Melanoma

P1, N=10, Active, not recruiting, University Hospital, Basel, Switzerland | Trial completion date: Jun 2025 --> Jun 2026 | Recruiting --> Active, not recruiting

P1/2, N=49, Recruiting, Toray Industries, Inc | Active, not recruiting --> Recruiting

Our findings underscore the utility of scRNA-seq in dissecting the cellular complexity of fibrotic skin diseases and highlight potential therapeutic targets. This study not only advances our understanding of fibroblast heterogeneity in fibrosis but also opens avenues for targeted therapeutic strategies, moving closer to personalized medicine for fibrotic diseases.

Given its crucial role in mediating DNA damage responses, we analyzed the p53 protein functionality and downstream target activation in a panel of UM cell lines in response to standard-of-care treatments (i.e., cisplatin and proton-beam irradiation)...Our results indicated a correlation between higher expression levels of Δ40p53α or Δ133p53γ isoforms and the development of more aggressive cancers. Our findings suggest that shorter p53 isoforms can promote cancer aggressiveness and therapy resistance, thereby providing crucial insights into UM pathogenesis.

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.

P1, N=77, Active, not recruiting, Amgen | Recruiting --> Active, not recruiting | N=535 --> 77

Core ICRG genes demonstrate elevated expression in both cell lines and clinical specimens, supporting their potential role as disease-associated genetic risk loci. ICRG modification patterns provide critical insights into TME infiltration heterogeneity, enabling refined prognostic assessment and therapeutic targeting strategies.

In vitro studies against B16F10 melanoma cells demonstrated potent synergistic effects: the system achieved significant cell killing (viability <50% at 50 μg/mL) and promoted marked apoptosis, as evidenced by the profound upregulation of key pro-apoptotic proteins (caspase-3: 1.85-fold; Bax: 2.26-fold) and downregulation of Bcl-2 (0.44-fold). Our work highlights MWCNTs/HSA-DOX as a promising nanomedicine that successfully integrates photothermal ablation with controlled chemotherapy to trigger enhanced apoptotic death in melanoma cells.

Stem-memory but not effector-memory cells exhibited similar antitumor efficacy and lymph node trafficking patterns to the naïve cells in mice with high-avidity neoantigen tumors. These findings highlight how differential tumor antigens shape divergent cellular fate and uncover a critical role of T cell trafficking in lymph nodes in shaping high-avidity neoantigen-specific antitumor responses.

6-MF targets PTBP1 to inhibit circPIAS1 biogenesis and reduce circPIAS1-108aa.6-MF inhibits PI3K-AKT pathway; combined with IFN-γ, it enhances STAT1 phosphorylation, inhibits SLC7A11/GPX4 pathway, promoting melanoma ferroptosis. Its combination with PD-1 inhibitor enhances antitumor efficacy, providing a novel therapeutic strategy for melanoma treatment.

Drug sensitivity profiling nominated imatinib (Vina score: -8.9 kcal/mol) and TTNPB as potential therapies for UBD-high tumors, validated by stable MD simulations. In esophageal carcinoma (ESCA), UBD expression escalated with tumor stage and predicted poor survival (p<0.05).UBD enhances the proliferation and migration of esophageal cancer cells by modulating the TP53 signaling pathway, as validated through transcriptomic analysis and functional assays. This study advances UBD as a prognostic indicator and therapeutic target, bridging molecular insights with clinical translation in precision oncology.

The ARS-LS-Gel platform's ability to simultaneously address oncogenic progression and tissue repair represents a significant conceptual and practical advancement in post-surgical cancer management. By bridging fundamental mechanistic discovery with engineered therapeutic delivery, our findings provide a robust foundation for imminent translational development in melanoma therapy and beyond.