Non Small Cell Lung Cancer

Notably, synthetic PAMP administration recapitulates these anti-tumor effects, effectively reducing intracellular proline levels and impairing tumor progression in cellular and animal models. Together, our findings uncover a previously uncharacterized lncRNA-encoded micropeptide that orchestrates proline metabolic reprogramming to restrain LUAD development, offering new opportunities for metabolic intervention in precision oncology.

P2, N=52, Not yet recruiting, Montefiore Medical Center | Trial completion date: Oct 2028 --> Feb 2029 | Initiation date: May 2026 --> Sep 2026 | Trial primary completion date: Dec 2027 --> Apr 2028

P=N/A, N=400, Recruiting, Sheba Medical Center

P2, N=32, Recruiting, Nanfang Hospital, Southern Medical University

This first documented case demonstrates the therapeutic efficacy of crizotinib in ALK-IR rearranged NSCLC, emphasizing the importance of comprehensive molecular profiling in guiding precision oncology.

The data indicate that miR-130a-3p exerts regulatory control over the ZDHHC5 gene, consequently modulating the function of CD28 on secreting Tregs, thereby promoting LUSC occurrence. These insights provide a novel theoretical foundation for the development of immunotherapeutic and targeted treatment strategies for LUSC.

In vitro, LEPR knockdown significantly inhibited proliferation and invasion while promoting apoptosis in LUSC cells. These findings suggest that LEPR may play a critical role in the development and progression of LUSC, providing a potential target for therapeutic intervention.

Our findings define GPNMB-ECD-driven resistance as a novel paradigm in NSCLC and identify a viable precision therapeutic strategy to overcome it.

Specific DEGs for NSCLC are present in platelets, including HSP90AB1, NPM1, CD44, and CD74, which may play a role in the early stages of NSCLC development. These genes exhibit a specific expression pattern, characterized by downregulation in early-stage (I and II) NSCLC, indicating their potential as biomarkers for early screening and diagnosis of NSCLC.

LY86-AS1 upregulates RB1CC1 expression by sponging miR-132-3p, thereby inhibiting the malignant progression of NSCLC and is a potential prognostic biomarker and therapeutic target for NSCLC.

Our study identifies CHCHD3 as a mitochondrial protein upregulated in lung cancer that contributes to tumor cell proliferation and survival.

MTT was the most common second-line treatment, however, outcomes were generally poor, emphasizing the unmet need for effective second-line treatments for HER2-mutant NSCLC.