P4, N=0, Withdrawn, SRH Wald-Klinikum Gera GmbH | N=101 --> 0 | Not yet recruiting --> Withdrawn

P2, N=25, Active, not recruiting, Fondazione Policlinico Universitario Agostino Gemelli IRCCS | Recruiting --> Active, not recruiting

The authors discuss adverse event management and the implications for integration into routine clinical practice. Clinicians caring for patients with low-grade serous ovarian carcinoma can use the drug knowledge and evidence outlined in this review to assist with implementing avutometinib and defactinib therapy.

KSR1 knockdown did not substantially affect ppERK responses to Type I½ RAF inhibitor (Encorafenib) in both cell types, whereas ppERK sensitivity slightly decreased for Type II RAFi (TAK-632) in MCF7 cells, aligning with simulations. The efficacy of MEKi (Cobimetinib) slightly increased in MCF7 cells following KSR1 knockdown but slightly decreased in PSN1 cells where higher MEKi concentrations were required to suppress ERK signaling, as predicted by the model. Our computational models predict, and experiments validate that in RAS-mutant cells, two conformation-specific RAF inhibitors used in combination suppress the ERK pathway more effectively than a combination of MEK and RAF inhibitors irrespective of KSR1 levels.

P2, N=36, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

Our findings demonstrate that laparoscopic caudate lobectomy after neoadjuvant therapy is a feasible approach for managing resectable HCC with high risk of recurrence located in the caudate lobe.

P2, N=24, Active, not recruiting, Providence Health & Services | Trial completion date: Jan 2027 --> Dec 2028 | Trial primary completion date: Jan 2026 --> Dec 2027

P=N/A, N=50, Active, not recruiting, Pierre Fabre Ltd | Recruiting --> Active, not recruiting

P2, N=50, Recruiting, Emory University | Trial completion date: Sep 2028 --> Sep 2029 | Trial primary completion date: Mar 2028 --> Mar 2029

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.