Non Small Cell Lung Cancer

P=N/A, N=100, Recruiting, Geneplus-Beijing Co. Ltd. | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Jun 2027

P1, N=75, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting

P2, N=19, Active, not recruiting, Georgetown University | Recruiting --> Active, not recruiting | N=54 --> 19

Nearly 7% of EGFR mutations in NSCLC patients were compound mutations, which is comparable to previous reports. The presence of multiple mutations, particularly those involving T790M , may be associated with potential resistance to first-line EGFR -TKIs. We describe a triple mutation involving del19 + G719X + S768I , which represents an uncommon scenario.

Our findings support a monoclonal origin for ASC, with smoking influencing divergent evolutionary trajectories and immune microenvironment characteristics between ACC and SCCC. These insights provide a molecular framework for personalized ASC therapies.

We developed and validated an interpretable, [18F]FDG PET/CT-based nomogram integrating SUVmax and clinical-pathological features to non-invasively predict PD-L1 high expression in resectable NSCLC. This study suggests that traditional LR offers comparable predictive accuracy to complex ML algorithms, while providing enhanced clinical transparency and a potential non-invasive adjunct for personalized nCIT decision-making.

Findings on EGFR mutations were consistent with the national and international literature. However, PD-L1 expression rates were higher than those typically reported in Brazilian studies, highlighting regional variation in biomarker prevalence.

The SCLC component dictated adjuvant cisplatin-etoposide regardless of the accompanying adenocarcinoma histology. This case report exemplifies the importance of integrated histologic and molecular evaluation, and the need to recognize potentially actionable mutations in combined SCLC. Comprehensive profiling not only clarifies clonal relationships and may guide therapeutic strategies, including in the context of recurrence or combined presentations.

STK11 mutations with KEAP1 or KRAS co-mutations are associated with significantly worse survival outcomes in mNSCLC compared with patients without these co-mutations. These findings underscore the urgent need for targeted therapies to improve prognosis in this high-risk population.

To augment signal analysis, we integrate deep learning-based segmentation using Cellpose and U-Net to extract quantitative data from single-cell and in vivo imaging, respectively. This AI-assisted workflow significantly improved measurement reproducibility and enabled high-content quantification of protease activity distributions and tumor-to-background ratios, establishing a robust platform for dual-protease sensing in complex biological systems.

APOBEC mutational signatures represent a robust predictive biomarker for ICI response in TMB-low metastatic NSCLC, identifying responders particularly among PD-L1-negative patients where biomarker guidance is most needed, detectable from targeted gene panels used in routine clinical practice.

In vivo, 5Z7 plus cisplatin suppressed resistant tumor growth without notable organ toxicity. This study establishes TAK1 as a key hub in cisplatin resistance and shows that 5Z7 reverses resistance by targeting TAK1 to coordinately regulate NF-κB/p53 signaling, providing a foundation for potential clinical translation.