Tumor organoids may be more suitable for clinical personalized chemotherapeutic drug screening in lung adenocarcinoma.

Objective: The formulation of precision treatment strategies and the analysis of drug-resistance mechanisms for lung adenocarcinoma are highly dependent on Methods: The study utilized a three-dimensional (3D) organoid model, a 2D adherent model, and an animal model constructed from the A549 cell line to dynamically monitor drug responses to chemotherapeutic treatments. We analyzed cell cycle arrest, proliferation inhibition, and the invasive regulatory features mediated by the human epidermal growth factor receptor 2(HER-2) mediated invasive regulatory features. The evolution of the resistance mutation spectrum was tracked through dynamic gene sequencing and compared with clinical resistance samples. Comparisons between two groups were performed using t-tests, while comparisons involving three or more groups were conducted using one-way analysis of variance (ANOVA). Results: In studies of four chemotherapy regimens (etoposide, paclitaxel, cisplatin, and carboplatin), organoid models showed a pharmacodynamic profile highly consistent with animal models. For drug-induced cell cycle block, the organoid model accurately replicated the animal model's G2/M phase block. Analysis showed similar Conclusion: The lung adenocarcinoma organoid model accurately simulates drug sensitivity and the evolution of drug resistance, providing a highly predictive