P2, N=40, Active, not recruiting, The University of Texas Health Science Center at San Antonio | Recruiting --> Active, not recruiting | Trial completion date: Mar 2026 --> Mar 2027

These findings suggest that rapamycin enhances the mechanistic efficacy of cisplatin by specifically targeting and reducing cisplatin-induced stemness (CD133+ CSC population). This study proposes a viable combination therapy for HNSCC involving an mTOR inhibitor and a platinum-based drug to overcome CSC-mediated resistance.

P2, N=12, Not yet recruiting, Huashan Hospital

In tumor necrosis factor-alpha (TNFα)-induced L6 myotubes, SA significantly suppressed inflammatory cytokine expression through inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and attenuated forkhead box O3a (FoxO3a)-dependent protein degradation, while restoring protein kinase B (Akt)/mechanistic target of rapamycin (mTOR)-dependent anabolic signaling to promote myogenic differentiation and protein synthesis...Furthermore, molecular docking analysis revealed that SA interacts with the activation pocket of phosphoinositide 3-kinase (PI3K), providing structural insight into the mechanism of anabolic signaling reactivation. Collectively, these findings demonstrate that SA mitigates immobilization-induced skeletal muscle atrophy by suppressing NF-κB-mediated inflammatory signaling and restoring muscle protein turnover through reactivation of the PI3K/Akt/mTOR signaling pathway, highlighting its potential as a functional compound for preserving skeletal muscle health under immobilization conditions.

This nine-BRM prognostic model serves as a potential prognostic stratification tool that may complement existing clinical parameters in evaluating the outcomes of KIRC patients.

We detail a two-step mechanism where mTORC1 first 'primes' the enzyme by relieving internal constraints, allowing mTORC2 to complete the activation process. By reconciling these different models and addressing long-standing questions about drug sensitivity, this review establishes a modern framework for S6K1 biology and identifies new opportunities for precise therapeutic intervention.

Several signaling pathways are crucial in CAF development, including fibroblast activation protein (FAP), phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR), Janus kinase/signal transducers and activators of transcription (JAK/STAT), nuclear factor κB (NF‑κB), transforming growth factor β (TGF‑β), ferroptosis, apoptosis and autophagy pathways...The present review summarized current studies on small molecule compounds that inhibit CAF progression, encompassing inhibitors of the PI3K/AKT/mTOR, JAK/STAT, TGF‑β and NF‑κB pathways, as well as activators of the FAP, ferroptosis, apoptosis and autophagy pathways. These small molecule compounds underscore the significance of CAFs in tumor progression and suggest novel strategies for cancer treatment by targeting CAFs in clinical settings.

P2/3, N=60, Not yet recruiting, Boston Children's Hospital | Trial completion date: Apr 2030 --> Sep 2030 | Initiation date: Apr 2026 --> Sep 2026 | Trial primary completion date: Apr 2030 --> Sep 2030

These modified compounds can be tested to determine which are most effective on cancer treatment. These findings are important in the development of multi-functionalized niclosamide and drug design therapy in the future.

In conclusion, our findings demonstrate that trapping cells in a state of high autophagic flux through simultaneous induction and late stage inhibition, is a potent strategy to trigger non-apoptotic cell death in leukemia. This approach represents a promising therapeutic strategy to overcome apoptosis-resistant leukemia.

Upon confirming KHE diagnosis, we initiated a combined sirolimus and prednisone treatment. In this report, we also discuss the clinical manifestations, imaging features, histopathological characteristics, and treatment options for this KHE subtype and review relevant literature. This case highlights the diagnostic features and therapeutic considerations of superficial KHE without KMP, emphasizing the importance of multidisciplinary evaluation.