Myung Shin Kim1, Eunsom Kim2, Jeong-Seok Heo3, Da-Jeong Bae4, Jong-Uk Wook Lee5, Tae-Hyeong Lee6, Hyeon Ju Lee7, Hun Soo Chang8, Jong Sook Park9, An Soo Jang10, Eun Suk Koh11, Hun Gyu Hwang12, Guneil Lim13, Soohyun Kim14, Choon-Sik Park15. 1. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Gumi Hospital, Gumi-Si, Gyeongsangbuk-Do, Republic of Korea. Electronic address: g72264@schmc.ac.kr. 2. Laboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea. Electronic address: kes0126@naver.com. 3. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: huccine@naver.com. 4. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: dnwls75@naver.com. 5. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: lajoal@nate.com. 6. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: halamadrid@naver.com. 7. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: 1204thgml@naver.com. 8. Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Wonmi-gu, Bucheon, Gyeonggi-do 420-767, Republic of Korea. Electronic address: hschang@sch.ac.kr. 9. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Gyeonggi-Do, Republic of Korea. Electronic address: js1221@schmc.ac.kr. 10. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Gyeonggi-Do, Republic of Korea. Electronic address: jas877@schmc.ac.kr. 11. Departmentof Anatomic Pathology, Soonchunhyang University Bucheon Hospital, Bucheon, Gyeonggi-Do, Republic of Korea. Electronic address: eskamd@schmc.ac.kr. 12. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Gumi Hospital, Gumi-Si, Gyeongsangbuk-Do, Republic of Korea. Electronic address: hwangpark@schmc.ac.kr. 13. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Gumi Hospital, Gumi-Si, Gyeongsangbuk-Do, Republic of Korea. Electronic address: guneil@schmc.ac.kr. 14. Laboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea. Electronic address: soohyun@konkuk.ac.kr. 15. Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Gyeonggi-Do, Republic of Korea. Electronic address: mdcspark@hanmail.net.
Abstract
OBJECTIVES: Interleukin (IL)-33 protects against infection and inflammation; however, few studies have explored the relevance of IL-33 in lung cancer patients. We evaluated relation of plasma IL-33 levels with development and progression of lung cancer. MATERIALS AND METHODS: A total of 160 patients with lung cancer and 160 controls with normal lungs were enrolled. Plasma IL-33 levels were measured using a specific sandwich ELISA; these levels were followed-up in 18 patients who underwent surgery and in 14 patients treated with chemotherapy. Malignant lesions and normal lung tissues from 10 cancer patients were subjected to immunohistochemical staining for IL-33. RESULTS: IL-33 levels were significantly lower in cancer patients than normal controls (0.08 vs. 0.38 ng/mL, p=0.005). Among cancer patients, IL-33 decreased in a stage-dependent manner from 0.76 ng/mL in stage I patients to 0.25 ng/mL in those with stage II, 0.08 ng/mL in those with stage III, and 0.08 ng/mL in those with stage IV (p=0.002). The levels were higher at stage I (p=0.041) and markedly lower at stages III and IV than those of controls (p=0.005 and p=0.001, respectively). A similar pattern was observed when IL-33 levels were analyzed by T stage; the levels were 0.39 ng/mL at T1/T2 vs. 0.08 ng/mL at T3/T4 (p=0.001). However, no difference was noted when stage N1 levels were compared with N2 and N3 levels (p=0.058), or between stage M0 and M1 levels (p=0.147). IL-33 levels gradually decreased after surgical resection of malignant lesions (from 1.075 to 0.756 ng/mL, p=0.006), but were unchanged after chemotherapy (0.705 vs. 0.829 ng/mL, p=0.875). On immunohistochemical staining, bronchial epithelial and vascular endothelial cells of normal lung tissues mainly expressed IL-33. CONCLUSIONS: Plasma IL-33 levels are associated inversely with progression of lung cancer. The observed decreases may be attributed to lung volume reduction containing bronchial epithelium and vascular endothelium as the sources of IL-33.
OBJECTIVES: Interleukin (IL)-33 protects against infection and inflammation; however, few studies have explored the relevance of IL-33 in lung cancerpatients. We evaluated relation of plasma IL-33 levels with development and progression of lung cancer. MATERIALS AND METHODS: A total of 160 patients with lung cancer and 160 controls with normal lungs were enrolled. Plasma IL-33 levels were measured using a specific sandwich ELISA; these levels were followed-up in 18 patients who underwent surgery and in 14 patients treated with chemotherapy. Malignant lesions and normal lung tissues from 10 cancerpatients were subjected to immunohistochemical staining for IL-33. RESULTS:IL-33 levels were significantly lower in cancerpatients than normal controls (0.08 vs. 0.38 ng/mL, p=0.005). Among cancerpatients, IL-33 decreased in a stage-dependent manner from 0.76 ng/mL in stage I patients to 0.25 ng/mL in those with stage II, 0.08 ng/mL in those with stage III, and 0.08 ng/mL in those with stage IV (p=0.002). The levels were higher at stage I (p=0.041) and markedly lower at stages III and IV than those of controls (p=0.005 and p=0.001, respectively). A similar pattern was observed when IL-33 levels were analyzed by T stage; the levels were 0.39 ng/mL at T1/T2 vs. 0.08 ng/mL at T3/T4 (p=0.001). However, no difference was noted when stage N1 levels were compared with N2 and N3 levels (p=0.058), or between stage M0 and M1 levels (p=0.147). IL-33 levels gradually decreased after surgical resection of malignant lesions (from 1.075 to 0.756 ng/mL, p=0.006), but were unchanged after chemotherapy (0.705 vs. 0.829 ng/mL, p=0.875). On immunohistochemical staining, bronchial epithelial and vascular endothelial cells of normal lung tissues mainly expressed IL-33. CONCLUSIONS: Plasma IL-33 levels are associated inversely with progression of lung cancer. The observed decreases may be attributed to lung volume reduction containing bronchial epithelium and vascular endothelium as the sources of IL-33.
Authors: Yujiang Fang; Lei Zhao; Huaping Xiao; Kathryn M Cook; Qian Bai; Elizabeth J Herrick; Xuhui Chen; Chenglu Qin; Ziwen Zhu; Mark R Wakefield; Michael B Nicholl Journal: Med Oncol Date: 2017-01-05 Impact factor: 3.064
Authors: Stefan Gröschel; Martin Bommer; Barbara Hutter; Jan Budczies; David Bonekamp; Christoph Heining; Peter Horak; Martina Fröhlich; Sebastian Uhrig; Daniel Hübschmann; Christina Geörg; Daniela Richter; Nicole Pfarr; Katrin Pfütze; Stephan Wolf; Peter Schirmacher; Dirk Jäger; Christof von Kalle; Benedikt Brors; Hanno Glimm; Wilko Weichert; Albrecht Stenzinger; Stefan Fröhling Journal: Cold Spring Harb Mol Case Stud Date: 2016-11