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Keywords {🔍}

pdl, cells, expression, nsclc, cancer, egfrtki, resistant, pubmed, lung, cmet, article, egfr, resistance, google, scholar, hgf, patients, cell, cas, immune, figure, egfrtkis, pcr, additional, fig, treatment, pathway, mutant, amplification, mapk, tumour, file, mutation, wang, mechanisms, signaling, results, activation, gefitinib, acquired, growth, pathways, nfkappa, tumours, human, lymphocytes, percentage, pikakt, escape, involved,

Topics {✒️}

pd-l1-deleted egfr-tkis sensitive egfr-tki resistant lung cancer pd-1/pd-l1 axis plays pd-1/pd-l1 therapies require c-met amplification-induced upregulation c-met si-rnas downregulate anti-pd-1/pd-l1 inhibitors pd-l1-induced primary resistance anti-pd-l1 antibodies restores anti-pd-1/pd-l1 therapies t790m-induced pd-l1 expression hgf-mediated pd-l1 expression egfr-tki resistant mechanisms related egfr-tki resistant nsclc cells egfr-related pd-l1 expression hgf-induced pd-l1 upregulation pd-1/pd-l1 immune checkpoint anti-pd-l1 monoclonal antibody hgf-induced pd-l1 expression anti-pd-1/pd-l1 therapy egfr-tkis resistant nsclc tumours egfr+/c-met+ mutant nsclc egfr+/c-met− mutant nsclc crispr-cas9 knockout lentiviruses anti-pd-l1 antibodies restored egfr-tkis resistant nsclc cells pi3k/akt/nf-kappab signaling pathway pc-9rpd-l1- tumours responded small-cell lung cancer crispr-cas9 knockout lentivirus cd3−cd16+cd56+ nk cells egfr-tki resistant nsclc egfr-tki resistant nsclc pd-1/pd-l1 inhibitors acquiring egfr-tki resistance generated egfr-tki sensitive pd-l1 expression induced dual pi3k/mtor inhibitors pc-9r pd-l1- xenografts c-jun si-rna generation egfr-tkis resistance [10] egfr-tkis resistant nsclc egfr-tkis resistant nsclc upregulate pd-l1 expression members including c-jun c-met sirna combined pc-9rpd-l1- tumours shows induce egfr-tkis resistance acquired egfr-tki resistance acquired egfr-tki resistance

Questions {❓}

• ATLANTIC: a sea change in immunotherapy for oncogene-driven lung cancer?
• Does c-met remain a rational target for therapy in patients with EGFR TKI-resistant non-small cell lung cancer?
• What does PD-L1 positive or negative mean?
• Org/study?

Schema {🗺️}

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         headline:EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression
         description:The ATLANTIC trial reported that higher PD-L1 expression in tumors was involved in a higher objective response in patients with EGFR+/ALK+ non-small cell lung cancer (NSCLC), indicating the possibility of anti-PD-1/PD-L1 therapy as a third-line (or later) treatment for advanced NSCLC. Therefore, the determination of status and regulatory mechanisms of PD-L1 in EGFR mutant NSCLC before and after acquired EGFR-TKIs resistance are meaningful. The correlation among PD-L1, c-MET, and HGF was analyzed based on TCGA datasheets and paired NSCLC specimens before and after acquired EGFR-TKI resistance. EGFR-TKI resistant NSCLC cells with three well-known mechanisms, c-MET amplification, hepatocyte growth factor (HGF), and EGFR-T790M, were investigated to determinate PD-L1 expression status and immune escape ability. PD-L1-deleted EGFR-TKIs sensitive and resistant cells were used to evaluate the immune escape ability of tumors in mice xenograft models. Positive correlations were found among PD-L1, c-MET, and HGF, based on TCGA datasheets and paired NSCLC specimens. Moreover, the above three resistant mechanisms increased PD-L1 expression and attenuated activation and cytotoxicity of lymphocytes in vitro and in vivo, and downregulation of PD-L1 partially restored the cytotoxicity of lymphocytes. Both MAPK and PI3K pathways were involved in the three types of resistance mechanism-induced PD-L1 overexpression, whereas the NF-kappa B pathway was only involved in T790M-induced PD-L1 expression. HGF, MET-amplification, and EGFR-T790M upregulate PD-L1 expression in NSCLC and promote the immune escape of tumor cells through different mechanisms.
         datePublished:2019-11-20T00:00:00Z
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            EGFR-TKIs resistance
            Signaling pathways
            Lung cancer
            Immunotherapy
            Cancer Research
            Oncology
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      headline:EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression
      description:The ATLANTIC trial reported that higher PD-L1 expression in tumors was involved in a higher objective response in patients with EGFR+/ALK+ non-small cell lung cancer (NSCLC), indicating the possibility of anti-PD-1/PD-L1 therapy as a third-line (or later) treatment for advanced NSCLC. Therefore, the determination of status and regulatory mechanisms of PD-L1 in EGFR mutant NSCLC before and after acquired EGFR-TKIs resistance are meaningful. The correlation among PD-L1, c-MET, and HGF was analyzed based on TCGA datasheets and paired NSCLC specimens before and after acquired EGFR-TKI resistance. EGFR-TKI resistant NSCLC cells with three well-known mechanisms, c-MET amplification, hepatocyte growth factor (HGF), and EGFR-T790M, were investigated to determinate PD-L1 expression status and immune escape ability. PD-L1-deleted EGFR-TKIs sensitive and resistant cells were used to evaluate the immune escape ability of tumors in mice xenograft models. Positive correlations were found among PD-L1, c-MET, and HGF, based on TCGA datasheets and paired NSCLC specimens. Moreover, the above three resistant mechanisms increased PD-L1 expression and attenuated activation and cytotoxicity of lymphocytes in vitro and in vivo, and downregulation of PD-L1 partially restored the cytotoxicity of lymphocytes. Both MAPK and PI3K pathways were involved in the three types of resistance mechanism-induced PD-L1 overexpression, whereas the NF-kappa B pathway was only involved in T790M-induced PD-L1 expression. HGF, MET-amplification, and EGFR-T790M upregulate PD-L1 expression in NSCLC and promote the immune escape of tumor cells through different mechanisms.
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      dateModified:2019-11-20T00:00:00Z
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         PD-L1
         EGFR-TKIs resistance
         Signaling pathways
         Lung cancer
         Immunotherapy
         Cancer Research
         Oncology
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      name:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China
      name:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China
      name:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China
      name:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China
      name:Center for Clinical Medicine Research, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China
      name:Divisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan
      name:Divisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan
      name:Divisions of Medical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan
      name:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China

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