Fiber-optic bronchoscopy showed a diagnostic accuracy rate of 100 % but played a poor therapeutic role with a case resolution of 10.7 %. Rigid bronchoscopy was the main technique, permitting the removal of the tracheobronchial foreign body in 97.2 % of patients.
The use of VATS at first spontaneous pneumothorax is justified in the interest of both patients and health administrations as demonstrated by the number of recurrences in patients in the first group and economy savings resulting from use of VATS.
Our study shows that 18F-FDG PET/CT improves the identification and characterisation of potentially malignant pulmonary nodules with a diameter < 1 cm. This technique could be a valid alternative to a surgical approach, currently the main method to investigate indeterminate lung nodules.
Background: Intrinsic or acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) is common, thus strategies for the management of EGFR-TKIs resistance are urgently required. Ferroptosis is a recently discovered form of cell death that has been implicated in tumorigenesis and resistance treatment. Accumulating evidence suggests that ferroptosis can be therapeutically exploited for the treatment of solid tumors; however, whether ferroptosis can be targeted to treat EGFR mutant lung cancer and/or overcome the resistance to EGFR-TKIs is still unknown.
Methods:The effect of ferroptosis inducers on a panel of EGFR mutant lung cancer cell lines, including those with EGFR-TKI intrinsic and acquired (generated by long-term exposure to the third-generation EGFR-TKI osimertinib), was determined using cytotoxicity assays. Further, drug candidates to enhance the effect of ferroptosis inducers were screened through implementing WGCNA (weighted gene co-expression network analysis) and CMAP (connectivity map) analysis. Flow cytometry-based apoptosis and lipid hydroperoxides measurement were used to evaluate the cell fates after treatment.Results: Compared with EGFR-TKI-sensitive cells, those with intrinsic or acquired resistance to EGFR-TKI display high sensitivity to ferroptosis inducers. In addition, Vorinostat, a clinically used inhibitor targeting histone deacetylase, can robustly enhance the efficacy of ferroptosis inducers, leading to a dramatic increase of hydroperoxides in EGFR mutant lung cancer cells with intrinsic or acquired resistance to EGFR-TKI. Mechanistically, Vorinostat promotes ferroptosis via xCT downregulation.Conclusions: Ferroptosis-inducing therapy shows promise in EGFR-activating mutant lung cancer cells that display intrinsic or acquired resistance to EGFR-TKI. Histone deacetylase inhibitor (HDACi)Vorinostat can further promote ferroptosis by inhibiting xCT expression.
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