Lung Adenocarcinoma

The study results confirm the reproducibility of HER2 status assessment using a unified diagnostic approach in a multicenter setting. The application of standardized HER2 interpretation criteria ensures data comparability and provides a methodological basis for further clinicopathological studies and for the implementation of HER2-targeted therapeutic strategies in clinical practice.

Radiomic modeling has been utilized to identify NSCLC histopathological features, proteomic mutational burden, responsiveness to surgical and immunotherapy interventions, and occult lymph node metastasis. This review article provides an overview of studies using radiomic features to model risk and radiomic predictive tools such as the Computer-Aided Nodule Assessment and Risk Yield (CANARY) that have been developed to provide insight and pre-operative risk stratification for resectable NSCLC.

Importantly, treating TPX2-overexpressing cells with the autophagy inhibitor chloroquine significantly reversed their enhanced migration, proliferation, and stemness marker expression. In vivo, TPX2 silencing in xenograft models reduced tumor growth and altered autophagy marker profiles. These findings unveil a novel mechanism whereby TPX2 promotes CSC properties in LUAD by driving autophagy, offering a promising therapeutic avenue targeting TPX2-mediated autophagy.

These findings support the further development of multi-target CDK inhibitors as promising candidates to overcome tumor progression and therapeutic resistance in lung cancer.

This study reveals that hypoxia-induced lactate elevation decreases SIRT2 expression to promote LUAD progression, with the mechanism related to promoting glycolysis by increasing LDHA acetylation. In addition, decreased SIRT2 expression has also been found to cause alterations in many metabolic pathways with no verification mechanism.

In conclusion, our results support the use of an immunohistochemical panel to diagnose YST-like tumors, considering not only the most frequently expressed makers (FOXA2 and HNF1β), but also the potential expression (particularly of HNF1β) by the associated somatic neoplastic components lacking an overt YST phenotype. The consistent expression of FOXA2 and HNF1β (but not SOX17) in our cohort underscores the phenotypic overlap between YST-like tumors and YSTs of germ cell origin (type II), including shared expression of multiple pioneer transcription factors which drive the YST phenotype.

We therefore present a working model in which a hypoxia-associated HIF-1α/S100A8/A9 axis may bypass RAGE inhibition and restore pro-tumor signaling; however, this mechanism requires direct experimental validation. Overall, our data highlight the importance of tumor-microenvironment context when interpreting RAGE-targeted interventions in LUAD.

p53 IHC, particularly using a ≥40% cut-off at 3+ intensity, is an accurate and accessible surrogate for TP53 mutation detection in LUAD patients. This method facilitates rapid molecular stratification, optimal resource utilization and informed prognostic and therapeutic decision-making in routine pathology practice.

This axis sustains the tumor-initiating and regenerative capacity of LUAD progenitor cells. By illuminating the role of L1CAM and PCP signaling in the generation of SOX2+ LUAD progenitors, our findings identify potential new targets to treat metastatic cancer.

As these genes have extra-P-body functions, the score serves as a transcriptomic proxy for P-body component enrichment, not a direct measure of P-body activity. Despite this limitation, it offers a clinically useful tool for risk stratification and mechanistic hypotheses.

Our study identifies a four-gene cell cycle signature associated with poor LUAD prognosis and demonstrates that astragalin induces apoptosis in LUAD cells. These genes are involved in a PANoptosis-related network, suggesting a potential mechanistic link requiring further validation.

The observed loss of phagocytic capacity reflects dynamic functional state transitions toward an inflammatory and hypoxic phenotype rather than the passive enrichment of a single subpopulation. These insights provide a single-cell evolutionary framework for metastasis-associated immune reprogramming and underscore the potential of CD74 as a target for therapeutic intervention.