title: Loss of phenotypic expression is related to tumour progression in early gastric differentiated adenocarcinoma.
abstract: OBJECTIVE
  To evaluate the relationship between phenotypic expression and tumour progression as represented by macroscopic features, submucosal invasion and lymph node metastasis in early differentiated gastric adenocarcinoma.
  
  
  METHODS
  One hundred and fifty-five cases of early gastric differentiated adenocarcinoma without any poorly differentiated components were studied. The mucosal and submucosal components of carcinomas and lymph node metastatic lesions were classified into four categories, gastric type (G-type), incomplete intestinal type (I-type), complete intestinal type (C-type) and unclassified type (U-type), based on the combination of the phenotypic expression of HGM (gastric foveolar epithelium), MUC 6 (gastric pyloric glands), MUC 2 (intestinal goblet cells) and CD 10 (small intestinal brush border). In addition, a new classification representing a phenotypic shift from mucosa to submucosa or from primary lesion to lymph node metastasis was established with the categories of preserved group (P-group), loss group (L-group) and acquired group (A-group).
  
  
  RESULTS
  (1) In submucosal carcinoma, U-type was more common in the submucosa (39%) than in the mucosa (9%). (2) U-type was more common in the metastatic lesions (42%) than in the primary lesions (5%). (3) The submucosal component and lymph node metastatic lesions were classified as P-group in 48% and 43% of cases, respectively, and as L-group in 50% and 52% of cases, respectively. (4) Lymph node metastatic lesions comprising undifferentiated carcinoma were classified as L-group in 100% of cases.
  
  
  CONCLUSIONS
  During the course of tumour progression, early differentiated adenocarcinoma at first tends to lose its phenotypic expression despite preserving its morphology, but subsequently morphological dedifferentiation occurs.
authors.affiliation: Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Yao
authors.forename: A
authors.initials: A
authors.lastname: Kabashima
authors.forename: K
authors.initials: K
authors.lastname: Nishiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Maehara
authors.forename: M
authors.initials: M
authors.lastname: Tsuneyoshi
mesh_terms: D000230:Adenocarcinoma / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D000368:Aged; D018450:Disease Progression; D005260:Female; D005752:Gastric Mucins / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008207:Lymphatic Metastasis / Q000473:pathology; D008297:Male; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins / Q000378:metabolism; D015260:Neprilysin / Q000378:metabolism; D010641:Phenotype; D013274:Stomach Neoplasms / Q000145:classification / Q000378:metabolism / Q000473:pathology*
chemical_list: D005752:Gastric Mucins; C524625:MUC2 protein, human; C524734:MUC6 protein, human; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins; D015260:Neprilysin