title: Gastric and intestinal phenotypic cell marker expressions in gastric differentiated-type carcinomas: association with E-cadherin expression and chromosomal changes.
abstract: Gastric and intestinal phenotypic cell markers are widely expressed in gastric carcinomas, irrespective of their histological type. In the present study, the relations between the phenotypic marker expression of the tumour, histological findings, expression of cell adhesion molecules, and the chromosomal changes in gastric differentiated-type carcinomas were examined. The phenotypic marker expression of the tumour was determined by the combination of the expression of the human gastric mucin (HGM), MUC6, MUC2 and CD10, and was evaluated in comparison with the expression of cell adhesion molecules, such as E-cadherin and beta-catenin, and chromosomal changes by comparative genomic hybridization (CGH) in 34 gastric differentiated-type carcinomas. Tumours were classified into the gastric- (G-), gastric and intestinal mixed- (GI-), intestinal- (I-), or unclassified- (UC-) phenotype according to the immunopositivity of staining for HGM, MUC6, MUC2, and CD10. G-phenotype tumours were significantly associated with a higher incidence of differentiated-type tumours mixed with undifferentiated-type component, compared with GI- and I-phenotype tumours (88.9 vs 33.3%, P=0.0498 and 88.9 vs 42.9%, P=0.0397; respectively). HGM-positive tumours were significantly associated with a higher incidence of tumours with abnormal expression of E-cadherin, compared with HGM-negative tumours (66.7 vs 21.1%, P=0.0135). GI-phenotype tumours were significantly associated with a higher incidence of tumours with abnormal expression of E-cadherin, compared with I-phenotype tumours (77.8 vs 21.4%, P=0.0131). HGM-negative tumours were significantly associated with higher frequencies of the gains of 19q13.2 and 19q13.3, compared with HGM-positive tumours (57.9 vs 20.0%, P=0.0382 and 63.2 vs 13.3%, P=0.0051; respectively). MUC6-positive tumours were significantly associated with higher frequencies of the gains of 20q13.2, compared with MUC6-negative tumours (71.4 vs 30.0%, P=0.0349). MUC2-positive tumours were significantly associated with the gain of 19p13.3, compared with MUC2-negative tumours (41.2 vs 5.9%, P=0.0391). I-phenotype tumours were significantly associated with higher frequencies of gains of 5p15.2 and 13q33-34, compared with G-phenotype tumours (66.7 vs 0%, P=0.0481, each) and also associated with higher frequencies of gain of 7p21, compared with GI-phenotype tumours (66.7 vs 0%, P=0.0481). Our present results show that gastric differentiated-type carcinomas have different characteristics according to the phenotypic marker expression of the tumour in terms of histological findings, E-cadherin expression and pattern of chromosomal changes.
authors.affiliation: Department of Surgery, Division of General and Gastroenterological Surgery, Showa University, School of Medicine, Tokyo, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Morohara
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Tajima
authors.forename: Kentaro
authors.initials: K
authors.lastname: Nakao
authors.forename: Nobukazu
authors.initials: N
authors.lastname: Nishino
authors.forename: Shigeo
authors.initials: S
authors.lastname: Aoki
authors.forename: Masanori
authors.initials: M
authors.lastname: Kato
authors.forename: Masaaki
authors.initials: M
authors.lastname: Sakamoto
authors.forename: Kimiyasu
authors.initials: K
authors.lastname: Yamazaki
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Kaetsu
authors.forename: Satoshi
authors.initials: S
authors.lastname: Suzuki
authors.forename: Akira
authors.initials: A
authors.lastname: Tsunoda
authors.forename: Tetsuhiko
authors.initials: T
authors.lastname: Tachikawa
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Kusano
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000096:biosynthesis* / Q000235:genetics; D015820:Cadherins / Q000096:biosynthesis*; D002277:Carcinoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002869:Chromosome Aberrations; D004273:DNA, Neoplasm / Q000032:analysis / Q000235:genetics; D005260:Female; D005752:Gastric Mucins / Q000096:biosynthesis / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins / Q000096:biosynthesis / Q000235:genetics; D015260:Neprilysin / Q000096:biosynthesis / Q000235:genetics; D009693:Nucleic Acid Hybridization; D010641:Phenotype; D013274:Stomach Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D051176:beta Catenin / Q000096:biosynthesis
chemical_list: D014408:Biomarkers, Tumor; D015820:Cadherins; D004273:DNA, Neoplasm; D005752:Gastric Mucins; C524625:MUC2 protein, human; C524734:MUC6 protein, human; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins; D051176:beta Catenin; D015260:Neprilysin