Lung Cancer

PACIFIC-5 met its primary endpoint of improved PFS after either cCRT or sCRT. Follow-up for overall survival is ongoing.

It underscores the necessity of genetic testing for MPC patients and demonstrates that aggressive management of primary tumors can improve the patient's quality of life. This case provides valuable insights for clinical research and treatment strategies for MPC.

The miR-3613-5p-XPO6 axis may act as a LC therapeutic target, and novel therapeutic strategies for LC could be developed based on this axis.

By further evaluating anti-proliferative, anti-migratory property with apoptotic inducing potential of Evo, we found there is a significant effect on A549 and A549CR cells. Together, these findings demonstrate that ZEB-2 can be an effective target of Evo mediating cisplatin resistance pathways and sensitize resistant lung cancer cells to cisplatin, providing a promising combinatorial therapeutic strategy to enhance NSCLC treatment efficacy.

It highlights the importance of understanding tumour-immune interactions in their full biological context, and explores current thinking on how to reshape the immune landscape of solid tumours. By addressing both immunological and physical barriers, future approaches may broaden the benefit of immunotherapy beyond its current scope, ultimately improving outcomes for patients with traditionally treatment-resistant cancers.

MDR analysis predicted the best interaction model (MSH2 118 T > C, IVS 1 + 9 G > C, T > C/-6) with a maximum CVC of 10/10 and the least prediction error of 0.355, accompanied by a significant p-value. Furthermore, MD simulations reveal that the Gly322Asp polymorphism in MSH2 induces pronounced structural destabilisation, which may compromise DNA binding and repair efficiency.

The ELK3-SERPINE1-PCBP2 axis promotes GEF resistance in lung cancer by inhibiting ferroptosis, providing a potential new therapeutic strategy for overcoming chemoresistance.

CL7 treatment also modulated the tumor microenvironment by increasing the population of M1 macrophages and CD8+ T cells, while decreasing the population of regulatory T cells. Our findings suggest that CL7 exerts antitumor effects in NSCLC by reprogramming the immunosuppressive landscape of the TME and enhancing antitumor immunity.

Collectively, we associated the redox status mediated by loss-function mutations of KEAP1 or STK11 to immune evasion and immunotherapeutic resistance by suppressing STING/MDA5 expression and interferon signaling of cancer cells. Our findings link redox homeostasis to STING/MDA5 expression and tumor immunogenicity, raising the possibility that targeting this axis could represent a future strategy to enhance ICI efficacy.

Our integrative model highlights the complex interplay between immune signaling, metabolic reprogramming, and autophagic regulation in NSCLC. Further findings offer mechanistic insights into the dual role of FOXO proteins in autophagy mediated cancer progression and present potential components for the development of personalized therapeutic strategies aimed at targeting the cGAS-STING-FOXO-autophagy axis.

For ALK mutations, the analysis showed that patients with ALK-positive tumors had distinct radiological features, including a higher occurrence in the lower lobes and fewer ground glass nodules compared to the WT group. The study concluded that specific radiological and pathological characteristics, along with EGFR and ALK mutation statuses, could be used to guide the treatment and diagnosis of lung adenocarcinoma.