P2, N=29, Recruiting, Seoul National University Hospital | Trial completion date: Dec 2027 --> Dec 2028 | Trial primary completion date: May 2026 --> Dec 2027

Moreover, in vivo studies in MOC2-induced tumor-bearing mice demonstrated a significant upregulation of ER stress markers, including PERK and PDI, as well as remodeling of macrophages, characterized by the upregulation of M1 markers, such as iNOS, TNF-α, and CD86. Thus, BTZ@GOT is an efficient nanotherapy that warrants further exploration for the treatment of oral carcinoma.

Gene enrichment analysis indicated pathways involving potassium channel regulation and thromboxane signaling to be implicated. This integrative metabolomic and genetic investigation supports a potential protective role of glycoursodeoxycholic acid in cardiovascular vulnerability and motivates larger, carfilzomib-specific studies to evaluate its utility for risk stratification.

P=N/A, N=12, Not yet recruiting, Zhejiang Xiaoshan Hospital; Hainan Dermavon Pharmaceutical Technology Co., Ltd.

The combination of rosuvastatin and bortezomib exerts a synergistic effect by inhibiting CCL3, thereby rebalancing bone remodeling and promoting osteogenesis. This strategy represents a promising novel therapeutic approach for mitigating MBD.

Rescue experiments used N-acetylcysteine (NAC) and chloroquine (CQ)...CQ but not MG-132 increased CD276 expression in ESCC cells...SLC1A5 enhances CD276 stability by suppressing ROS-autophagy signaling, promoting ESCC progression. Targeting glutamine metabolism to enhance CD276 degradation might be a novel therapeutic strategy for ESCC.

We then focus on hematological malignancies, especially multiple myeloma, where recent reports implicate the autophagy-related protein GABARAP in bortezomib-induced ICD. Finally, we discuss the translational implications, including rational combinations of autophagy modulators with ICD-inducing chemotherapies, targeted drugs, and cellular immunotherapies, and outline the remaining challenges for safely harnessing the autophagy-ICD axis in the clinical setting.

Factors related to MM may influence systemic cytokine levels in BIPN patients, limiting conclusions on their role in BIPN pathophysiology and their utility as drug targets.

Energy decomposition analysis identifies key interacting residues Pro171, Ile174, and Ala66 that anchor the inhibitors. Although both ligands induce subtle constriction of the channel pores, Bacopaside II establishes a more persistent hydrogen bonding network, underscoring its unique energetic contribution to the inhibition profile. Overall, these findings provide a detailed mechanistic blueprint for AQP1 inhibition by Bacopasides and offer a structural framework for the rational design of next-generation AQP1-targeted anticancer therapies.

P2, N=42, Completed, University of Chicago | Active, not recruiting --> Completed

Treatment of MM cells with the selective AURKA inhibitor LY3295668 induced dose-dependent cytotoxicity, caspase-3/7 activation, and cellular senescence. These findings underscore AURKA expression as a prognostic marker in plasma cell disorders and support the therapeutic potential of combining AURKA inhibition with selinexor for bortezomib-resistant MM and PCL. To explore biomarker-driven strategies for optimizing therapeutic outcomes, future studies are warranted.

Serial assessments were performed before and during treatment with bortezomib and dexamethasone for MM, and later with daunorubicin/cytarabine for AML. It demonstrates the earliest events in pDC-AML evolution. Furthermore, the immature immunophenotype raises the question of appropriate treatment, since a diagnosis of acute undifferentiated leukemia can be established.