title: Monoclonal origin of an esophageal carcinosarcoma producing granulocyte-colony stimulating factor: a case report.
abstract: BACKGROUND
  Carcinosarcomas are comprised of carcinomatous and sarcomatous elements, and their histogenesis remains unclear. The authors examined the serum concentrations of hematopoietic growth factors and performed immunohistochemical studies on an esophageal carcinosarcoma from a patient with marked granulocytosis to determine its histopathogenesis and clonality.
  
  
  METHODS
  The authors examined the case of a 63-year-old man with a polypoid tumor of the esophagus associated with marked leukocytosis (131 x 10(9) per liter). Immunohistochemical staining of the esophageal tumor was performed using monoclonal antibodies against granulocyte-colony stimulating factor (G-CSF), keratin, epithelial membrane antigen (EMA), and vimentin.
  
  
  RESULTS
  The patient's leukocyte count was increased (124 x 10(9) per liter) on admission. Because mature granulocytes predominantly were increased despite the absence of apparent infection, the patient's serum G-CSF concentration was examined and found to be 286.0 pg/mL and to increase with time. After thoracic esophagectomy was performed, granulocyte count and serum G-CSF concentration rapidly normalized. G-CSF concentration was 50-fold higher in the tumor tissue extract than in the extract from normal esophageal tissue. Microscopic examination of the resected specimens revealed that the tumor was comprised of squamous cell carcinoma (SCC) and spindle-shaped sarcomatous elements, and transitional features were observed within these two components. Immunohistochemical examination disclosed cells that were positive for keratin and EMA in the carcinomatous element and vimentin positive cells in the sarcomatous element. However, both types of tumor cells were positive for G-CSF.
  
  
  CONCLUSIONS
  The presence of G-CSF in both SCC cells and spindle-shaped sarcomatous cells indicated that these two components originated from a single clone.
authors.affiliation: The Third Department of Internal Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ota
authors.forename: A
authors.initials: A
authors.lastname: Kato
authors.forename: H
authors.initials: H
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Yonezumi
authors.forename: J
authors.initials: J
authors.lastname: Yamaguchi
authors.forename: M
authors.initials: M
authors.lastname: Musashi
authors.forename: M
authors.initials: M
authors.lastname: Imamura
authors.forename: M
authors.initials: M
authors.lastname: Asaka
mesh_terms: D002296:Carcinosarcoma / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000097:blood; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D016179:Granulocyte Colony-Stimulating Factor / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D016179:Granulocyte Colony-Stimulating Factor