personalized medicine in NSCLC treatment in Spain.

These findings demonstrate that aPFs mediate the cross-talk between cholangiocytes and hepatocytes, regulate hepatocyte functions, and that Msln-Muc16 signaling in aPFs is pathogenic for cholestatic fibrosis and HCC. Msln and Muc16 may become novel targets for anti-fibrotic therapy and HCC patients with sclerosis cholangitis.

The proportion of the patients benefitting of the treatment and its safety profile justify larger, controlled studies to further investigate the added role of combining cabozantinib with metronomic temozolomide. ClinicalTrials.gov identifier: NCT04893785.

Using the IsoTar target prediction tool, we identified STAT3 as a key regulator and confirmed STAT3 protein downregulation upon transfection with miR-411ed. We further investigated the effect of miR-411ed in vivo, observing a reduction in tumor size with miR-411ed in combination with Osimertinib but not with miR-411ed or Osimertinib treatment alone, confirming the effectiveness of miR-411ed in TKI response.

MCPIP1 plays a protective role against inflammation-driven hepatocarcinogenesis, particularly in females, by restraining fibrotic remodeling and oncogenic signaling. The downregulation of MCPIP1 expression promotes a tumor-promoting microenvironment through the coordinated activation of the β-catenin, STAT3, and CREB1 pathways.

The use of molecular testing has increased significantly in the last 20 years, and the -adaptation of new targeted therapies has been rapid.