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

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

Molecular docking and 100-ns molecular dynamics simulations against BRAF kinase (PDB: 6V34) suggested that Myfracone A and Myfracone G may interact stably with the target protein (RMSD < 3 Å). These findings provide preliminary insight into potential bioactive constituents of mace oleoresin and support further bioactivity-guided investigation.

Additionally, consistent "Rho GTPase signaling" changes were observed across both proteomic and phosphoproteomic analyses, underscoring the functional reactivation of this pathway in resistant tumors. In summary, these findings reveal molecular signatures of early response and acquired resistance to vemurafenib and offer a valuable resource for future investigation of BRAF-targeted therapy.

These findings suggest that delivering vemurafenib in polymeric nanocapsules produces delayed but sustained cytotoxic and apoptotic effects in ATC cells in vitro, warranting further investigation of this nanocarrier approach for thyroid cancer treatment. Altogether, the biological results reported in this study are derived from in vitro experiments and require further validation in in vivo models.

The CRHBP-UCN2 axis critically regulates KIRC prognosis and immune microenvironment remodeling. CRHBP serves as a reliable prognostic biomarker and a potential anticancer peptide target, while dabrafenib is a promising therapeutic agent for KIRC.

Furthermore, the combination of vemurafenib with cysmethynil, a proof-of-concept ICMT inhibitor, showed efficacy in combating RAC1P29S-driven resistance of BRAFV600E melanoma cells in both in vitro and in vivo settings...We further validated the role of TAZ in RAC1P29S-driven resistance by demonstrating that introducing a constitutively-active TAZ mutant enhanced the resistance to MAPK pathway inhibitors in native cells, phenocopying the effect of RAC1P29S. The novel application of MAPK pathway inhibitors and cysmethynil combination in RAC1P29S-driven MAPK-pathway-inhibitor-resistant melanoma cells extends the potential utility of ICMT inhibitors, and also provides a new mechanism for targeting ICMT in cancer.

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.

Our findings identify TYRP1 as a marker of a highly proliferative melanoma subpopulation that promotes tumor progression through the GPNMB-Notch1-SOX10/MITF axis. The TYRP1-SOX10-MITF feedback loop represents a key driver of melanoma proliferation and a potential biomarker for stratifying therapeutic response, offering a novel avenue for precision treatment in melanoma.

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

P=N/A, N=82, Completed, Novartis Pharmaceuticals