title: A different pattern of cytotoxic T lymphocyte recognition against primary and metastatic tumor cells in a patient with nonsmall cell lung carcinoma.
abstract: BACKGROUND
  Lung carcinoma represents the most frequent cause of cancer death worldwide because of tumor metastases. The objective of the current study was to analyze the immunologic response during the progress of lung carcinoma metastasis.
  
  
  METHODS
  The authors established two tumor cell lines that were derived from primary and metastatic lesions in a patient with lung carcinoma (Patient G603). One cell line (G603L) was established from the primary lesion, and the other cell line (G603AD) was established from a metastatic lesion in the right adrenal gland 7 months after the patient underwent surgery for the primary lesion. Autologous regional lymph node lymphocytes were stimulated with CD80-transfected G603L cells, then cytotoxic T lymphocytes (CTLs) were induced against both lung carcinoma cell lines.
  
  
  RESULTS
  Both G603L cells and G603AD cells expressed Class I human leukocyte antigen, intracellular cell adhesion molecule 1, and lymphocyte-associated antigen type 3 (LFA-3), but not Fas or Fas ligand on their surfaces. By stimulation with CD80-transfected G603L cells, 2 CTL clones (H2/17 and H2/36) were established from the bulk CTLs. CTL clone H2/17 lysed G603L cells but not G603AD cells, suggesting that the antigen recognized by CTL clone H2/17 was abrogated during the process of metastasis. In contrast, CTL clone H2/36 lysed both G603L cells and G603AD cells, indicating that the antigen recognized by CTL clone H2/36 was maintained in the tumor cells throughout tumor progression.
  
  
  CONCLUSIONS
  The results demonstrated the possibility that some tumor-associated antigens may be abrogated during the process of metastasis, although others are maintained. The identification of these antigens will lead to a better understanding of their immunologic role during disease progression in patients with lung carcinoma.
authors.affiliation: Second Department of Surgery, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. tetsuya@med.uoeh-u.ac.jp
authors.forename: Tetsuya
authors.initials: T
authors.lastname: So
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Takenoyama
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Ichiki
authors.forename: Makiko
authors.initials: M
authors.lastname: Mizukami
authors.forename: Tomoko
authors.initials: T
authors.lastname: So
authors.forename: Takeshi
authors.initials: T
authors.lastname: Hanagiri
authors.forename: Kenji
authors.initials: K
authors.lastname: Sugio
authors.forename: Kosei
authors.initials: K
authors.lastname: Yasumoto
mesh_terms: D000368:Aged; D000917:Antibody Formation; D000951:Antigens, Neoplasm / Q000276:immunology*; D002289:Carcinoma, Non-Small-Cell Lung / Q000276:immunology* / Q000473:pathology*; D018450:Disease Progression; D005434:Flow Cytometry; D006801:Humans; D007167:Immunotherapy; D008175:Lung Neoplasms / Q000276:immunology* / Q000473:pathology*; D008297:Male; D009362:Neoplasm Metastasis / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014162:Transfection; D014407:Tumor Cells, Cultured
chemical_list: D000951:Antigens, Neoplasm