title: Malignant potential regarding mucin phenotypes and endocrine cell differentiation in gastric adenocarcinoma.
abstract: BACKGROUND
  This study was designed to define the relationship between the mucin phenotype and differentiation in endocrine cells, including their biological behavior in gastric adenocarcinoma.
  
  
  METHODS
  A total of 337 cases of solitary gastric adenocarcinoma were studied. The depth of tumor invasion was the mucosa in 58 cases, the submucosa in 206 cases and the muscularis propria in 73 cases. The mucin phenotype was divided into four phenotypes (gastric, intestinal, mixed and null types) based on immunohistochemical staining (HGM, Muc2 and CD10) and histochemical staining (PCS). Endocrine cells were identified by immunohistochemical staining (serotonin, gastrin, pancreatic polypeptide and Chromogranin A staining) in order to examine their relationship to mucin phenotype. Lymph node metastasis was used as a major indicator of the malignant potential.
  
  
  RESULTS
  When lymph node metastasis was analyzed for tumors with submucosa(sm) or muscularis propria invasion, the incidence was significantly higher in the endocrine cell-positive [ECs(+)] group than in the endocrine cell-negative [ECs(-)] group. Namely, in gastric type, the incidence was 22.7% for the ECs(+) group and 0% for the ECs(-) group (p < 0.05). In intestinal type it was 26.9% for the ECs(+) group and 4.5% for the ECs(-) group (p < 0.05). When the 5-year survival rate of patients with a depth of sm or mp carcinoma was analyzed in relation to the mucin phenotype, no significant difference was seen in the survival rate according to the mucin phenotype, but the prognosis tended to be less favorable in the ECs(+) group than in the ECs(-) group (p = 0.06).
  
  
  CONCLUSIONS
  The expression of endocrine cells was thus found to be more important as a prognostic factor than the mucin phenotype.
authors.affiliation: Department of Surgery, Department of Pathology, Chikushi Hospital, Fukuoka University, 377-1 Zokumyoin, Chikushino City, Fukuoka, Japan.
authors.forename: Kazuya
authors.initials: K
authors.lastname: Naritomi
authors.forename: Kitaro
authors.initials: K
authors.lastname: Futami
authors.forename: Sumitaka
authors.initials: S
authors.lastname: Arima
authors.forename: Akinori
authors.initials: A
authors.lastname: Iwashita
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology*; D002454:Cell Differentiation / Q000502:physiology; D053379:Chromogranin A; D002864:Chromogranins / Q000378:metabolism; D019858:Enteroendocrine Cells / Q000378:metabolism / Q000473:pathology*; D005755:Gastrins / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008207:Lymphatic Metastasis; D009077:Mucins / Q000378:metabolism*; D010191:Pancreatic Polypeptide / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*
chemical_list: D053379:Chromogranin A; D002864:Chromogranins; D005755:Gastrins; D009077:Mucins; D012701:Serotonin; D010191:Pancreatic Polypeptide