title: Preoperative steroid pulse therapy for invasive thymoma: clinical experience and mechanism of action.
abstract: BACKGROUND
  Glucocorticoid was used in thymomas. The purpose of the study was to evaluate the efficacy of intravenous high-dose glucocorticoid (steroid pulse) therapy in patients with previously untreated advanced thymoma. Causes were also sought for a possible underlying mechanism of the effect of steroid on thymoma.
  
  
  METHODS
  Seventeen patients with invasive thymoma who had not received previous chemotherapy or radiation therapy were enrolled in the study. All cases were treated with 2 courses of glucocorticoid therapy before surgery. Tumor response was assessed by computed tomography (CT) scan 1 week after the steroid pulse therapy. Lymphocytes associated with thymoma were analyzed for their CD4/CD8 phenotype and glucocorticoid receptor (GR). TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining was used to analyze the apoptotic lymphocytes and epithelial cells.
  
  
  RESULTS
  The overall response rate to the steroid pulse therapy was 47.1% (8 of 17). The reduction in tumor size was most prominent in type B1 thymomas; there were significant differences between type AB and type B1 thymomas (P = .0234) and type B1 and type B3 thymomas (P = .0068). The reduction in tumor size was accompanied with a marked reduction in the CD4+8+ double-positive immature thymocytes that expressed higher levels of glucocorticoid receptor. Apoptotic changes were observed in both neoplastic epithelial cell and lymphocyte components after glucocorticoid therapy.
  
  
  CONCLUSIONS
  The efficiency of preoperative steroid pulse therapy in type B1 thymoma was most prominent, which is probably related to the specific effect on GR-rich CD4+8+ double-positive immature lymphocytes, which are abundant in this type of thymoma.
authors.affiliation: Department of Surgery II, Nagoya City University Medical School, Nagoya, Japan. shogen@med.nagoya-cu.ac.jp
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Fujii
authors.forename: Motoki
authors.initials: M
authors.lastname: Yano
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Sasaki
authors.forename: Haruhiro
authors.initials: H
authors.lastname: Yukiue
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Haneda
authors.forename: Eriko
authors.initials: E
authors.lastname: Suzuki
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Endo
authors.forename: Osamu
authors.initials: O
authors.lastname: Kawano
mesh_terms: D000328:Adult; D000368:Aged; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D003131:Combined Modality Therapy; D005260:Female; D005434:Flow Cytometry; D005938:Glucocorticoids / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D013945:Thymoma / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D013953:Thymus Neoplasms / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology
chemical_list: D015704:CD4 Antigens; D016827:CD8 Antigens; D005938:Glucocorticoids