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Background: This study investigated the relationship between inflammatory biomarkers (lymphocyte ratio [NLR], monocyte-to-lymphocyte ratio [MLR], and platelet-to-lymphocyte ratio [PLR]) and the treatment outcomes of patients with non-small cell lung cancer (NSCLC) treated with afatinib.
Methods: The patients with NSCLC treated with afatinib between June 2014 and February 2018 were retrospectively reviewed. Their inflammatory biomarkers and clinical outcomes (progression-free survival [PFS] and tumor response) were explored using univariate and multivariate analyses.
Results: Among 325 patients, those with an NLR >2.18, MLR >0.19, and PLR >177.73 had significantly worse PFS than those with lower values. After adjusting for performance status, stage, and liver metastasis, the PFS was still unfavorable for a baseline NLR >2.18, MLR >0.19, or PLR > 177.73. Among 188 patients with paired inflammatory values, those whose NLR decreased by >29.5%, MLR decreased by >57.9%, and PLR increased by <18.8% had significantly better PFS. After adjusting for performance status, stage, and liver metastasis, the PFS was significantly unfavorable for an NLR decrease of <29.5% and MLR decrease of <57.9%. Among the patients with tumor response, NLR, MLR, and PLR significantly decreased after treatment (all p < 0.05).
Conclusions: Our study presented the NLR, MLR, and PLR as prognostic factors for patients with NSCLC treated with afatinib. Further investigation into these markers representing the tumor microenvironment and their association with cancer status is crucial for evaluating prognosis and clinical outcomes in patients with NSCLC.
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http://dx.doi.org/10.1111/1759-7714.15338 | DOI Listing |
EMBO J
September 2025
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University; Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences; Wuhan University, Wuhan, 430071, China.
Inadequate antigen presentation by MHC-I in tumor microenvironment (TME) is a common immune escape mechanism. Here, we show that glycine decarboxylase (GLDC), a key enzyme in glycine metabolism, functions as an inhibitor of MHC-I expression in EGFR-activated tumor cells to induce immune escape by a mechanism independent of its enzymatic activity. Upon EGFR activation, GLDC is phosphorylated by SRC and subsequently translocated to the nucleus in human NSCLC cells.
View Article and Find Full Text PDFZhonghua Jie He He Hu Xi Za Zhi
September 2025
Department of nursing, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, China.
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) are important treatments for EGFR mutant non-small cell lung cancer (NSCLC). However, the first and second generation EGFR-TKI face clinical limitations due to acquired resistance, such as the T790M mutation. Irreversible EGFR-TKI can significantly prolong the survival of patients by enhancing the inhibition of drug-resistant mutations through the covalent binding mechanism.
View Article and Find Full Text PDFLung Cancer
September 2025
Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-Shimbashi, Minato-ku, Tokyo, Japan; Division of Next-Generation Drug Development Research, Research Center for Medical Sciences, The Jikei University School of Medicine, 3-25-8 Ni
Background: The risk factors associated with treatment resistance to consolidation durvalumab following chemoradiotherapy (CRT) for locally advanced non-small cell lung cancer (NSCLC) have not been well established.
Methods: Extracellular vesicles (EVs) were isolated from the pretreatment serum of 73 patients treated with consolidation durvalumab. Isolation was performed using CD9/CD63 antibodies, and EV proteins were identified using liquid chromatography-tandem mass spectrometry (LC-MS).
Biochem Soc Trans
September 2025
Department of Biochemistry, McGill University, Montréal, QC, Canada.
The MET receptor tyrosine kinase is a pivotal regulator of cellular survival, motility, and proliferation. Mutations leading to skipping of exon 14 (METΔex14) within the juxtamembrane domain of MET impair receptor degradation and prolong oncogenic signaling, contributing significantly to tumor progression across multiple cancer types. METΔex14 mutations are associated with aggressive clinical behavior, therapeutic resistance, and poor outcomes.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Radiation Oncology, Yonsei Cancer Center, Heavy Ion Therapy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Volumetric modulated arc therapy (VMAT) for lung cancer involves complex multileaf collimator (MLC) motion, which increases sensitivity to interplay effects with tumour motion. Current dynamic conformal arc methods address this issue but may limit the achievable dose distribution optimisation compared with standard VMAT. This study examined the clinical utility of a VMAT technique with monitor unit limits (VMATliMU) to mimic conformal arc delivery and reduce interplay effects while maintaining plan quality.
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