P2, N=35, Completed, Melanoma Institute Australia | Active, not recruiting --> Completed

P1, N=31, Recruiting, M.D. Anderson Cancer Center | Not yet recruiting --> Recruiting

Our work redefines an immune-cell death paradox, revealing how tumors exploit IFN-β to evade therapy. We propose CADS as a translational biomarker for identifying tumors reliant on this pathway and validate a mechanism-based combination therapy that selectively targets dormancy-associated death resistance, offering a promising strategy to improve CRC outcomes.

Trametinib monotherapy offers limited CB in patients harboring NRAS-mutant malignancies. Future research should further explore the biological and clinical significance of specific NRAS codon mutations to identify biomarkers and optimize treatment approaches.

Progression-free survival was 12.8 months and overall survival reached 44.4 months. This case underscores the importance of early molecular profiling and supports the integration of targeted therapies into routine clinical practice for tumors with limited effective therapeutic options.

P1/2, N=4, Not yet recruiting, Verastem Inc.

Patients with high RCDI exhibited higher sensitivity to several targeted therapies, including Vorinostat and Trametinib. The RCDI model effectively stratifies HCC patients based on RCD-related molecular features, providing a valuable tool for predicting survival and therapeutic responses. The identification of key genes offers new insights into the molecular mechanisms of HCC and potential therapeutic targets.

Due to the lesion's inoperable location and risk of vascular and biliary compression, targeted therapy with the MEK inhibitor selumetinib was indicated. The patient is currently awaiting provision of the medication. This case underscores the importance of careful monitoring and early initiation of targeted therapy in NF1 patients with extensive plexiform neurofibromas, particularly those caused by large NF1 gene deletions, which result in complete loss of neurofibromin and extensive infiltrative benign tumor growth.

Targeted therapy with trametinib achieved partial radiologic response before further progression. The patient remains clinically stable under ongoing therapy and multidisciplinary care. This case underscores the critical role of molecular diagnostics in risk stratification and treatment selection, particularly in infants with atypically aggressive PLGG.

P2, N=57, Active, not recruiting, University Health Network, Toronto | Trial completion date: Sep 2026 --> Sep 2027 | Trial primary completion date: May 2026 --> May 2027

Patients with specific chimeric RNAs, such as BRAF and JAK2, exhibited favorable responses to trametinib or ruxolitinib, and those with more neoantigens may benefit from immunotherapy. In subcutaneous xenograft models, tumors bearing Ctsc-Rab38 responded better to anti-PD1 therapy, highlighting its potential as a biomarker and therapeutic target. These findings indicate that chimeric RNAs can produce novel fusion proteins and neoantigens, disrupt the expression and function of partner genes, and guide clinical treatment stratification in ESCC.

P1, N=16, Active, not recruiting, Pfizer | Recruiting --> Active, not recruiting