Single-atom and double-atom catalysts have emerged as new frontiers in many fields due to their high atom-utilization efficiency, excellent catalytic properties and good durability. In this decade, Fe-based atomic catalysts...
BackgroundThis study was designed to compare toxicities, disease control, and survival outcomes for limited disease small-cell lung cancer (LD-SCLC) treated with once daily (QD) versus twice daily (BID) radiotherapy.MethodsAll of the patients received four to six cycles of platinum plus etoposide. In the QD group, irradiation was given via conventional radiotherapy with a dose of 60 Gy at 2 Gy per once-daily fraction. In the BID group, the dose was 45 Gy at 1.5 Gy per twice-daily fraction.ResultsData from a total of 143 LD-SCLC patients treated at the Shandong Cancer Hospital & Institute were retrospectively analyzed. Statistically significant differences were found in the rates of both grade 2 or higher esophagitis (P = 0.036) and pneumonitis (P = 0.043) between QD and BID groups, respectively. Grade 3 esophagitis occurred in 6% of patients receiving QD and 19% of those receiving BID therapy. The median overall survival (OS) of all patients was 30.4 months: 29.5 months for QD therapy, and 31.4 months for BID therapy. The two-year OS rate was 43.3% for QD therapy, and 48.8% for BID therapy. The two-year locoregional recurrence-free survival (LRFS) rate was 45% versus 63.4% for the QD group versus the BID group, respectively.ConclusionsPneumonitis was more common in the QD group, and esophagitis was more common in the BID group. Although there were no significant differences in OS and LRFS between the QD and BID groups, there was a trend toward improved local control in the BID group.
Introduction: Osimertinib is a potent epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC). However, the emergence of acquired resistance due to the EGFR-Del19/T790M/C797S mutation limits the clinical application of osimertinib. Feiyiliu Mixture (FYLM), a clinical experience formula of Chinese medicine, was used to treat lung cancer with good clinical efficacy. In this study, we aimed to investigate the mechanism by which Feiyiliu Mixture delays osimertinib resistance in EGFR-mutant cell lines and EGFR-mutant cell tumor-bearing mice.Methods: The osimertinib-resistant cell models were established in mouse Lewis lung carcinoma (LLC) cells transfected with EGFR-Del19/T790M/C797S mutant lentivirus. In cell experiments, after 48 h of treatment with Feiyiliu Mixture-containing serum, MTT assay was used to detect the relative cell viability, and western blotting was used to detect EGFR protein phosphorylation expression. In animal experiments, C57BL/6J mice were subcutaneously injected with Lewis lung carcinoma cells stably expressing EGFR-Del19/T790M/C797S mutations to construct a xenograft model. After 2 weeks of Feiyiliu Mixture and/or osimertinib treatment, the expression of proliferation-related, apoptosis-related and PRC1/Wnt/EGFR pathway markers was detected by real-time qPCR, western blotting and immunohistochemistry.Results: The results showed that when combined with osimertinib, Feiyiliu Mixture synergistically reduces proliferation and increases apoptosis to improve drug resistance. In vitro, Feiyiliu Mixture-containing serum reduced the EGFR phosphorylation. In vivo, Feiyiliu Mixture downregulated the expression of cyclin B1 and Bcl-2 while upregulating the level of cleaved Caspase-3 protein, indicating that Feiyiliu Mixture promotes apoptosis. Furthermore, Feiyiliu Mixture reduced the expression of p-EGFR, p-Akt, PRC1 and Wnt pathway-related proteins such as β-catenin, c-Myc and c-Jun.Conclusion: The present study identified that Feiyiliu Mixture inhibited PRC1/Wnt/EGFR pathway activation, reduced proliferation, and promoted apoptosis, thereby increasing the sensitivity of EGFR-mutant non-small cell lung cancer to osimertinib. Our study provided a new idea for Chinese medicine to play a role in enhancing efficacy and reducing toxicity in the treatment of non-small cell lung cancer.
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