title: Members of the EpCAM signalling pathway are expressed in gastric cancer tissue and are correlated with patient prognosis.
abstract: BACKGROUND
  We investigated the expression of members of the epithelial cell adhesion molecule (EpCAM) signalling pathway in gastric cancer (GC) testing the following hypotheses: are these molecules expressed in GC and are they putatively involved in GC biology.
  
  
  METHODS
  The study cohort consisted of 482 patients. The following members of the EpCAM signalling pathway were analysed by immunohistochemistry and were correlated with various clinico-pathological patient characteristics: extracellular domain of EpCAM (EpEX), intracellular domain of EpCAM (EpICD), E-cadherin, β-catenin, presenilin-2 (PSEN2), and ADAM17.
  
  
  RESULTS
  All members of the EpCAM signalling pathway were differentially expressed in GC. The expression correlated significantly with tumour type (EpEX, EpICD, E-cadherin, β-catenin, and PSEN2), mucin phenotype (EpEX, EpICD, β-catenin, and ADAM17), T-category (EpEX, E-cadherin, and β-catenin), N-category (EpEX and β-catenin), UICC tumour stage (EpEX, EpICD, β-catenin, and PSEN2), tumour grade (EpEX, EpICD, E-cadherin, β-catenin, and PSEN2), and patients' survival (EpEX, EpICD, and PSEN2). A significant coincidental expression in GC was found for EpEX, EpICD, E-cadherin, β-catenin, PSEN2, and ADAM17. Decreased immunodetection of EpEX in locally advanced GC was not associated with decreased EpCAM mRNA levels.
  
  
  CONCLUSIONS
  All members of the EpCAM signalling pathway are expressed in GC. The expression correlated significantly with each other and with various clinico-pathological patient characteristics, including patients' survival. Thus, the EpCAM signalling pathway is a highly interesting putative therapeutic target in GC.
authors.affiliation: Department of Pathology, Christian-Albrechts-University, Arnold-Heller-Strasse, D-24105 Kiel, Germany.
authors.forename: V S
authors.initials: VS
authors.lastname: Warneke
authors.forename: H-M
authors.initials: HM
authors.lastname: Behrens
authors.forename: J
authors.initials: J
authors.lastname: Haag
authors.forename: S
authors.initials: S
authors.lastname: Krüger
authors.forename: E
authors.initials: E
authors.lastname: Simon
authors.forename: M
authors.initials: M
authors.lastname: Mathiak
authors.forename: M P A
authors.initials: MP
authors.lastname: Ebert
authors.forename: C
authors.initials: C
authors.lastname: Röcken
mesh_terms: D051722:ADAM Proteins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D000072198:ADAM17 Protein; D000368:Aged; D000951:Antigens, Neoplasm / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D015331:Cohort Studies; D000071858:Epithelial Cell Adhesion Molecule; D005260:Female; D057809:HEK293 Cells; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009367:Neoplasm Staging; D053766:Presenilin-2 / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D011379:Prognosis; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000378:metabolism* / Q000473:pathology; D051176:beta Catenin / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism
chemical_list: D000951:Antigens, Neoplasm; C495270:CTNNB1 protein, human; D015820:Cadherins; D015815:Cell Adhesion Molecules; C499379:EPCAM protein, human; D000071858:Epithelial Cell Adhesion Molecule; C508861:PSEN2 protein, human; D053766:Presenilin-2; D012333:RNA, Messenger; D051176:beta Catenin; D051722:ADAM Proteins; D000072198:ADAM17 Protein; C000606462:ADAM17 protein, human