P2, N=54, Completed, Hospices Civils de Lyon | Unknown status --> Completed | Trial completion date: Oct 2023 --> Jun 2026 | Trial primary completion date: Oct 2023 --> Jun 2026

In addition, mTOR pathway activity and responsiveness to mTOR inhibitors (rapamycin and ipatasertib) and chemotherapeutic agents (cisplatin) were assessed. Compared with 2D monolayer cultures, 3D TMSs exhibited reduced mTOR signaling activity, which led to significantly decreased sensitivity to mTOR inhibition. These findings indicate that 3D bioprinted breast cancer models recapitulate key structural and signaling features of in situ tumors more accurately than 2D systems, highlighting their potential value for preclinical drug testing and mechanistic studies.

IL-22 promotes LUAD progression by activating the PI3K/AKT signaling pathway and inducing EMT, while its upregulation is modulated by promoter hypomethylation and miR- 21-5p suppression. The IL-22/PI3K/AKT axis represents a potential therapeutic target for LUAD management.

Importantly, cotreatment with venetoclax and the clinically available AKT inhibitor capivasertib effectively restored sensitivity in both cell lines and patient-derived primary AML samples with high EVI1 expression. Overall, our findings reveal a novel molecular mechanism underlying EVI1-mediated venetoclax resistance through PI3K/AKT-driven MCL-1 stabilization and suggest a combination strategy involving AKT inhibition as a promising approach for overcoming therapeutic resistance in this high-risk AML subset.

Notably, the oncogenic effects of GJB6 ablation could be pharmacologically reversed by the AKT inhibitor capivasertib, suggesting a potential therapeutic strategy for GJB6-deficient ESCC patients. Collectively, our findings establish GJB6 as both a critical suppressor and a clinically actionable prognostic biomarker, highlighting the potential of drug repurposing approaches for ESCC treatment.

The drug is administered orally once weekly and is well tolerated. Dordaviprone offers a new targeted systemic therapy for DMG with proven safety, good tolerability, and meaningful clinical benefit.

This study defines an oncogenic axis wherein ELYS promotes HCC stemness and metastasis by activating PI3K/AKT, triggering a FOXO6-NUP205 cascade to drive Hedgehog, representing a pivotal mechanism and therapeutic target.

Drug sensitivity analyses identified candidate agents such as YM201636 and AT7867, though their applicability to VS requires dedicated validation. This study contributes to understanding the molecular mechanisms of Schwann cells in benign nerve sheath tumors while providing preliminary evidence for future therapeutic investigation.

This study identified oxidative stress-correlated DEGs and prognostic risk model in sevoflurane-treated GBM for computationally predicting potential immunotherapy response and drug sensitivity. Therefore, THBS1 mediated a protective response against sevoflurane-induced cytotoxicity and migration inhibition in GBM via PI3K/AKT activation, highlighting a potential molecular interaction between anesthetic exposure and tumor cell behavior.

β-Ecd attenuates Ang II-induced premature senescence in HASMCs by enhancing autophagy and limiting oxidative stress, a process mediated by suppressed AKT/mTOR signaling.

The recent ONC201 FDA approval, however, suggests DIPG therapy is tractable...A proof-of-concept in vivo mouse xenograft experiment demonstrated a reduction in tumor volume beyond antibody treatment alone. The work here represents an important milestone in preclinical development of a novel deruxtecan-based ADC agent for an intractable pediatric brain cancer, concurrent with other ADC agents demonstrating real-world clinical efficacy and gaining approvals in multiple disease indications.