Non Small Cell Lung Cancer

P2, N=19, Not yet recruiting, Shanghai Chest Hospital

P=N/A, N=56, Active, not recruiting, Fudan University | Not yet recruiting --> Active, not recruiting | Trial completion date: Jun 2024 --> Aug 2026 | Trial primary completion date: Jun 2023 --> Apr 2026

P1/2, N=151, Recruiting, Takeda | Not yet recruiting --> Recruiting

P=N/A, N=10000, Recruiting, Spanish Lung Cancer Group | Trial completion date: Dec 2030 --> Dec 2031 | Trial primary completion date: Dec 2026 --> Dec 2030

P1, N=6, Suspended, UNC Lineberger Comprehensive Cancer Center | Not yet recruiting --> Suspended | Trial primary completion date: Jun 2026 --> Jun 2027

P3, N=327, Enrolling by invitation, Avistone Biotechnology Co., Ltd. | Trial completion date: Dec 2026 --> Jun 2030 | Trial primary completion date: Jan 2026 --> Jun 2028

Disruption of the amphiregulin-EGFR axis prevents early niche formation and abrogates tumour initiation. Conservation of this programme in KRASG12D-inducible human alveolar organoids and early-stage lung adenocarcinoma tissues identifies epithelial-microenvironment communication as a therapeutically actionable vulnerability and suggests that intercepting niche formation may prevent progression to treatment-resistant disease.

The proposed model achieved an AUC of 0.735 and an accuracy of 0.724, outperforming traditional supervised pretraining (AUC 0.695) and single-task MAE (AUC 0.712). These results demonstrate that combining self-supervised learning, multi-task learning, and GAN-based augmentation enables a reproducible and standardized model-based prediction of clinically reported PD-L1 status from CT images, providing a non-invasive complementary tool for treatment decision-making.

Clinically, an elevated FGL1/TRIM21 protein ratio is associated with poor prognosis in NSCLC. Collectively, these findings elucidate a post-translational regulatory mechanism of FGL1 in tumor progression and support the development of a rational combination immunotherapy strategy for NSCLC treatment.

Silencing of BiP markedly attenuated SAG-induced apoptosis and ferroptosis, confirming its essential role in this process. Mechanistically, SAG up-regulates BiP expression and activates the protein kinase R-like endoplasmic reticulum kinase (PERK)/eIF2α/C/EBP homologous protein (CHOP)/GADD34 signaling axis of ER stress (ERS), ultimately leading to dual induction of apoptosis and ferroptosis in vitro and in vivo.

PRO scores were maintained during osimertinib treatment of unresectable stage III EGFR-mutated NSCLC after definitive chemoradiotherapy. Together with significant PFS benefit and expected, manageable safety, the PRO data support osimertinib treatment in this setting.