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      Circulating plasma lncRNAs as novel markers of EGFR mutation status and monitors of epidermal growth factor receptor‐tyrosine kinase inhibitor therapy

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          Abstract

          Background

          Epidermal growth factor receptor (EGFR) gene mutations predict tumor response to EGFR tyrosine kinase inhibitors (EGFR‐TKIs) in non‐small cell lung cancer (NSCLC). However, even patients with EGFR‐sensitive mutations in NSCLC have limited efficacy with EGFR‐TKI. Studies have shown that long noncoding RNA (lncRNA) is related to diagnosis and prognosis with NSCLC. This study aimed to explore the correlation between lncRNA in NSCLC patients with EGFR mutation status and EGFR‐TKI efficacy.

          Methods

          The amplification‐refractory mutation system method was used to test the EGFR mutation status in tumor tissues and pleural effusions of NSCLC patients. Three EGFR‐mutant patients and three EGFR wild‐type patients were selected. Differential lncRNA was performed on the pleural effusions of the two selected groups of patients using Clariom D Human chip technology. Five lncRNAs significantly associated with EGFR mutation status were screened by FC value and GO analysis, and then evaluated by real‐time quantitative polymerase chain reaction in NSCLC patients' pleural effusions. Three were further analyzed in NSCLC patients' plasma.

          Results

          There were 61 significant differences in lncRNA between EGFR mutation‐positive and wild‐type patients. Among them, SCARNA7, MALAT1, NONHSAT017369, NONHSAT051892, and FTH1P2 were significantly associated with EGFR mutation status. SCARNA7, MALAT1, and NONHSAT017369 showed consistent results with plasma in pleural effusions compared to EGFR wild‐type, all upregulated in the EGFR mutation group.

          Conclusion

          This study shows that lncRNAs can be used not only as potential biomarkers for predicting the mutation status of EGFR and the efficacy of EGFR‐TKI, but also for monitoring the efficacy of EGFR‐TKI.

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          Most cited references22

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          Current and future perspectives of liquid biopsies in genomics-driven oncology

          Precision oncology seeks to leverage molecular information about cancer to improve patient outcomes. Tissue biopsy samples are widely used to characterize tumours but are limited by constraints on sampling frequency and their incomplete representation of the entire tumour bulk. Now, attention is turning to minimally invasive liquid biopsies, which enable analysis of tumour components (including circulating tumour cells and circulating tumour DNA) in bodily fluids such as blood. The potential of liquid biopsies is highlighted by studies that show they can track the evolutionary dynamics and heterogeneity of tumours and can detect very early emergence of therapy resistance, residual disease and recurrence. However, the analytical validity and clinical utility of liquid biopsies must be rigorously demonstrated before this potential can be realized.
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            Detection and Dynamic Changes of EGFR Mutations from Circulating Tumor DNA as a Predictor of Survival Outcomes in NSCLC Patients Treated with First-line Intercalated Erlotinib and Chemotherapy.

            Blood-based circulating-free (cf) tumor DNA may be an alternative to tissue-based EGFR mutation testing in NSCLC. This exploratory analysis compares matched tumor and blood samples from the FASTACT-2 study.
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              Distribution of M1 and M2 macrophages in tumor islets and stroma in relation to prognosis of non-small cell lung cancer

              Background Non-small cell lung cancer (NSCLC) remains the most common cause of cancer related death worldwide. Tumor-infiltrating macrophages are believed to play an important role in growth, progression, and metastasis of tumors. In NSCLC, the role of macrophages remains controversial; therefore, we aimed to evaluate the distribution of macrophages (M1 and M2) in tumor islets and stroma and to analyze their relations to patients’ survival. Methods Lung tissue specimens from 80 NSCLC patients who underwent surgical resection for NSCLC (pathological stage I-III) and 16 control group subjects who underwent surgery because of recurrent spontaneous pneumothorax were analyzed. Immunohistochemical double staining of CD68/iNOS (markers for M1 macrophages) and CD68/CD163 (markers for M2 macrophages) was performed and evaluated in a blinded manner. The numbers of M1 and M2 macrophages in tumor islets and stroma were counted manually. Results Predominant infiltration of M1 and M2 macrophages was observed in the tumor stroma compared with the tumor islets. M2 macrophages predominated over M1 macrophages in the tumor tissue. Tumor islets-infiltrating M1 macrophages and the number of total tumor-infiltrating M2 macrophages were independent predictors of patients survival: high infiltration of M1 macrophages in tumor islets was associated with increased overall survival in NSCLC (P < 0.05); high infiltration of total M2 macrophages in tumor (islets and stroma) was associated with reduced overall survival in NSCLC (P < 0.05). Conclusions This study demonstrated that high infiltration of M1 macrophages in the tumor islets and low infiltration of total tumor-infiltrating M2 macrophages were associated with improved NSCLC patients’ survival. Trial registration ClinicalTrials.gov NCT01955343, registered on September 27, 2013
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                Author and article information

                Contributors
                lvpanpan307@163.com
                liuxiaoqing0612@163.com
                Journal
                Thorac Cancer
                Thorac Cancer
                10.1111/(ISSN)1759-7714
                TCA
                Thoracic Cancer
                John Wiley & Sons Australia, Ltd (Melbourne )
                1759-7706
                1759-7714
                05 November 2019
                January 2020
                : 11
                : 1 ( doiID: 10.1111/tca.v11.1 )
                : 29-40
                Affiliations
                [ 1 ] Academy of Military Medical Science Beijing China
                [ 2 ] PLA Rocket Force Characteristic Medical Center Beijing China
                [ 3 ] Department of Pulmonary Oncology The Fifth Medical Centre, Chinese PLA General Hospital Beijing China
                Author notes
                [*] [* ] Correspondence

                Xiaoqing Liu, Department of Pulmonary Oncology, The Fifth Medical Centre, Chinese PLA General Hospital, No. 8 East Street, Fengtai District, Beijing 100071, China.

                Tel: +86 01066947164

                Fax: +86 01066947164

                Email: liuxiaoqing0612@ 123456163.com

                Author information
                https://orcid.org/0000-0003-2277-400X
                Article
                TCA13216
                10.1111/1759-7714.13216
                6938758
                31691525
                9ab0cced-2589-45a1-82ce-cd8259eefe94
                © 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 17 June 2019
                : 20 September 2019
                : 22 September 2019
                Page count
                Figures: 5, Tables: 4, Pages: 12, Words: 7169
                Funding
                Funded by: Beijing Municipal Science & Technology Commission
                Award ID: Z181100001718074
                Funded by: Chinese National Instrumentation Program
                Award ID: 2011YQ170067
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                January 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.4 mode:remove_FC converted:01.01.2020

                biomarker,epidermal growth factor receptor,long noncoding rna,non‐small cell lung cancer,tyrosine kinase inhibitor

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