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NSCLC

Overcoming Microenvironmental Resistance to PD-1 Blockade in Genetically Engineered Lung Cancer Models

[Science Translational Medicine] Investigators found that antiangiogenic treatment facilitated non–small cell lung cancer tumor infiltration by PD-1+ regulatory T cells, which were more efficiently targeted by the PD-1 antibody than CD8+ T cells.

Preparation and Characterization of Palladium Derivate-Loaded Micelle Formulation In Vitro as an Innovative Therapy Option against Non-Small Cell Lung Cancer Cells

[Chemistry & Biodiversity] A549 and H1299 non-small lung cancer cell types were used for cytotoxicity using SRB and ATP assays. Fluorescent staining and M30 antigen assay were carried out for cell death evaluation.

Identification of Prognostic Markers by Weighted Gene Co-Expression Network Analysis in Non-Small Cell Lung Cancer

[Bioengineered] All hub genes were overexpressed in tumor tissue, and high expression of AURKB, CDC20, TPX2, and KIF2C correlated with the poor prognosis of non-small cell lung cancer patients. In vitro experiments confirmed that CDC20 knockdown inhibited cell proliferation and growth.

USP12 Downregulation Orchestrates a Protumourigenic Microenvironment and Enhances Lung Tumor Resistance to PD-1 Blockade

[Nature Communications] Scientists showed that the deubiquitinase USP12 was commonly downregulated in the KrasG12D-driven mouse lung tumour and human non-small cell lung cancer owing to the activation of AKT-mTOR signalling.

Combined Inhibition of SHP2 and CXCR1/2 Promotes Anti-Tumor T Cell Response in NSCLC

[Cancer Discovery] The authors found that SHP2 inhibitor treatment depleted alveolar and M2-like macrophages, induced tumor-intrinsic CCL5/CXCL10 secretion and promoted B and T lymphocyte infiltration in Kras- and Egfr-mutant non-small cell lung cancer.

Coregulation of Pathways in Lung Cancer Patients with EGFR Mutation: Therapeutic Opportunities

[British Journal of Cancer] Scientists highlight regulatory mechanisms and signaling pathways that cause therapy-induced resistance to epidermal growth factor receptor tyrosine kinase inhibitors.

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