title: [Effect of EGFR-TKI on lymphangiogenesis of lung cancer with EGFR mutation].
abstract: OBJECTIVE
  This study aims to explore the effect of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKIs) on the lymphangiogenesis of lung cancer with EGFR mutation, as well as to determine the function of EGFR targeted therapy in relation to the inhibition of lymphangiogenesis during lung cancer treatment.
  
  
  METHODS
  The EGFR double mutant lung cancer cell line NCI-H1975 is used to construct lung cancer xenograft models. The models are divided into two groups: the solvent control group and the EGFR-TKI treatment group. Each group includes five mice. The inhibitory effect of EGFR-TKI on the growth of transplanted tumors was observed. Immunohistochemical method and lymphatic endothelium specific antibody D2-40 were used in the experiment to observe the influence of EGFR-TKI on lymphangiogenesis in lung cancer.
  
  
  RESULTS
  The weight and relative volume of tumors in the EGFR-TKI treated group were less than those in the solvent control group. The average lymphatic vessel density of EGFR-TKI-treated mice was 6.44 per case. This value was 10.70 per case in the solvent control group. Lower density of lymphangiogenesis was found in the EGFR-TKI treated group (P=0.023). The area and longest diameter of neonatal lymphatic vessel of the EGFR-TKI treated group were less than those of the solvent control group. Moreover, EGFR-TKI exhibited no significant effect on the invasion of tumor cells into the lymphatic vessel (P=0.519).
  
  
  CONCLUSIONS
  EGFR-TKI can inhibit lymphangiogenesis in EGFR mutant lung cancer while suppressing vessel diameter and expansion area.
authors.affiliation: Department of Thoracic Cancer, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai Lung Tumor Clinical Medical Center, Shanghai 200030, China.
authors.forename: Minghui
authors.initials: M
authors.lastname: Cai
authors.affiliation: Shanghai Institute of Materia Medical, Chinese Academy of Sciences, Shanghai 201203, China.
authors.forename: Xinying
authors.initials: X
authors.lastname: Yang
authors.affiliation: Shanghai Institute of Materia Medical, Chinese Academy of Sciences, Shanghai 201203, China.
authors.forename: Baohong
authors.initials: B
authors.lastname: Jiang
authors.affiliation: Shanghai Institute of Materia Medical, Chinese Academy of Sciences, Shanghai 201203, China.
authors.forename: Fukang
authors.initials: F
authors.lastname: Teng
authors.affiliation: Department of Pharmacy, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Pan
authors.affiliation: Department of Thoracic Cancer, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai Lung Tumor Clinical Medical Center, Shanghai 200030, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Mao
authors.affiliation: Department of Thoracic Cancer, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai Lung Tumor Clinical Medical Center, Shanghai 200030, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Shen-Tu
mesh_terms: D000077716:Afatinib; D000818:Animals; D045744:Cell Line, Tumor; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000235:genetics*; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy*; D042583:Lymphangiogenesis / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D011799:Quinazolines / Q000627:therapeutic use
chemical_list: D047428:Protein Kinase Inhibitors; D011799:Quinazolines; D000077716:Afatinib; D066246:ErbB Receptors