Melanoma

P=N/A, N=58, Active, not recruiting, Wake Forest University Health Sciences | Recruiting --> Active, not recruiting | N=244 --> 58

P1, N=40, Active, not recruiting, Iovance Biotherapeutics, Inc. | Recruiting --> Active, not recruiting

P2, N=7, Active, not recruiting, H. Lee Moffitt Cancer Center and Research Institute | Trial primary completion date: Jan 2027 --> Dec 2025

P2, N=20, Not yet recruiting, M.D. Anderson Cancer Center

SAM.1 hydrogel acted as a two-in-one scaffold, controlled release and an immunomodulatory agent, to enhance the persistence and antitumor function of Vγ9Vδ2 T cells. This strategy provided a new paradigm for γδ T-cell-based immunotherapy in melanoma.

Additionally, knockdown of the core risk gene keratin 17 (KRT17) inhibited the invasion and proliferation of B16 cells, demonstrating the role of KRT17 in the progression of SKCM. This study proposed a novel STIRS model and selected the core risk gene KRT17 for functional validation, which had potential as a prognostic tool and a guide for creating personalized therapies for SKCM patients.

We report here a patient on encorafenib who developed numerous new pigmented lesions within 3 weeks of therapy...This case underscores that BRAF inhibition may enhance PRAME expression in benign melanocytic nevi, potentially through mechanisms involving mitogen-activated protein kinase (MAPK) activation, altered Erk phosphorylation, or disruption of retinoic acid (RA) signaling. This case also brings awareness to the potential of medication-induced PRAME expression and encourages both dermatologists and dermatopathologists to avoid overdiagnosis as PRAME continues to gain prominence as a diagnostic biomarker.

These co-regulated proteins highlight the integration of BRAF signaling with critical processes, such as cell cycle control, apoptosis, DNA damage response, and protein synthesis in melanoma. Our analysis suggests that targeting BRAF-interacting proteins may also modulate oncogenic signaling pathways and represent promising biomarkers for melanoma diagnosis and therapy.

Moreover, increased proapoptotic signaling (SK-MEL-1) was clearly observed, with increased expression of caspase-3 (UVA) and caspase-8 (CBG or UVA). Thus, CBG does not explicitly promote apoptosis but influences it by regulating oxidative and inflammatory processes in a cell-type-dependent manner.

The study's complete pipeline identified Ombuin as a potential hit compound. In the future, in vitro and in vivo studies should be conducted to confirm its therapeutic potential against melanoma and breast cancer.

The efficacy of the CD40 agonist was partially dependent on CD8⁺ T cells. Our findings underscore the complex role of IL-1 signaling in modulating immune responses in PDAC and caution against pursuing IL-1R1 blockade, either as monotherapy or combined with agonistic CD40 antibodies, in clinical trials for PDAC.

P2, N=101, Recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Sep 2026 | Trial primary completion date: Jun 2026 --> Sep 2026