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Autoreactive napsin A-specific T cells are enriched in lung tumors and inflammatory lung lesions during immune checkpoint blockade - PubMed

Autoreactive napsin A-specific T cells are enriched in lung tumors and inflammatory lung lesions during immune checkpoint blockade - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/36054337/

Cancer treatment with immune checkpoint blockade (ICB) often induces immune-related adverse events (irAEs). We hypothesized that proteins coexpressed in tumors and normal cells could be antigenic targets in irAEs and...


Conclusion: DITAS successfully identified self-antigens, including napsin A, that likely mediate effective antitumor T cell responses in NSCLC and may simultaneously underpin lung irAEs.

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Log odds of positive lymph nodes is a robust predictor of survival and benefits from postoperative radiotherapy in stage IIIA-N2 resected non-small cell lung cancer - PubMed

Log odds of positive lymph nodes is a robust predictor of survival and benefits from postoperative radiotherapy in stage IIIA-N2 resected non-small cell lung cancer - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/36054738/

doi: 10.1111/1759-7714.14617. Online ahead of print. 1 Department of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China. 2 Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai,...


Conclusions: The LODDS classification not only exhibited the best prognostic performance in predicting LCSS and OS in stage IIIA-N2 disease, but also could help tailor individualized PORT.

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MiR-504-3p Has Tumor-Suppressing Activity and Decreases IFITM1 Expression in Non-Small Cell Lung Cancer Cells

Source : https://www.liebertpub.com/doi/10.1089/gtmb.2021.0158

Objective: To analyze the impact of expression of miR-504-3p on the proliferation, migration, cell cycle transit and rate of apoptosis of NSCLC cells and explore the underlying mechanisms.


Conclusion: miR-504-3p inhibits cell proliferation and migration and promotes cell apoptosis in NSCLC cells. MiR-504-3p decreases IFITM1 expression in NSCLC cells, which may be a potential mechanism of its tumor-suppressive functions in NSCLC.

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Overall Survival Benefits of First-Line Treatments for Asian Patients with Advanced Epidermal Growth Factor Receptor-Mutated NSCLC Harboring Exon 19 Deletion: A Systematic Review and Network Meta-Analysis - PubMed

Overall Survival Benefits of First-Line Treatments for Asian Patients with Advanced Epidermal Growth Factor Receptor-Mutated NSCLC Harboring Exon 19 Deletion: A Systematic Review and Network Meta-Analysis - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/35884423/

1 Department of Clinical Oncology, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. 2 School of Public Health, LKS Faculty of Medicine,...


Conclusions: In patients from Asia with 19del, both EGFR-TKIs and treatments in which therapies were combined exhibited no OS benefits in comparison with standard chemotherapy treatments. Additional research is required to study TKIs' resistance mechanisms and possible combined approaches for individuals harboring this common mutation.

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RELAY, ramucirumab plus erlotinib versus placebo plus erlotinib in untreated EGFR-mutated metastatic non-small cell lung cancer: exposure-response relationship

RELAY, ramucirumab plus erlotinib versus placebo plus erlotinib in untreated EGFR-mutated metastatic non-small cell lung cancer: exposure-response relationship

Source : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360106/

Cancer Chemotherapy and Pharmacology In RELAY, ramucirumab plus erlotinib (RAM + ERL) improved progression-free survival (PFS) in patients with untreated, metastatic, EGFR-mutated, non-small cell lung cancer (NSCLC). Here, we present the exposure-response...


Conclusions: No association was observed between RAM exposure and response, suggesting that the RELAY regimen of RAM 10 mg/kg Q2W with ERL is an optimized, efficacious, and safe first-line treatment for patients with untreated, metastatic, EGFR-mutated NSCLC.